The Tip of the Iceberg – the much bigger problem of high insulin levels

The US and Canada and much of the westernized world is in the midst of a Diabetes epidemic but this is just the tip of the iceberg when it comes the underlying metabolic disruption caused by insulin. The part of the iceberg that is visible and that people know about is hyperglycemia (elevated blood sugar) but the part that is invisible and that few are aware of  hyperinsulinemia (elevated blood insulin levels) which often precedes a diagnosis of pre-diabetes or Type 2 Diabetes by decades. It is this high circulating level of insulin that contributes to the significant risk of developing cardiovascular disease including heart attack and stroke, hypertension (high blood pressure), elevated cholesterol and triglycerides, non-alcoholic fatty liver (NAFLD), Poly Cystic Ovarian Syndrome (PCOS), Alzheimer’s disease and other forms of dementia, as well as certain forms of cancer including breast and colon / bowel cancer.

High blood sugar may or may not be a symptom of high levels of insulin levels and in the early stages of metabolic dysfunction almost 75% of people will have normal fasting blood glucose yet have abnormally high levels of circulating insulin.  As a result, these people are at increased risk of the metabolic diseases mentioned above but unlike someone already diagnosed with Type 2 Diabetes they have no idea!

High circulating levels of insulin is entirely missed by most routine lab tests because blood sugar is being monitored as the first indication that someone is becoming insulin resistant.  By the time blood glucose levels are abnormal, the β-cells of the pancreas that produce insulin are already being over-taxed to the point of exhaustion.  Physicians have “answers” (lab test results) but oftentimes are asking the wrong questions. That is, having normal fasting blood sugar or even HbA1C (3-month blood sugar average) does not necessarily mean everything is “fine”.  Most sobering is that by the time a person is diagnosed with Type 2 Diabetes they have already lost ~ 40% of their beta-cells mass sometimes more – cell loss which is currently thought to be unrecoverable.

The healthy human body maintains blood sugar in a tightly-regulated range between 60-100 mg/dl (3.3-5.5 mmol/L).  When a healthy person eats food containing carbohydrate – whether as the starch in bread, pasta and rice, the sugar in milk (lactose), fruit (fructose), simple table sugar (sucrose) or high fructose corn syrup in commercially prepared foods, special glucose-sensing cells in the small intestine release signalling hormones called incretin hormones in response to the presence of these carbohydrates. The incretin hormones tell the pancreas to release insulin which in turn tells the body’s cells what to do with the energy from the food we eat; either (1) burn it or (2) send it to the liver to store it, first as glycogen, and the remainder as fat (adipose tissue).  This is called fuel partitioning. When metabolic processes respond appropriately, blood sugar rises modestly after eating carbohydrate-based food but is quickly restored to its normal, tightly-regulated range soon afterwards.

Metabolic problems begin because people eat foods that contain some form of carbohydrate every few hours which results in frequent release of insulin. Glycogen levels in the muscle and liver remain close to full due to the steady supply of refined or processed carbohydrate-based food compounded by the reality that body’s cells are rarely challenged to use stored energy. In the early stages cells simply stop responding appropriately to insulin’s signal. This is called insulin resistance. Insulin resistance is the decreased ability of our cells to partition fuel. It can be compared to someone hearing a noise such as their neighbour playing music, but after a while their brain “tunes out” the noise.  Even if the neighbour gradually turns up the volume of the music, the person’s brain compensates by further tuning out the increased noise. To compensate for insulin resistance, the β-cells of the pancreas begin producing and releasing more insulin, which results in hyperinsulinemia – too much insulin in the blood.

In the early stages the body is simply trying to keep blood sugar levels within its normally tightly regulated range by making and releasing more insulin to force the cells of the body to take up the excess glucose and burn it, but this just makes the problem worse. It is the increasingly high circulating levels of insulin that contribute to the health risks and metabolic disease listed above.

Just as high blood sugar is not necessarily associated with high circulating levels of insulin, neither is obesity.  Approximately 1/3 of insulin-resistant people are lean. A person who is obese simply makes more fat cells (adipocytes) in order to store the excess energy as sub-cutaneous fat (fat under the skin) which serves as a protective mechanism. Contrary to what most people assume, people don’t become insulin resistant because they are fat; becoming fat may be a protective response to high levels of circulating insulin. Those who are lean but insulin-resistant are thought to have a lower ‘personal fat threshold’ than those that become overweight of obese. That is, they are limited in terms of how many new fat cells their body can make to store excess energy, so they store the excess energy in and around their organs in what’s called visceral fat.  This is where the metabolic disruption occurs.  Whether the person is obese or lean, once they have exceeded their personal fat threshold, the result is the same.

Assessing whether my clients have higher than ideal levels of insulin is as important as assessing whether they already have higher than ideal levels of blood sugar, in fact it is even more important. When people already have pre-diabetes or Type 2 Diabetes, they’ve likely been told by their doctors that they are increased cardiovascular risk and that this is a risk factor for other metabolically related conditions, including high blood pressure, fatty liver disease, Alzheimer’s and other forms of dementia and certain types of cancer. Having normal blood sugar many are told “everything is fine” when very often it is not.  These people are at risk and don’t even know it.

It is important that my clients know whether they have symptoms of hyperinsulinemia and to help them understand the factors that contribute to it. This helps people to have the motivation to make necessary dietary and lifestyle changes to reduce their disease risk and totally avoid the progression to Type 2 Diabetes, long before blood sugar levels begin to rise.

For those that already are pre-diabetic or been diagnosed as having Type 2 Diabetes, it is not too late. A carbohydrate-modified diet as well implementing very specific lifestyle changes makes the reversal of symptoms entirely possible and does not require dietary or exercise extremes.

I think that for too long we as clinicians have tackled this as an insulin problem caused by overweight and created by “eating too much and moving too little” rather than as the exact opposite; that people get overweight because of an underlying insulin problem. When we address hyperinsulinemia, weight, blood sugar, blood pressure and high cholesterol and triglycerides are corrected. There are studies documenting this (covered in previous articles) and my “A Dietitian’s Journey” tells my own sample-set-of-one story reversing Type 2 Diabetes that I had for 10 years, as well as the related conditions of high blood pressure and abnormal cholesterol and triglycerides. It can be done.

Have questions as to how I can help you either in-person in my office or via Distance Consultation? Please send me a note using the Contact Me form above and I will reply as soon as I am able.

To our good health!

Joy


you can follow me at:

 https://twitter.com/lchfRD

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References

Reaven, G., Insulin resistance, type 2 diabetes mellitus, and cardiovascular disease: the end of the beginning. Circulation, 2005. 112(20): p. 3030-2.

Reaven, G.M., Pathophysiology of insulin resistance in human disease. Physiol Rev, 1995. 75(3): p. 473-86.

Taylor, R. and R.R. Holman, Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Clin Sci (Lond), 2015. 128(7): p. 405-10.

Reaven, G., The metabolic syndrome or the insulin resistance syndrome? Different names, different concepts, and different goals. Endocrinol Metab Clin North Am, 2004. 33(2): p. 283-303.

Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.

Ludwig, D.S. and M.I. Friedman, Increasing adiposity: consequence or cause of overeating? JAMA, 2014. 311(21): p. 2167-8.

Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Alzheimer’s Disease as Glucose Dysfunction in the Brain

I’d heard of Alzheimer’s disease (AD) being referred to by some clinicians as “Type 3 Diabetes” but until yesterday the link between AD and abnormalities in glucose metabolism in the brain was an academic interest. Now it’s personal. You see, yesterday I found out that my dad (90 years old) was diagnosed with Alzheimer’s disease. His once-sharp mind is no longer capable of recalling what happened yesterday or in fact what just happened. It is as though he has “partial amnesia”.

The majority of those that are diagnosed with AD (95%) have the same form of the disease that my dad has called sporadic Alzheimer’s disease. Only 5% are diagnosed with a genetically-linked form inherited from the maternal side of the family [2].

In sporadic Alzheimer’s disease the first part of memory that is affected is the person’s unique memory of specific events (called episodic memory).

I remember three or four years ago asking my dad to recount the details of our family history from his side of the family that he often told yearly at holiday dinners – yet he couldn’t even remember their existence! I tried prompting him with parts of the story to try and trigger the memory but was met with “I’m sorry dear, I don’t recall”.  I was dumbfounded because he told this same exact story over and over again for years, and then suddenly it was gone. From his perspective, it didn’t exist. His behaviour and other forms of memory were completely normal, so I discounted his forgetfulness to “aging” but I now know this was the first noticeable indication that something was not working as it should.

As Healthy People Age

As healthy people age, brain cells waste away (atrophy) and are not replaced such that brain volume decreases at a rate of about 1.6% / decade after the age of 30 years old [1]. So, at 40 years old, a person is expected to have a 1.6% decrease in brain volume, at 50 years old a 3.2% decrease, and so on. At 90 years old, a healthy person would be expected to have lost a little less than 10% of their brain volume.

My maternal grandmother was healthy and lived until well over 100 years old and I can see in retrospect that the kinds of memory changes my dad was showing a few years ago (at age ~85) were not simply part of normal aging.

Changes in Alzheimer’s Disease

Over the last 30 years, there has been a lot of progress in terms of understanding changes in brain energy metabolism during AD as compared with what occurs in normal, healthy aging. Until recently, many thought that lower brain function of those developing AD led to less use of glucose by the brain, but now it is thought that it is actually the other way around; that decreased glucose uptake into the cells of the brain leads to decrease metabolism in the brain. This decrease glucose uptake into the cells of the brain are believed to be a critical part of the early development of AD and that significantly lower brain glucose metabolism may be present long before the onset of any clinically measurable mental decline in AD [2].

It is now widely believed that there is decreased glucose metabolism in the brain in those with AD. When compared with healthy aged-matched people, those with AD have ~25% more brain atrophy than would be expected for their age. This is, after correction for age-associated brain atrophy, the majority of PET scan studies conducted from 1981- until the present, show that glucose utilization by the brain is decreased by as much as ~25% in AD [2].

While healthy, normal aging is associated with some slow brain atrophy, it is not thought to be associated with decreased glucose metabolism. 

Normal Brain Glucose Use

The brain, heart, liver and kidneys together use ~ 60% of the body’s resting metabolic energy needs and while the heart and kidneys are metabolically more active than the brain, the brain is larger. As a result, the brain uses about ¼ of the body’s total energy needs [2]. This energy is used for blood flow in the brain, use of oxygen by the brain and for glucose metabolism – but most of the glucose used by the brain is used to maintain a glucose gradient (difference) between glutamate neurons which enable communication along this neurotransmitter system.

Glucose transporters (GLUTs) bring glucose into the brain in a three-step process: (i) Transport across the blood-brain barrier (ii) transport into the brain cells (astrocytes) and (iii) transfer of the glucose into the neurons of the glutamate neurotransmitters.

When the brain is active, the Adenosine Triphosphate molecule (ATP) which is the “currency” of energy transfer inside cells decreases, and the brain needs more glucose, so glucose uptake is stimulated by the cell. It is unknow at what point partial reduction in glucose transport begins to limit brain function in AD.

Brain Glucose Use in Alzheimer’s Disease

Alzheimer’s Disease is a neurodegenerative disease that results in progressive worsening of memory and cognitive function, as well as behavior changes and disorientation.

Even though normal healthy aging is not associated with AD. Aging itself is the main risk factor for sporadic AD, with rates ~doubling every five years after 65 years of age [3] and affecting more than 60% of people over the age of 95 years of age [4].

The brain of those with AD is marked by an accumulation of βeta-amyloid plaques between brain cells and by neurological “tangles” within brain cells.  As mentioned earlier, there are two types of AD – familial / early onset AD and sporadic / late onset AD. The early onset type is much rarer (~5% of all AD) and is inherited from the maternal (mother’s) side of the family. Except for a different age of onset, what is seen clinically, and the progression of decreased cognitive function is not significantly different between the two types of AD. The βeta –amyloid plaques occur slowly before any change in memory or understanding become apparent. The progressive brain atrophy speeds up later in the disease process, bringing the cognitive decline frequently associated with AD.

There are also other forms of dementia besides Alzheimer’s disease, including fronto-temporal dementia and vascular dementia but these are very different from either of the two sub types of AD.

PET scan studies point to lower brain glucose metabolism in AD, with difference between normal aging subjects and those with AD being as much as ~20–25% lower in AD with most of the atrophy occurring in the region of the brain called the hippocampus, which is involved in memory processing.

Mild Cognitive Impairment (MCI)

There is intermediate stage between normal healthy aging and AD, called Mild Cognitive Impairment (MCI) which includes some decreased thinking ability (cognitive decline). When these thought process changes and memory loss are present in the elderly, but don’t significantly affect daily life or interactions it is considered to be MCI. There are a few studies of glucose metabolism in MCI which show that it is lower than in healthy aged-match controls but less than in moderate to severe AD.

As MCI progresses to AD, glucose usage decreases in additional regions of the brain (cingulate, inferior parietal lobes, temporal lobes) [2].

Nutritional Factor that Affects Glucose Metabolism

The omega-3 fatty acid found mainly in fatty fish known as Docosahexaenoic acid (DHA; 22:6ω3) is known to have an important role in normal brain development. In animal studies,  supplementation with DHA was found to increase expression of the glucose transporters (GLUTs) that bring glucose into the brain and in primate studies, brain DHA concentration was found to be directly proportional to brain glucose uptake in the same region of the brain [2]. Insufficient intake of DHA and/or low levels in the hippocampus (the region of the brain initially impacted by AD) may play a role in cognitive decline in older adults.

Metabolic Factors that Affect Glucose Metabolism

While the glucose transporters (GLUTs) involved in getting glucose across the blood-brain barrier and into the brain cells (GLUT1) and across glutamate neurons (GLUT3) are not sensitive to insulin, GLUT4 which is another glucose transporter involved in memory and cognition in areas of the brain including the hippocampus are insulin-sensitive [5]. It is thought that brain insulin signaling may be defective in AD [5].

Older adults and the elderly often develop glucose intolerance which often progresses to Type 2 Diabetes then to Metabolic Syndrome which is a combination of Type 2 Diabetes, high blood pressure (hypertension), increased waist circumference (visceral obesity) and abnormal cholesterol tests (dyslipidemia).

Insulin resistance, which often comes before glucose intolerance / high blood sugar tops the list of known risk factors to cognitive decline [5, 6] and younger adults that are obese are predisposed to Metabolic Syndrome which is associated with increased risk of degenerative changes in the brain [6].

Decreased skeletal muscle mass (sarcopenia) in older adults and the elderly may contribute to the increased risk of insulin resistance associated with aging, as muscle is the main site of insulin-mediated glucose utilization in the body. In older adults, adequate dietary protein intake as well as incorporating some form of resistance training of large muscle groups may play a role in decreasing cognitive decline by increasing glucose update from the blood to the muscle where it can then be transported to areas of the brain.

Ketones: the body’s preferred alternative fuel

In healthy people that haven’t eaten in while (such as after an overnight fast or a during relatively long period of time between meals) ketone bodies (ketones) are the body’s key replacement fuel which maintains brain function. The brain even has a separate transport system for ketones which is independent of glucose transport [2].

When blood sugar levels drop over a period of several hours or even days during fasting the energy requirements of the body are dependent on the availability of two ketonesacetoacetate and β-hyydroxybutyrate for normal function.  During prolonged fasting over a period of days and in starvation up to ~60% of the human brain’s energy requirements can be met by a combination of acetoacetate and β-hydroxybutyrate [7].

The brain can convert ketones to ATP, the energy “currency” of the cell by oxidizing ketones (converting β-hydroxybutyrate to acetoacetate, acetoacetate to acetoacetyl CoA, and acetoacetyl CoA to acetyl CoA which then is used to generate ATP).  While brain cells (astrocytes) can beta-oxidize fatty acids [8] to produce ketones, transport of fatty acids across the blood-brain barrier is too slow to make fatty acids as useful alternative as fuel for the brain.

Ketones cannot fully replace glucose as a brain fuel as a small quantity of glucose is essential for the brain, however this does not need to be supplied in the diet but can be manufactured by the liver (as well as to a lesser degree by the kidneys and the intestines) from fat or protein in a process known as gluconeogenesis (literally “making new glucose”).

The body can make ketones from fat stores in a process called ketogenesis but first there needs to be a lowering of blood glucose, which will result in decreased blood insulin levels. This can occur during fasting, as well as by following a low-carbohydrate diet. When insulin level decreases, free fatty acids from fat cells (adipose tissue) can be freed into the blood. These long chain fatty acids are then brought to the liver where they are broken down (β-oxidized) to acetyl CoA, which are then condensed into ketones.

Use of a Therapeutic Ketogenic Diet in Alzheimer’s Disease

It is thought that in Alzheimer’s disease the combination of brain glucose insufficiency and the inadequate supply of naturally-produced ketones (which normally would naturally be produced by the body in response to low blood glucose) puts the high energy consuming areas of the brain in mild, but constant shortage of energy.

Since the brain can’t get its main fuel source which is glucose nor its preferred back- up fuel source which are ketones (because blood glucose doesn’t drop) this forces the brain to rely on a third, but inadequate source of energy – which is making glucose from fat stores or protein (gluconeogenesis).

Over time, specific regions of the brain such as the hippocampus are thought to be put in a situation of long-term chronic fuel shortage and gradually these brain cells ‘burn out’, which leads to the brain changes seen in Alzheimer’s Disease [2].

It is thought that if brain ketone metabolism is unaffected in AD – or at least is affected less than glucose, a ketogenic diet may provide the brain with ketones it can use as an alternative fuel to glucose, enabling it to function more normally, reducing cognitive decline resulting from brain glucose insufficiency.

If you have questions about how eating a low carbohydrate diet can significantly reduce insulin resistance, a major risk factor for Alzheimer’s disease, as well as reverse symptoms of Metabolic Syndrome, please send me a note using the “Contact Me” form on this web page and I’ll be glad to reply as soon as I’m able. Remember, I provide services via Distance Consultation (via secured Skype) as well as in-person in my Coquitlam office.

To our good health!

Joy


you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

 

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

References

  1. Svennerholm, L., K. Boström, and B. Jungbjer, Changes in weight and compositions of major membrane components of human brain during the span of adult human life of Swedes. Acta Neuropathol, 1997. 94(4): p. 345-52.
  2. Cunnane, S., et al., Brain fuel metabolism, aging, and Alzheimer’s disease. Nutrition, 2011. 27(1): p. 3-20.
  3. Canadian study of health and aging: study methods and prevalence of dementia. CMAJ, 1994. 150(6): p. 899-913.
  4. Brayne, C., et al., Dementia before death in ageing societies–the promise of prevention and the reality. PLoS Med, 2006. 3(10): p. e397.
  5. Watson, G.S. and S. Craft, Modulation of memory by insulin and glucose: neuropsychological observations in Alzheimer’s disease. Eur J Pharmacol, 2004. 490(1-3): p. 97-113.
  6. Raffaitin, C., et al., Metabolic syndrome and risk for incident Alzheimer’s disease or vascular dementia: the Three-City Study. Diabetes Care, 2009. 32(1): p. 169-74.
  7. Cahill, G.F., Fuel metabolism in starvation. Annu Rev Nutr, 2006. 26: p. 1-22.
  8. Guzmán, M. and C. Blázquez, Is there an astrocyte-neuron ketone body shuttle? Trends Endocrinol Metab, 2001. 12(4): p. 169-73.

 

When Fat Became the Villain

Those who are younger than 40 years old probably grew up hearing that saturated fat is “bad” and polyunsaturated fat is “good”, but where did we get this idea and is it true?

The process of what I call the “vilification of fat” began when researcher Ancel Keys presented a graph at a talk at Mount Sinai Hospital in New York in January 1953 and later published it in a research paper titled Atherosclerosis: a problem in newer public health [1]. It was said to show the relationship between ‘fat calories as a percentage of total fat” and the number of ‘deaths from degenerative heart disease per 100,000 people’ for men between the ages of 45-49 and 55-59. The linear relationship of these data points from the Six Country Study (Japan, Italy, England & Wales, Australia, Canada and the USA) suggested that there was a strong relationship between the amount of fat calories as a percentage of dietary intake and deaths from degenerative heart disease for men aged 55-59. At the time of publication of the Six Country Study, Keys said that it was possible to only get complete data from those 6 countries [1] at the time. He concluded;

“Whether or not cholesterol etc. are involved, it must be concluded that dietary fat somehow is associated with cardiac diseases mortality, at least in middle age [1].

In Key’s mind, the total amount of dietary fat was “somehow associated” with cardiac death in middle aged men, but he expressed doubt whether or not cholesterol was involved.

In 1957, Yerushalamy and Hilleboe [2] published data from 22 countries which showed there was no linear relationship between ‘fat calories as a percentage of total fat” and the number of ‘deaths from degenerative heart disease per 100,000 people’.

Keys went onto conduct what became known as the Seven Country Study which collected data on almost 13,000 men aged 40-59 from the USA, Finland, the Netherlands, Yugoslavia, Greece and Japan. Findings were only published in 1970 in the journal Circulation in several papers from separate countries [3]. Keys no longer believed that total fat was associated with heart disease but that saturated fat was the villain. Keys concluded that the average consumption of animal foods (with the exception of fish) was positively associated with 25-year heart disease death rates and that the average intake of saturated fat was strongly related to 10 and 25-year coronary heart disease death rates.

What solidified this association was that the 1970 publication on the Seven Country Study contained Keys’ 1953 graph from the Six Country Study (above) [4]. Even though it indicated a linear relationship between total fat intake and degenerative heart disease it became tied in the minds of many that this graph “proved” that saturated fat was linked to heart disease—even though that is not what the graph shows at all.  It isn’t even about saturated fat. Keys also neglected to mention Yerushalamy and Hilleboe’s data from 22 countries showed no relationship between total fat consumption and heart disease.

The Diet Heart Hypothesis

The diet-heart hypothesis originated with Ancel Keys and is the belief that eating foods high in saturated fat contributes to heart disease. Keys believed that replacing fat from meat, butter and eggs with newly-created polyunsaturated vegetable oils such as soybean oil would reduce heart disease and deaths by lowering blood cholesterol levels.

The Sugar Industry Funding of Research Vilifying Fat

In the mid-1960’s, the Sugar Research Foundation (predecessor of the Sugar Association) wanted to offset research that had been published and that suggested that sugar was a more important a cause of heart disease and stroke from atherosclerosis than dietary fat. The Sugar Research Foundation invited Dr. Fredrick Stare and the late Dr. D. Mark Hegsted of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board and then approved $6,500 in funds ($50,000 in 2016 dollars) to support a review article that would respond to the research showing the danger of sucrose [5]. Letters exchanged between the parties came to light a November 2016 article published by Kearns et al [6] which said that the Sugar Research Foundation had tasked the Harvard researchers with preparing “a review article of the several papers which find some special metabolic peril in sucrose and, in particular, fructose [7]”.

The Sugar Industry paying researchers to blame dietary fat and vindicate sugar for heart disease seems a little like the tobacco industry having secretly funded articles demonstrating that something other than smoking was responsible for lung cancer.

In August 1967 the New England Journal of Medicine published the first review article written by Drs. Stare, Hegsted and McGandy titled “Dietary fats, carbohydrates and atherosclerotic vascular disease” which stated;

Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol”.

The report concluded;

the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.”

The Harvard researchers went on to say;

there can be no doubt that levels of serum cholesterol can be substantially modified by manipulation of the fat and cholesterol of the diet” and that “on the basis of epidemiological, experimental and clinical evidence, that a lowering of the proportion of dietary saturated fatty acids, increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit.

At no point did Stare, Hegsted and McGandy disclose that they were paid by the Sugar Research Foundation for the two-part review.

A commentary in the Journal of Accountability in Research [8] summarized the significance of those articles as follows;

“Researchers were paid handsomely to critique studies that found sucrose [sugar] makes an inordinate contribution to fat metabolism and heart disease leaving only the theory that dietary fat and cholesterol was the primary contributor.”

The same Dr. Hegsted that was funded by the Sugar Industry to write the above articles vindicating sugar and vilifying dietary fat went on to work on editing the 1977 US Dietary Guidelines [9], which entrenched the vilification of fat into the US Food Pyramid for the next 40+ years. The rest, they say, is history.

The same year (1977), Canada’s Food Guide recommended that Canadians limit fat to <30% of daily calories with no more than 1/3 from saturated fat but did not specify an upper limit for dietary cholesterol. This was based on the belief that total dietary fat and saturated fat were responsible blood levels of LDL cholesterol levels and total serum cholesterol [10]. Cholesterol in general (total cholesterol) and LDL cholesterol was assumed to be tied to heart disease, so the focus was on lowering the proxy measurements of LDL cholesterol and total cholesterol.

Recommendations for the continued restriction of dietary fat continued in both the US and Canada in the 2015 revision of the Dietary Guidelines based on the enduring belief that lowering saturated fat in the diet would lower blood cholesterol levels and reduce heart disease.

The question is does it?

A 2018 study published in the journal Nutrients looked at health and nutrition data from 158 countries from 1993-2011 and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease and that high carbohydrate consumption,  particularly as cereals and wheat was most associated with the risk of cardiovascular disease [11]. Significantly, both of these relationships held up regardless of a nation’s average national income.

These findings support those of the 2017 PURE (Prospective Urban and Rural Epidemiological) study, the largest-ever epidemiological study which recorded dietary intake of 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations. The PURE study found an association between raised cholesterol and lower  cardiovascular risk and that “higher carbohydrate intake was associated with higher risk of total mortality”. It also reported that “total fat and individual types of fat were related to lower total mortality (death)” [12].

A recent study published in the American Journal of Clinical Nutrition reports that long-term consumption of the saturated fat found in full-fat dairy products is not associated with an increased risk of cardiovascular disease (atherosclerosis, coronary artery disease, etc.) or other causes of death, and may actually be protective against heart attack and stroke [13].

This recent large-scale epidemiological data provides strong evidence that eating a diet containing saturated fat is not associated with heart disease. While eating saturated fat raises blood levels of LDL cholesterol, we now know that there is more than one type of LDL cholesterol and only the small, dense LDL cholesterol is linked to atherosclerosis. The large, fluffy LDL is protective [14].

We now know that fat was made out to be the villain in scientific reviews paid for by the sugar industry and this combined with Ancel Key’s Diet-Heart Hypothesis ended up being the impetus for the creation of an entire food industry designed to extract fat from industrial seed oils, such as soybean oil and rapeseed (Canola). These industrial seed oils are the so-called “healthy polyunsaturated fats” that we are encouraged to eat instead of so-called “dangerous” saturated fat, yet these industrial seed oils are only able to be produced using solvent-based chemical extraction under very high temperature. Should we be confident in industrial fats brought to us by the same industry that brought us “trans fats”? With a lack of evidence that natural fats such as butter or cream are dangerous, perhaps eating a bit of real animal fat and plenty of natural plant-based monounsaturated fats such as olive oil is the better way to go?

For more than forty years, generations of Americans and Canadians have avoided eggs, full fat cheese and creamery butter – and done so because they have believed that saturated fat raising LDL cholesterol predisposed them to heart disease. We know much more than we did in the 1970s when the first Dietary Guidelines were created in the US (under the watchful editorial oversight of one of the researchers that had been paid by the sugar industry to vilify fat).  We now know that eating foods with saturated fat will raise LDL-cholesterol, but not all LDL-cholesterol is “bad”[14]. Before we knew this high total LDL-cholesterol (LDL-C) was seen as a good proxy (indirect substitute) measurement for heart disease risk, but no longer.

It has been known since the early 1990s that a high TG:HDL ratio is very good estimator of coronary heart disease risk [15].

The measurement of the LDL-cholesterol particle number (LDL-P) which measures the actual number of LDL particles is a much stronger predictor of cardiovascular events than LDL-C [16] because the more particles there are, the more small, dense LDL there are.

The ratio of apolipoprotein B (apoB): apolipoprotein A (apoA) is another good estimator of cardiovascular risk. Lipoproteins are particles that transport cholesterol and triglycerides (TG) in the blood stream and are made up of apolipoproteins, phospholipids, triglycerides and cholesterol. Apolipoprotein B is an important component of many of the lipoprotein particles associated with atherosclerosis, such as chylomicrons, VLDL, IDL, LDL – with most found in LDL. Since each lipoprotein particle contains one apoB molecule, measuring apoB enables the determination of the number of lipoprotein particles that contribute to atherosclerosis and for this reason that ApoB is considered a much better predictor of cardiovascular disease risk than LDL-C [17].

In light of the recently published epidemiological evidence and much stronger proxy measurement of cardiovascular risk we must update our thinking that fat in general, or saturated fat in particular is the “villain”. It’s not.

Perhaps you could use some help as to which fats you should eat more of and in what amounts, or on deciding on what ratio of protein to fat in your diet will best help you reach your health and weight goals? I can help.

I provide services via Distance Consultation (Skype, long distance telephone) as well as in-person in my Coquitlam office.

If you have questions on my services, please send me a note using the Contact Me form located on the tab above, and I will reply as soon as I’m able.

To our good health!

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Keys, A., Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp N Y, 1953. 20(2): p. 118-39.
  2. Yerushalamy, J. and Hilleboe HE, Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med, 1957. 57(14): p. 2343-54.
  3. Coronary heart disease in seven countries. Summary. Circulation, 1970. 41(4 Suppl): p. I186-95.
  4. Harcombe, Z., An examination of the randomised controlled trial and epidemiological evidence for the introduction of dietary fat recommendations in 1977 and 1983:  A systematic review and meta-analysis. 2015, University of the West of Scotland.
  5. Husten, L., How Sweet: Sugar Industry Made Fat the Villain. 2016.
  6. Kearns, C.E., L.A. Schmidt, and S.A. Glantz, Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med, 2016. 176(11): p. 1680-1685.
  7. McGandy, R.B., D.M. Hegsted, and F.J. Stare, Dietary fats, carbohydrates and atherosclerotic vascular disease. N Engl J Med, 1967. 277(4): p. 186-92 contd.
  8. Krimsky, S., Sugar Industry Science and Heart Disease. Account Res, 2017. 24(2): p. 124-125.
  9. Hegsted D.M. Introduction to the Dietary Goals for the United States. p. 17 of 130.
  10. McDonald, B.E., The Canadian experience: why Canada decided against an upper limit for cholesterol. J Am Coll Nutr, 2004. 23(6 Suppl): p. 616S-620S.
  11. Grasgruber, P., et al., Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries. Nutrients, 2018. 10(4).
  12. Dehghan, M., et al., Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet, 2017. 390(10107): p. 2050-2062.
  13. de Oliveira Otto, M.C., et al., Serial measures of circulating biomarkers of dairy fat and total and cause-specific mortality in older adults: the Cardiovascular Health Study. Am J Clin Nutr, 2018.
  14. Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
  15. Manninen, V., et al., Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. Circulation, 1992. 85(1): p. 37-45.
  16. Cromwell, W.C., et al., LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study – Implications for LDL Management. J Clin Lipidol, 2007. 1(6): p. 583-92.
  17. Lamarche, B., et al., Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Québec cardiovascular study. Circulation, 1996. 94(3): p. 273-8.

 

 

Important Warning Signs of Developing Type 2 Diabetes

INTRODUCTION: To avoid ignoring important warning signs that our body is not working as it should, we first need to understand how it is supposed to work and what begins to go wrong — long before we receive a diagnosis of Type 2 Diabetes. That way we can make the necessary dietary and lifestyle changes to prevent it from ever progressing further. Type 2 Diabetes can be prevented and this article explains what to look for.


When the human body is healthy, it maintains blood sugar between 3.3-5.5 mmol/L (60-100 mg/dl). The beta (β) cells of the pancreas produce the hormone insulin, store it and release it into the blood in the correct amount and at the right time. The β-cells of healthy people are constantly making insulin and storing most of it within the cell until it receives a signal that food with carbohydrate has been eaten. β-cells constantly release a little bit of insulin all the time in very small pulses called basal insulin. This basal insulin allows the body to use blood sugar even when the person hasn’t eaten for several hours or even longer.

Normal insulin and glucose curves (adapted from Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.)

The rest of the insulin stored in β-cells is only released when blood sugar rises after the person eats foods containing carbohydrate. This insulin is released in two phases [1]. The first-phase insulin response occurs as soon as the person begins to eat and peaks within 30 minutes and can be seen at 30 minutes on the graph above.

The amount of the first-phase insulin release is based on how much insulin the body is used to needing each time the person eats. Provided the person eats more or less the same amount of carbohydrate-based food at each meal, the amount of insulin in the first-phase insulin response will be enough to move the excess glucose from the food into the cells, returning blood sugar to ~5.5 mmol/L (100 mg/dl). If there is not enough insulin in the first-phase insulin response, the β-cells will release a smaller amount of insulin within an hour to an hour and a half of the person beginning to eat. This is the second-phase insulin response [1] and can be seen at 60 minutes on the graph above.

In healthy people, the combination of the larger first-phase insulin response and the smaller second-phase insulin response is sufficient to keep blood sugar level from rising above 7.8 mmol/L (140 mg/dl), even after the person has eaten a lot of carbohydrate. In healthy people whose β-cells are working properly and receiving the correct signals from their small intestines, blood sugar levels will return to their normal fasting level between 4.6-5.5 mmol/L (83-100 mg/dl range) by 2 hours.

 Dysfunctional Insulin Release & Insulin Resistance

In the early stages when people are becoming insulin resistant, receptors in the liver and muscle cells begin to stop responding properly to insulin’s signal. To compensate, the β-cells of the pancreas begin producing and releasing more insulin (hyperinsulinemia). This can be seen on the graph below (in black), which is superimposed over the normal glucose and insulin curve (light grey).

As a result of the insulin resistance of the liver and muscle cells, it takes more insulin to move the same amount of glucose into the cells.

Beginning of insulin resistance and hyperinsulinemia (adapted from Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.)

At this point, only 3% of people will meet the criteria for diagnosis with Type 2 Diabetes [2].

Insulin resistance doesn’t come by itself but is accompanied by hyperinsulinemia — too much insulin in the blood. Hyperinsulinemia is the result of the body trying to compensate for insulin resistance by making more and more insulin to try to keep blood sugar levels normal. With ongoing high intake of carbohydrate, especially refined carbohydrate the amount of insulin that has to be released from the β-cells is enormous (see the dashed black line on the graph below compared to the dashed grey line of a healthy person).

Advancing insulin resistance and hyperinsulemia (adapted from Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.)

The first-phase insulin response won’t produce enough insulin be able to clear the extra blood glucose after a high carbohydrate meal into the cells and even the second-phase insulin response won’t be enough to overcome the insulin resistance of the cells. At this point, the β-cells of the pancreas are unable to make enough insulin to clear the excess glucose from the blood and blood glucose rises above the normal high peak of 7.8 mmol/L (140 mg/dl), to levels of 9.0 mmol/L (160 mg/dl) or higher.

In this case, since blood glucose is able to be returned to baseline after 2 hours, only 7% of people will be diagnosed with Type 2 Diabetes (T2D) [2] but clearly these people’s insulin response and blood glucose response (in black) is very dysfunctional compared to that of a healthy person (in grey).  In fact, almost 30% of people will have normal blood glucose, but they already have hyperinsulinemia and insulin resistance.

If the body is forced to continue to process a high refined-carbohydrate diet, it will make more and more insulin but not without a cost to the β-cells of the pancreas. β-cell failure will begin to occur as a result of this high demand [3].

Since most physicians only monitor fasting blood glucose (FBG) to detect whether their patients are becoming insulin resistant or Diabetic, they and their patients have no idea that between ½ and 1 hour after beginning a meal, the person’s blood sugar had reached levels well in excess of the normal high peak of 140 mg/dl (7.8 mmol/L). Blood sugar in these individuals often goes as high as 9.0 mmol/L (160 mg/dl ) and even higher but no one knows because no one is checking for it.

A standard fasting blood glucose test won’t pick this up and even if a doctor requisitions a two-hour oral glucose tolerance test (OGTT) where the person is required to fast and then drink a standard amount of glucose and have their blood sugar checked, glucose levels are only measured at baseline when the person is fasting (FBG) and after 2 hours, by which time blood sugar has returned to normal, so this huge peak in blood sugar won’t be seen.

People with these abnormal insulin-glucose responses are at significantly increased risk for developing Type 2 Diabetes and the cardiovascular disease (heart attack and stroke) that often accompanies it, but if no one checks, no one knows.

We can only obtain the right answers if we ask the right question, but often we are asking the wrong questions.

Severe insulin and glucose dysfunction (adapted from Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.)

By the time people’s insulin and glucose curves look like above in black, ~75% of people will already meet the diagnostic criteria Type 2 Diabetes [2].

When people’s fasting blood sugar and glycated hemoglobin (HbA1C) falls in the normal range, it can’t simply be assumed that “everything’s fine” if these same individuals also have other symptoms that are known to be associated with hyperinsulinemia, including high blood pressure  (hypertension), high triglycerides (TG) and/or low HDL cholesterol [4]. If fasting blood glucose and/or HbA1C lab test results comes back within normal range and the person has some of these other symptoms and/or a family history of them, then requisitioning a fasting insulin test along with a fasting blood glucose test will enable some calculations to be done to estimate insulin resistance using the homeostasis model assessment (HOMA-IR) described in previous articles, but assessing hyperinsulinemia is a more involved process as it requires assessing both insulin response and glucose response simultaneously over several hours. The problem is that hyperinsulinemia is mechanistically linked to Metabolic Syndrome (described below), Type 2 Diabetes and as a result, cardiovascular disease (atherosclerosis, thrombosis) and other diseases associated with Metabolic Syndrome.  Hyperinsulinemia is also an independent risk factor for specific cancers (including breast and colon/rectum, Alzheimer’s disease and other forms of dementia and non-alcoholic liver disease [3].  Hyperinsulinemia is a silent disease, with no overt symptoms.  Clinical tools such as assessing insulin and glucose at the same time in response to a glucose load (called a ‘Kraft Assay’) may be useful to predict those who are at risk.  In order to be able to prevent people from receiving this diagnosis, clinicians must ask the right questions.

If a doctor is willing to requisition a 2-hour glucose tolerance test, then something as simple as having blood glucose checked at baseline, 1/2 an hour, 1 hour and 2 hours — and not just at baseline and at 2 hours will “catch” abnormal spikes after a carbohydrate load. While it is not as involved as a Kraft Assay which assesses insulin levels simultaneously with glucose levels over several hours, it can provide some useful information.  Such a simple addition is not very expensive and can go a very long way to enabling a person to make dietary and lifestyle changes to reverse hyperinsulinemia and as a result, decrease insulin resistance and avoid a diagnosis of Type 2 Diabetes. Certainly, left on its own, there is a good chance these individuals will be diagnosed even though their blood sugar didn’t reflect the risk far enough in advance.

Someone taking their own blood sugar reading at 1/2 hour and an hour after eating a high carbohydrate meal can provide them with sufficient early warning to look further.  I have loaned glucometers to my clients for just this purpose. It doesn’t need to be complicated. We simply need to ask the right questions.

If people already have some form of cardiovascular disease (CVD),  essential hypertension (high blood pressure that has no identifiable cause), Polycystic Ovarian Syndrome (PCOS) or non-alcoholic fatty liver disease (NAFLD) we need to consider that insulin resistance and hyperinsulinemia are very often associated [4].

We need to look past the what appears on the surface to be ‘normal’, because we may be overlooking early warning signs because we didn’t ask the right questions.

Perhaps you have questions about whether you may be insulin resistant or have hyperinsulinemia even though your blood sugar is normal or are concerned that your family history puts you at increased risk of developing Type 2 Diabetes and you want to make some simple dietary and lifestyle changes to avoid what seems as “inevitable”.  Please send me a note using the Contact Me form on the tab above and I’d be pleased to reply as soon as I can.

I provide services by Distance Consultation (Skype, long distance telephone) as well as in person in my Coquitlam office. Detailed information can be found on the Services tab, as well as in the Shop. You can download the Intake and Service Option Form under the package of your choice if you would like to get started and please let me know if you need more information.

To your good health,

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Del Prato, S., P. Marchetti, and R.C. Bonadonna, Phasic insulin release and metabolic regulation in type 2 diabetes. Diabetes, 2002. 51 Suppl 1: p. S109-16.
  2. Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.
  3. Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.
  4. Halban, P.A., et al., β-cell failure in type 2 diabetes: postulated mechanisms and prospects for prevention and treatment. Diabetes Care, 2014. 37(6): p. 1751-8.
  5. Reaven, G., The metabolic syndrome or the insulin resistance syndrome? Different names, different concepts, and different goals. Endocrinol Metab Clin North Am, 2004. 33(2): p. 283-303.

American Diabetes Association (ADA) Makes Sense of Carbs

A June 2018 article written by Sacha Uelmen, RDN, CDE, Director of Nutrition at the American Diabetes Association (ADA) sheds much light on the expanded role for low carb diets in the treatment and management of Type 2 Diabetes [1].

In answering the question “should people with Diabetes cut back on carbs?”, Uelmen says;

“It’s true that foods high in carbohydrate have the biggest impact on blood glucose compared with foods high in protein and fat. Carbohydrates break down into glucose after they are digested, so it makes sense to think that cutting carbs would lead to lower blood glucose levels and better diabetes management. “

Without going into the fact that our body can make glucose from fat and protein, Uelmen says that while our brain needs glucose “there’s a lot of debate around what is the ideal mix of carbohydrate, protein, and fat needed by people with Diabetes” and adds “we don’t have any evidence that one specific proportion will be right for everyone.”

I am in complete agreement.

Uelmen makes the same point that I did in part 3 of my 4-part series titled Some Carbs Are Better Than Others that “what kind of carb is just as important as how much“. This is something that I explain in detail to each one of my clients when I am teaching them their Meal Plan. I agree with her when she says that “some carbs are better for you than others”.

Uelmen explains,

“Refined” carbs refer to foods made with white flour and sugar, such as pretzels, cookies, cakes, and white breads. These foods raise your blood glucose levels quickly, and do not provide much nutritional value. On the other hand, carbs found in vegetables, beans, lentils, fruit, and whole grains break down slower and are packed with fiber, vitamins, and minerals that provide many health benefits.

Unfortunately, what she didn’t explain was the role of food processing in how foods such as legumes (beans and lentils) and grains will raise blood sugar. As I covered in part 1 of my article on The Perils of Food Processing, there are a number of factors other than how many grams of carbohydrate are in a food that will affect how much a food will raise blood sugar. These factors include the amount and types of food processing, including simple grinding, pressing or pureeing, as well as how the food is cooked and for how long. From that article;

Mechanical processing of a food doesn’t change the amount of carbohydrate that is in it. That is, when we compare 60g of whole apple with 60 g of pureed apple or 60g of juiced apple, there is the same amount of carbohydrate each. When we compare the Glycemic Index of these three, the results are very similar so this isn’t very helpful to tell us about the blood glucose response to actually eating these different foods. When these foods are eaten, the blood glucose response 90 minutes later is significantly  different.

In the ADA article, Uelmen explains that legumes and whole grains “break down slower” than “refined carbs” such as those made with white flour, but fails to mention that ground beans and lentils or grains will result in a much higher release of glucose and much quicker than legumes or grains that are whole and intact. As well, how they are cooked and for how long will also affect how quickly they release blood sugar. You can read more about that in this article. In short this means that hummus will not have the same effect on blood sugar as the same amount of whole chickpeas. As well, what most people consider “whole grain bread” (i.e. whole wheat bread) has the same Glycemic Index (GI) and Glycemic Load (GL) as white bread. That is, they will both raise blood sugar just as quickly.

“Whole wheat bread” is what most people think of when they hear “whole grain bread” and whole wheat bread has a Glycemic Index of 74 ± 2 and white bread isn’t much worse at 75 ± 2. Compare these to the GI of whole grain rye bread which is 53 [2]. One slice of white bread has a Glycemic Load of 10 and so does one slice of whole wheat bread, but the GL of a real whole grain rye bread is much lower at 7 [2]. Breads made with the whole intact grain or grain that is only coarsely cracked, such as German-style pumpernickel are very different than the “whole grain” bread available in most supermarkets and affect blood sugar much less.

Uelmen makes another point which is correct, but also neglects to mention information that is important.  She says;

“The timing and amount of carbs you eat are also important. Eating a lot of carbs in one meal, even if they are high quality carbs, can cause a spike in your blood sugar.”

This is true and I agree with her recommendation;

“Try to spread them [the amount of carbs] across your meals and snacks throughout the day based on your personal carb goal”.

…but there are two things that she fails to mention.

The first omission is that when carb-based foods are eaten at a mixed meal along with fat, they will raise blood sugar significantly more than at meals where carb-based foods are eaten without fat.  This is due to the combined effect of carbs and fat on the incretin hormone GIP, from the K-cells. As well, carbohydrate-based foods will spike blood sugar much less if they are eaten at the end of the meal, after protein and fat foods. Secondly, Uelman omits to mention that eating snacks (which are really just smaller meals) frequently results in an overall greater amount of insulin being released than if one eats larger meals less often. When one is trying to lower insulin resistance, eating snacks between meals makes things worse than eating the same amount of food over three (or two) meals. You can read more about both of these in part 2 of The Perils of Food Processing.

Uelmen makes other excellent points;

“Remember, there are many other factors that can affect your blood glucose. Things like changes in activity or sleep, timing and dose of diabetes medicine, and stress can all have an impact on your blood glucose. It’s not always just about food!”

She offers this terrific advice;

“When deciding how much carb is best for you, start by looking at what you are eating on a regular basis. How many grams of carbohydrate are you eating in each of your meals and snacks?”

If people are normally eating 200-300 g of carbohydrate per day, starting a “low carb diet” at 130 g per day will provide significantly better blood sugar control, if the carbs that are selected have a minimum of food processing (grinding) and cooking. Then, carbohydrate amount can be lowered as needed to help achieve clinical and metabolic outcomes.

Uelmen advises;

“If you are considering a low carb eating pattern, be sure to think about how much time you are willing to devote to meal planning. Strict low carb eating patterns, such as the ketogenic (keto) diet, require careful planning and regular visits to your doctor to ensure you are getting all of the vitamins and minerals you need to stay healthy.”

I’m not sure where she arrived at the idea that eating low carb requires people to devote more time to meal planning.  When meals center around a protein food and low-carb veggies — with a few nuts or seeds or cheese thrown in, they are super easy and fast to cook.

I agree with Uelmen that for people following a “strict low carb eating pattern, such as the ketogenic (keto) diet” require regular visits to their doctor, but not for the reasons she lists. Yes, a doctor can run tests to check for vitamin or mineral deficiency, however when a Meal Plan is done by a Dietitian that knows how to design a well-formulated ketogenic diet, it takes into consideration adequate intake of vitamins and minerals. Low nutrient intake is likely going to be less of an issue than when the person was eating a Standard American Diet. That said, people following a low carb or ketogenic diet do require regular visits to their doctor IF they are taking any medications that lower blood glucose or blood pressure. Please read this article if you fall in this category.

Uelman says;

“What can we all agree on when it comes to carbohydrates? Whether you follow a Mediterranean, vegan, keto, low carb, or any other eating pattern, one thing is for sure: Eat plenty of colorful non-starchy vegetables. They are full of vitamins, minerals, dietary fiber, and antioxidants to name just a few.”

…and this is excellent advice!

She concludes her article with two excellent suggestions that I long to hear reflected by Diabetes Canada in the days ahead. The first one is;

“How many carbohydrates should you eat each day? Well, that choice is yours. With careful review of your blood glucose trends and your usual eating patterns, you can often find the right balance that meets your daily nutrition needs and health goals as well as satisfying your appetite. Remember, the best meal plan for YOU is the one that you can stick with while meeting your health goals and feeling good!

Her second recommendation is that if people need more help following a low carb or ketogenic diet that they should find a Registered Dietitian with RD or RDN credentials to help them.

Final thoughts…

At present, Diabetes Canada 2018 Clinical Practice Guidelines continue to recommend that those with Diabetes still eat ~half or more (45% to 65%) of their daily calories as carbohydrate and limit dietary fat regardless of its source to 20% to 35% of daily calories.

Why is this?

Both Americans and Canadians based their dietary recommendation on the exact same Dietary Reference Intakes (DRIs) yet the American Diabetes Association does not hold rigidly to the Acceptable Macronutrient Distribution Ranges (AMDRs) for macronutrients as a percentage of total energy for Diabetics; which are 45% to 65% of energy as carbohydrate, 10% to 35% of energy as protein and 20% to 35% of energy as fat.

What I don’t understand is why Diabetes Canada continues to recommend that Diabetics keep following the same macronutrient distribution (percent of carbs, protein and fat) as the general population when the American Diabetes Association now supports both low carb and ketogenic (keto) diets for Diabetics?

Both Diabetes Canada and the ADA freely admit that carbohydrate-containing foods have the biggest impact on blood glucose compared with foods high in protein and fat, so why are American Diabetics supported in their desire to follow a ketogenic diet, but not Canadian Diabetics?

Or is it just that the Canadian recommendations haven’t yet caught up with the American recommendations?

If you have questions as to how I can help support your preference to follow a low carb lifestyle, please send me a note using the “Contact Me” form on this web page and I’ll reply as soon as possible.

To our good health,

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Uelmen S, American Diabetes Association, Diabetes Food Hub, June 2018, Ask the Experts: All About Carbs
  2. Glycemic Index Foundation, https://www.gisymbol.com/product/burgen-rye-bread/

 

Consumption of Dairy Fat Doesn’t Increase the Risk of CVD — may protect

A new study published this week in the American Journal of Clinical Nutrition reports that long-term consumption of the saturated fat found in full-fat dairy products is not associated with an increased risk of cardiovascular disease (atherosclerosis, coronary artery disease, etc.) or other causes of death, and may actually be protective against heart attack and stroke[1].

The study which took place over almost a quarter of a century measured three specific fatty acids found in dairy products in 2,900 older adults, aged 65 years and above— first in 1992, again in 1998 and finally in 2015. The three fatty acids they measured were pentadecanoic, heptadecanoic, and palmitoleic acids.

During the 22 year period, 2,428 of the participants died of which 833 were due to heart disease.  When the data was analyzed, none of the three fats was associated with the risk of total mortality (death) or heart disease — in fact, high levels of heptadecanoic acid was associated with a lower risk of death from heart disease and stroke.

This is significant because while higher amounts of saturated-fat consumption, including the saturated fats in this study increase blood LDL cholesterol, they also increase HDL cholesterol and decrease triglycerides[2], both of which are protective. Since it was unknown what the ‘net effect’ on total mortality (death) and cause-specific death, this study was done to determine what effect, if any increased dairy fats had on these outcomes.

The results were clear.

Not only did long-term consumption of these three dairy fats have no effect on either total death or heart disease, high levels of one of the fats found in full-fat dairy was actually found to be associated with a lower risk of heart disease and stroke!

The authors of the study conclude;

“For decades dairy fat consumption has been hypothesized to be a risk factor for CVD, as well as potentially diabetes, weight gain, and cancer, little empirical evidence for these effects existed from studies of clinical events. In current years, a growing number of prospective studies have shown generally neutral or protective associations between self-reported dairy foods and dairy fat consumption with the risk of CVD, diabetes, weight gain and cancers, raising questions about this conventional wisdom.”

The results of this long-term study with almost 3,000 older adults demonstrates that the saturated fat found in full-fat dairy is not associated with cardiovascular disease (CVD), diabetes or cancer and may even be protective against both heart attack and stroke.

Final Thoughts…

With both the American and Canadian Dietary Guidelines currently being revised— and “front of label labeling” in Canada to advise against foods high in saturated fat, it is time for both the US Office of Disease Prevention as well as Health Canada to review their respective recommendations with regards to consumption of low-fat dairy, in light of current research.

Dairy protects play an important role in health and nutrition and are rich sources of calciumpotassium, and phosphorus and are a ready supply protein and essential fat not only to growing children, but to older adults who risk osteoporosis and sarcopenia (muscle wasting). Given the results of this study on the saturated fat in dairy, as well as the results of a recent 158-country study which found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease, it is time to  re-evaluate the long-held belief that animal fat (whether in meat or dairy), is somehow ‘dangerous’.

A Few Words “Fat Phobia”

I regularly come across people in my practice who grew up in the last 40 years and who have spent their entire lives avoiding any form of animal fat.  The very idea of eating the yolk in egg is a source of anxiety — and it need not be so.

I am not suggesting that these folks suddenly start eating copious amounts eggs, meat, cheese, cream and butter but often suggest they start with things such as avocado, olives, nuts and seeds that are rich in monounsaturated fats that have been less villainized than saturated fat. I encourage them to use a little cream on top of fresh berries or use a bit of butter to cook with. In time, I may show them delightful egg recipes that have other foods they are used to eating and enjoy, such as a spinach-ricotta pie, which makes a lovely summer-time dinner when it’s too hot too cook.

Overcoming “fat phobia” takes time — especially when it has been ingrained in you since you’re young. I understand. When we work together, you set the pace.

People are sometimes concerned than they can’t follow a low-carbohydrate lifestyle because they “can’t eat all that fat”, but the truth is, not all low-carb diets have large amounts of fat. It’s only because fat has 2  1/2 times the calories as protein and carbs that some types of low-carb diet are still considered “high fat”. There is a whole range of low-carb diets which you can read about here as well as different types of ketogenic (“keto”) diets that you can read about here.

Have questions about which type of low carbohydrate diet may be best for you? Or perhaps you have questions about my services and their costs.  Maybe you’d just like to meet me for a one-hour consultation (in-person or via Skype) to ask questions and see if this may be an option for you. Please send me a note using the “Contact Me” form on this web page and I’ll be glad to reply as soon as I’m able.

To our good health!

Joy


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Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. Otto MC , Lemaitre, RN, Song, X et al; Serial measures of circulating biomarkers of dairy fat and total and cause-specific mortality in older adults: the Cardiovascular Health Study,The American Journal of Clinical Nutrition, https://doi.org/10.1093/ajcn/nqy117
  2. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr 2003;77(5):1146–55

 

Evidence that Refined Carbs with Vegetable Oils Cause Weight Gain

It has been my conviction for some time that the “perfect storm” which underlies the current obesity epidemic was the marketing of novel food products that were a combination of refined carbohydrates and manufactured vegetable oils and today I came across evidence that the food industry has known for some time that this specific combination results in significant weight gain. The proof wasn’t in a remote journal article, but in a product that was deliberately designed from refined carbohydrates and manufactured vegetable oils and marketed for the specific purpose of causing weight gain.  Yes, you read that correctly.

Just 5 years after the first manufactured vegetable oil product, Crisco® was created in 1911 — the brainchild of soap manufacturer Proctor and Gamble, a product called Wate On® was created by Dendron Distributors [1] of Chicago, Illinois in 1916 and promoted to doctors and the general public to promote weight gain through its “proven weight building elements”.

Wate On® boasted in magazine and newspaper ads that it was “loaded with concentrated calories so prepared to be far easier to be used by the system in building wonderful body weight“.

So what was its specially prepared formula?

It was the combination of vegetable oil and refined carbohydrates with added vitamins and minerals together in one easy-to-take product.

Early advertisement for Wait-On

Here are the words of the ad, above;

“if you are skinny, thin and underweight, mail this coupon for the latest discovery of modern medical science. It’s called WATE ON and anyone in normal health may quickly gain 2, 4 as much as 5 lbs. in a week…then 10 pounds, 20 pounds and more so fast, it’s amazing! Not a medicine, not intended to cure anything. Instead WATE ON is a new different formula that’s pleasant to take as directed and is loaded with concentrated calories so prepared to be far easier to be used by the system in building wonderful body weight. Cheeks fill out, neck and bust-line gain, arms, legs, thighs, ankles, skinny underweight figures fill out all over the body.”

Wate-On®‘s formulation was no secrete and was published in their advertisements.

Actress June Wilkinson, in an ad from the early 1960s in referring to the two formulations, WATE-ON® and SUPER WATE-ON® writes”both forms of WATE-ON are super-concentrated with weight-building calories, vitamins, minerals, quick energy elements”. In other parts of the same ad, it lists that the product is “saturated with calories from maize oil” and that SUPER WATE-ON has “extra calories from energy-giving sucrose and easy-to-digest vegetable oils“.

Wate-On ad featuring June Wilkinson, early 1960s

The obesity crisis should have come as no surprise.

In the 1940s, 50s and 60s, manufactured vegetable oils combined with sucrose (the refined carbohydrate of table sugar) were sold and promoted for weight gain.

Then, in the early 1950’s, Ancel Keys proposed his diet-heart hypothesis  (the belief that eating foods high in saturated fat contributed to heart disease) which was followed by publication of his Six Country Study in 1953 where he claimed to have demonstrated that there was an association between dietary fat as a percentage of daily calories and death from degenerative heart disease. Despite the fact that 4 years later (1957)  Yerushalamy  et al published a paper with data from 22 countries which showed a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s Six Countries Study data, the link between saturated fat and heart disease endured (see this earlier article for more details and references.)

In August of 1967, Stare, Hegsted and McGandy – the 3 Harvard researchers paid by the sugar industry published their review in the New England Journal of Medicine — which vindicated sugar as a contributor of heart disease and laid the blame on dietary fat and in particular, saturated fat and dietary cholesterol.

This vilification of saturated fat laid the foundation for the food industry to promote their novel vegetable fats to the general consumer as a ‘healthy’ alternative to ostensibly ‘unhealthy’ saturated fats.

…and promote them they did!

In the late 1980s, the food industry marketed their manufactured vegetable fats to an unsuspecting public by providing “teaching resources” to future Dietitians to promote their products as “healthy oils”. I know.  I was one of them (more in this article). Then came the proliferation of manufactured “convenience foods” and “fast foods— sold as products to make life easier, but which made us fatter instead. These products were (and are) the very combination of manufactured vegetable oil and refined carbohydrates of which weight-gain products of years-gone-by were made from!

Can the food industry claim — like the tobacco industry before them that they didn't know fast food and convenience food would result in ill health, stemming from overweight and obesity? I don't think so.

The food industry knew that the combination of manufactured vegetable oil and refined carbohydrates would lead to weight gain because before they were sold together as ‘convenience food’ and ‘fast food’, they were sold together in products deliberately designed to promote weight gain.

I remember when when the tobacco industry was challenged and how very long it took before a final verdict was reached and marketing and selling of disease-causing tobacco products to the public was legislated. How long will it take for foods containing a combination of manufactured vegetable oil and refined carbohydrates that we KNOW cause weight gain, to be likewise legislated?

How many more millions of people will die from food-related death or live poor quality-of-life due to obesity and obesity-related metabolic disease before the food industry is challenged?


Final Thoughts…

Having read this article, I would encourage you to begin reading labels of the foods you buy  and see how many of them have this combination of manufactured vegetable oil and refined carbohydrates. Start with ones in your pantry or fridge, then begin to read labels before you purchase them. 

The manufactured vegetable oils to look for are mainly soybean oil, canola oil and corn oil [also called maize oil in imported products] and the refined carbohydrates can be anything from white flour to various types of sugar (sucrose, glucose, other words ending in —ose). 

Then, look for healthful alternatives available in the marketplace. Monounsaturated fats such as olive oil and avocado oil are great alternatives and many of the products that have added sugars and vegetable oils really don’t need them, such as salad dressing or peanut butter!

Finding healthy products rarely requires shopping at a “health food store”, but simply shopping wiser at an ordinary supermarket  and realizing the the products you and others buy are the ones that stores will restock. If your store doesn’t have a healthy alternative to a product, then ask to speak to the department manager to request that they stock some. 

When you have some time, ask for the ingredient list to the products you buy at your local fast food restaurant or coffee house or go online and find them. By law (in both Canada and the US), food service companies are required to make these available. Ask. Read them. Look for they types of fats that are used and the types of refined carbohydrates.

Then, make food purchases for yourself and your family based on what you know and what you learned in this article about products that contain a combination of manufactured vegetable fats and refined carbohydrates.

If you need help to make healthier food choices, I can help.

Please send me a note using the Contact Me form located on the tab above and I will reply soon.

To our good health,

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

References

  1. OTCToolbox, DDD seeks brands to distribute in the UK, Nov 11 2014, https://www.otctoolbox.com/news/archive-2014/ddd-seeks-brands-to-distribute-in-the-uk.aspx
  2. The History of Dendron http://www.dendron.co.uk/history

Some Carbs Are Better Than Others – Part 4 – the Insulin Index

In previous articles in this series on Some Carbs are Better than Others, I’ve covered both Glycemic Index  (GI) and Glycemic Load (GL) which are useful measures of how easily carbohydrate-based foods raise the blood sugar of healthy people. For those that are insulin resistant or have Type 2 Diabetes, Insulin Index is much more useful because it indicates how much insulin is required for a specific food. Insulin is the hormone that tells our body to store excess energy as glycogen or fat, and that is also responsible for lowering blood sugar.

Unlike GI and GL, the Insulin Index is not limited to carbohydrate-based foods because protein-based foods (have no carbohydrate in them) still cause an insulin response. Some foods that have a low GI or GL result in a lot of insulin being released — and knowing this is important to those who are insulin resistant or have already been diagnosed with Type 2 Diabetes and are working at lowering their fasting insulin levels.

As presented in Part 3 of this series Some Carbs are Better than Other (for Diabetics), I demonstrated how 25 g of carbs made from highly processed flour and sugar produced a very different glucose response a Type 2 Diabetic (me!) than 25 g of carbs of an unrefined (intact) food — even though at the time I did this ‘experiment’,  I had been eating very low carb for over a year.

Why the difference when both had 25 g of carbs?

The 25 g of carbs as a cracker with chocolate was a combination of highly refined white flour and fat (chocolate) which raises blood glucose to a much higher degree than a food that contains carbohydrates alone (see The Perils of Food Processing, Part 2) . The 25g of carbs as intact chickpeas that were cooked from soaked, dry ones were fully intact — as they were prepared with the minimum necessary cooking.  As covered in Part 1 of the series on The Perils of Food Processing, highly refined and carb-based processed foods cause a much higher and more immediate glucose response due to the incretin hormone GIP, than foods with the same number of carbs that has its plant structure intact (i.e. the chickpeas). This explains WHY I had three times the glucose response with the cracker, as I did with the chickpeas — even though both foods had the same amount (25 g) of carbohydrate in them.

What about Insulin Response in response to these two foods?

The 25 g of carbs as a cracker with chocolate would have resulted in a huge stimulation of the gut (incretin) hormone GIP in the upper intestine and resulted in a pronounced release of insulin. The 25 g of carbs as cooked chickpeas would not have resulted in a huge stimulation of GIP because they were intact and as a result, the starch in them was not readily available to the enzyme that digests it (α-amylase). In fact, some of the carbohydrate in the chickpeas would have passed through the gut undigested.

The insulin response of these two foods (each with 25 g of carbohydrate) would have been very different.

What is the Insulin Index?

Shortly after I was diagnosed as having Type 2 Diabetes in 2007, I came across a research paper from 1997 called “An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods”. In this paper, the Insulin Score of a food was determined by feeding individual foods that contained exactly 239 calories (kcals) / 1000 kilojoules each to non-diabetic subjects and then measuring their insulin response over three hours. The results from each food were then compared to the insulin response of pure glucose, which was assigned an arbitrary value of 100%. The Insulin Index ranks each individual food compared to the insulin response of pure glucose.

Below is a graph from that paper:

Holt S, Brand-Miller J & Petocz P (1997). An insulin index of foods

At the time, the graph was quite puzzling to me as eggs, cheese, fish and beef —which have no carbohydrate in them at all, still caused insulin to be released. It would take close to 10 years for me to better understand this.

As far as I could see, there were two major limitations to the Insulin Index; the first was that there were only 38 foods evaluated. One really can’t make any inferences based on only 38 foods!  The second limitation was that it measured the insulin response in healthy, non-diabetic people.

Last year, I had heard that a PhD researcher from the University of Sydney , under the oversight of Prof. Jennie Brand Miller (who had worked on the original study in 1997) had conducted a research project on the clinical application of the Insulin Index to Diabetes (Type 1). In addition to her thesis, she had also created a database of the Insulin Index of a large number of foods.

This was huge!

As it turned out, some foods that were high in protein and low in fat (such as lean steak or fish) resulted in a large insulin release and foods such as navy beans or All Bran® cereal resulted in a relatively low insulin response. As it turns out, it’s not only the amount of carbohydrate in a food that influences insulin release, but also protein and fiber.

What is especially helpful about the Insulin Index and the database of Insulin Scores is that it enables those with Type 1 or insulin-dependent Type 2 Diabetes to more accurately estimate their injected insulin needs.

However, for those with insulin-dependent Type 2 Diabetes, there is another option.

Results from recent research studies such as the one-year data from the Virta study have been published and demonstrate that reversal of Type 2 Diabetes symptoms is possible — even for those injecting themselves with insulin!

At the beginning of the study, 87% of participants were taking at least one medication for Diabetes but after only 10 weeks of following a well-formulated ketogenic diet, almost 57% had one or more Diabetes medications reduced or eliminated. At the end of a year, sulfonylurea medication was entirely eliminatedInsulin therapy was reduced or eliminated in 94% of of those following the well-formulated ketogenic diet at a year.

For those taking any of the types of medication listed below, following a well-designed ketogenic diet requires one’s doctor’s oversight. As I wrote about in a previous article, medical supervision is absolutely required  before a person changes the amount of their carbohydrate intake if they have been prescribed any of the following medications;

(1) insulin

(2) medication to lower blood glucose such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc. and other types of glucose lowering medication such as Victoza, etc.

(3) medication for blood pressure such as Ramipril, Lasix (furosemide), Lisinopril / ACE inhibitors, Atenolol / β₁ receptor antagonists

(4) mental health medication such as antidepressants, medication for anxiety disorder, and mood stabilizers for bipolar disorder and schizophrenia.

I don’t provide low carbohydrate / ketogenic dietary services those taking insulin (either Type 1 Diabetes or Type 2 Diabetes), I encourage those that are taking it to consult with their endocrinologist and work with a knowledgeable healthcare professional with CDE certification.

As I said previously, people taking any of these medications should not adjust the dosage of their medication without first consulting with their doctor and being instructed by them to do so. The consequences can be very serious, even life-threatening. For example, people taking SGLT2 inhibitors such as Invokana or Jardiance and who decrease insulin dosage suddenly are at increased risk for a life-threatening condition called “Diabetic ketoacidosis (DKA)”.  Medication dosages and timing must be adjusted by a doctor.

If you are not taking insulin — or have been stable for a period of time after having had insulin withdrawn by your doctor, I’d be happy to work with you to coordinate dietary and lifestyle changes with you and your doctor, as they monitor your health and adjust the levels of prescribed medications. In complex cases, I will ask for written consent to coordinate care with your doctor depending on medications you are prescribed, as your doctor will need to know in advance what level of carbohydrates you have been advised to eat, so that they can monitor your health and make adjustments in your medication dosage.

If you have questions as to how I can help you or how I’d work with you and your doctor as they oversee you adopting a low carb lifestyle please feel free to drop me a note using the Contact Me form on the tab above.

To your good health!

Joy


 https://twitter.com/lchfRD

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References

Holt S, Brand-Miller J & Petocz P (1997). An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods. Am J Clin Nutr 66, 1264-1276. The American journal of clinical nutrition. 66. 1264-76.

Bell K, University of Sydney, School of Molecular and Microbial Bioscience, Clinical Application of the Food Insulin Index to Diabetes Mellitus, May 14, 2014. https://ses.library.usyd.edu.au/handle/2123/11945


Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

The Perils of Food Processing – Part 2

This article on the Perils of Food Processing is based on a lecture given by Gabor Erdosi, MSc, MBA– Food News Conference, May 19, 2018 – Prague, Czech Republic.

Part 1 can be read here.


INTRODUCTION: In the first part of this article on the Perils of Food Processing, we considered the effect of different types of simple food processing such as grinding and cooking on the hormonal response of the incretin hormones to carbohydrate intake. While interesting, we rarely eat meals that are only made up carbohydrate, without any fat or protein. Even if we eat a slice of bread or toast and put peanut butter on top, it is now mixture of carbohydrate, fat and protein. How does a ‘mixed meal” with fat and protein affect the body’s hormonal response to carbohydrate?  How does the presence of fiber impact this hormonal response?  Does it matter how often we eat, or how fast? This and more are covered in this article.

Response of Incretin Hormones to Meal with Fat and Carbohydrate

In the first study we’re going to look at, the researchers designed a sandwich that produced a very stable glucose response in healthy individuals.  The sandwich was made of 120 g of white bread, 20 g of butter and 10 g of dried meat. As can be seen from curve A, blood sugar rose to ~150 mg/dl (~8.3 mmol/L) and stayed relatively stable for the next 3 hours (180 minutes).

But what happened to the insulin response when these foods were eaten separately and together in a sandwich?

Effect of fat and protein on incretin effect of a mixed meal – – Gabor Erdosi – Food News 2018

Looking at curve B (bottom), it can be seen when subjects ate only the dried meat, blood insulin levels didn’t rise much at first, but then rose a little bit at ~ 90 minutes and stayed relatively constant. When subjects ate only the butter, insulin levels rose a little bit more and then only increased slightly over the next several hours. But when they ate the sandwich with the white bread, butter and dried meat, you can see that blood insulin levels rose quite steeply, beginning before 30 minutes, reaching a maximum level at 60 minutes, and then decreased very slowly over the next several hours. This makes sense, because of the presence of the carbohydrate in the bread.

What is interesting is what happens to the two gut hormones, GIP (from the K-cells) and GLP-1 (from the L-cells) in response to eating these foods.

Contribution of fat and protein to the incretin effect of a mixed meal – – Gabor Erdosi – Food News 2018

Looking at the second curve (graph on the right) it can be seen that in response to the ‘mixed meal’ of the sandwich, GIP from the K-cells (high up in the intestine) is released rapidly and in large amounts. That is, a mixed meal results in a large stimulation of both insulin and glucagon release. Insulin moves the glucose into the cell for storage at the level of the fat cells increases lipoprotein lipase, which increases triglyceride storage. This is an anabolic process of storing nutrients for use later.

As can be seen from the first curve, when a ‘mixed meal’ is eaten, GLP-1 is released from the L-cells lower down in the intestine responded but is much less pronounced. That is, in response to GLP-1 secretion, insulin is released to a small extent, but there is little of the signalling to decrease glucagon, which means little effect on the hunger signal and little satiety (feeling full).

Incretin Response to a Standard Western Diet Meal versus a Paleo-style Meal

In this next study, we can see the same effect in a plant-based meal, using a reference meal and a paleolithic style meal (called PAL2) that both had the same number of calories (~1600 kcals) and very similar macronutrient distributions (carbohydrate, fat, protein). The only difference between the reference diet and the Paleolithic type diet is the amount of processing.

Plant-rich Paleo-type Meal versus Standard Western-type Meal – – Gabor Erdosi – Food News 2018

The reference meal was made up of cooked, long grain rice, mango and boiled carrots, some fish cooked over dry heat and some olive oil.

The paleo type meal was made up of raw strawberries, raw apple, as well as the same significantly more fish cooked over dry heat, raw mushrooms, seedless raisins, zucchini (courgettes), flax seed, cinnamon and capers. While both of these meals had the same number of calories, as can be seen, there was a significant difference in the weight between these two meals – with the reference meal weighing only 248 g, uncooked and the paleo type meal weighing 718 g.

In each of these two types of meals, the response of the two gut incretin hormones, GIP from the upper intestine K-cells and GLP-1 from the lower intestinal L-cells were very different!

Looking at the bottom of the 3 graphs, it can be seen that GIP from the K-cells (high up in the intestine) was released rapidly and in large amounts in the reference meal – a meal that is quite similar to the Standard Western Diet. Recall that the GIP from the K-cells acts on the pancreas to trigger both insulin release from the beta-cells and to trigger glucagon release from the alpha cells. The insulin results in the body storing glucose from the meal and the glucagon release signals the body to release stored glucose, if the blood sugar falls too low. The rise of GIP in response to the paleo-type meal was very slow and gradual and didn’t rise very high, which means that much less insulin was triggered to be released from the pancreas’ beta-cells and much less glucogon was triggered to be released from the alpha-cells.

What happened to GLP-1 release from the L-cells in the lower intestine in response to these two different types of meals?

The Western-type meal (the reference meal) caused a very short rise in GLP-1 from the lower L-cells, which decreased back to baseline quickly.  That means that very little additional insulin was released to move additional glucose into the cells and significantly, there was very little decrease of glucagon which means that appetite was not decreased and there was little to no stimulus to increase satiety (feeling full) and little to no signal to decrease food intake.

The paleo-type meal resulted in significant release of GLP-1, which caused the pancreas to release insulin from the beta-cells and also decreases glucagon release from the alpha-cells of the pancreas – which at the level of the brain, acts to decrease appetite and increase satiety.

This is key; based on this study, a meal based on a Standard Western Diet did not trigger the signal that the body had taken in sufficient food and that appetite could now decrease.

The Effect of Food Texture even Greater than the Effect of Macronutrient Distribution

This next study is very interesting – showing that food texture has an even greater effect on obesity induced from diet than macronutrient content of the diet.

Disrupted food texture versus a high-fat and high sugar diet – – Gabor Erdosi – Food News 2018

The top graph demonstrates that mice fed a “high fat diet” – which was really high in both sugar and fat (not just high in fat) gained significantly more weight than mice fed standard mice chow.

The bottom graph shows that if you take the standard mice chow and grind it fine into a powder and feed it to the mice, they gain weight to the same degree as when fed a diet high in fat and sugar.  That is, the degree of food processing in the diet has at least as great an effect on obesity as the amount of fat and sugar in the diet itself.

There is something about grinding the food that changes the satiety/hunger signal.

Meal Size and Meal Frequency

Common advice given by nutritionists and Dietitians is that it is better to eat small, frequent meals than large meals less often, but there are some studies that support that it as far as hunger and satiety signalling are concerned, it is better to eat fewer, larger meals due to the effect of the incretin hormones.

The Effect of Meal Size and Meal Frequency on Incretin Hormones – – Gabor Erdosi – Food News 2018

[study on right hand side of slide]

After a low-calorie smaller meal, insulin response is proportionately higher compared to a larger meal. That is, a small meal triggers a proportionately greater insulin response that a larger meal, so if one eats small meals frequently, there is an overall greater amount of insulin released than if one eats larger meals less often.

Interestingly, it is the same for those with Type 2 Diabetes.  It is possible to modulate the beta-cell sensitivity to glucose by giving obese people and those with Type 2 Diabetes fewer large meals compared to more frequent smaller meals.

Eating Speed

If one eats more slowly the incretin hormones that trigger satiety (feeling full) are released in a more pronounced manner.  This holds true even when obese subjects eat calorically dense foods such as ice-cream. More of the satiety hormones are released when people eat slowly.

Glycemic Load as a Proxy for the Amount of Carbohydrate Processing

Glycemic Load indicates how a healthy person’s body will respond to amount of carbohydrate in one serving of a food. One usual serving of a food would be considered to have a very high Glycemic Load if it is ≥ 20, a high Glycemic Load if it is between 11-19 and a low Glycemic Load if it is ≤10.

Glycemic Load as a proxy for amount of carbohydrate processing – – Gabor Erdosi – Food News 2018

When one compares the Glycemic Load estimated from ancient diets at the time of the Agricultural Revolution (A on the graph) compared with the Industrial Revolution (B on the graph), the Glycemic Load at the Industrial Revolution is approaching 20, and after that point, continues to go up in an almost vertical manner.  That is, Glycemic Load is a fairly accurate proxy for the degree of food processing of the diet; the more processed the diet, the higher the Glycemic Load.

Amount of Fiber as a Proxy for the Amount of Carbohydrate Processing

This next graph shows the consumption of total carbohydrate over the last century – from 1909-2000 and the amount of carbohydrate from fiber as a percentage.

Consumption of total carbohydrate from 1909-2000 and the amount of carbohydrate from fiber as a percentage – – Gabor Erdosi – Food News 2018

As can be seen, at the beginning of the century, the total amount of carbohydrate started off high and gradually decreased until about 1954, leveled off, then began to increase again. The decrease in the fiber content in carbohydrate-based foods is also evident on this graph from ~ 1960 onward.

What happened?

Perhaps it was the introduction of supposedly “healthy” polyunsaturated vegetable oils (industrial seed oils) in the 1960s that contributed to the dramatic increase in the consumption of ultra-refined carbohydrates.

At the very same time that ultra-refined carbohydrate appeared on the scene, so were novel industrial seed oils – ultra-refined fats.  Perhaps it is the combination of the two in many processed food products which contributed to carbohydrate content of the diet climbing exponentially – and along with it, obesity and metabolic diseases.

Structure and Speed of Absorption

Recall from Part 1 of this article that there are several nutrient-sensing hormones in the small intestine, but with respect to the effect of food processing, SGLT1 is a glucose sensor and both K-cells and L-cells contain this nutrient-sensing receptor.

Intact versus disrupted structure affects the speed of absorption in morbidly obese – Gabor Erdosi – Food News 2018

In the morbidly obese, intestinal glucose absorption high up in the intestine is accelerated due to SGLT-1 from the K-cells.  SGLT-1, along with GIP from the K-cells results in high insulin and high glucagon release, which results in both hyperinsulinemia and hyperglycemia.

Intact structures in grain are not accessible to the digestive enzyme amylase (which breaks down starch to glucose), so when grain is consumed intact, this delays gastric emptying and creates a barrier to starch digestion.  The degree to which grain is intact was found to be more effective in improving glucose metabolism than dietary fiber, irrespective of the type of cereal

Evidence for Why We Get Hungry 3-4 Hours After Eating Refined Carbohydrate

Recall from Part 1, the hormone ghrelin is the only hormone that can increase hunger.

Effect of Eating Refined Carbs on Ghrelin and Blood Glucose – Gabor Erdosi – Food News 2018

Looking at the graph in the top left, we can see that when one eats carbohydrate, ghrelin decreases at first below baseline for the first two hours (120 minutes), but then begins to rise. It continues to rise, exceeding baseline at three hours (180 minutes) and continues rising until four hours; resulting in significantly increased hunger.

At the same time as ghrelin (the hunger hormone) is increasing between 3 and 4 hours after eating refined carbs, serum glucose has dipped below baseline in response to eating refined carbs (as demonstrated in Part 1 of this article) and from 3 hours to 4 hours (180 minutes – 240 minutes), so that serum glucose remains low.

That is, in response to eating refined carbohydrates alone (without combining them with protein) you end up having low blood sugar and feel hungry 3-4 hours later. Blood glucose only gradually begins to increase until it is returns to baseline again at 6 hours (360 minutes).

This next study is a comparison between normal weight and obese people.

Satiety and Hunger Signaling in Normal-Weight and Obese Subjects – Gabor Erdosi – Food News 2018

On the right-hand side, at the top one can see that normal weight people have normal signalling. Satiety (feeling full) goes up and one can see that PYY correspondingly goes up, hunger goes down and correspondingly, ghrelin goes down.

Below that, one can see that in the morbidly obese, their signalling for hunger and satiety is dysregulated. Satiety is going down even after they’ve eaten and correspondingly, PYY shows this dysregulation in that it also goes down. While hunger goes down and the hormone ghrelin also goes down, it is to a much lesser degree that in normal subjects.

So, the obese individuals may feel slightly less hungry, but they don’t feel satiated. This holds true whether obese individuals eat carbohydrate, protein or fat but it is especially pronounced when carbohydrate is eaten. That is, signalling is largely preserved in the morbidly obese when it comes to protein and fat, but it is lost when it comes to carbohydrate.

Obese people should avoid eating diets high in refined carbohydrate because their hunger and satiety signals are dysfunctional and they don’t receive signals that they have eaten.

Here is another study showing that in obese Chinese men, a high protein meal or a high fat meal produces more satiety and better appetite hormonal response after eating than a high carbohydrate meal.

High protein or high fat meal produces more satiety than high carbohydrate meal – Gabor Erdosi – Food News 2018

In another study, different conditions were looked at such as whether it made a difference in the hunger hormone, ghrelin, if the carbohydrate food was eaten first or last.  It turned out that it is best to eat carbs last, as ghrelin continues to decrease for 2 ½ hours (150 minutes) after eating carbohydrate.

This next illustration shows that there is positive feedback mechanism between insulin and GIP.

 

Insulin drives GIP expression but requires glucose – Gabor Erdosi – Food News 2018

Insulin drives GIP expression but requires glucose to do it. When you eat food with carbohydrate, GIP in the upper intestines is released, resulting in insulin being released. If you keep eating carb-based foods, there is lots of glucose present, which continues to drive the release of more and more GIP, triggering more and more insulin to be released.

This next slide shows a study with two kinds of sugar, sucrose which is ordinary table sugar and isomaltulose, which is made up of the exact same molecules of fructose and glucose, just attached together in a different configuration.

Sucrose’s effect on Plasma Glucose and GIP, GLP-1 – Gabor Erdosi – Food News 2018

As can be seen, sucrose causes a huge spike in plasma GIP secreted from the K-cells high up in the intestine compared to isomaltulose which triggers high insulin and high glucagon release and which results in both hyperinsulinemia and hyperglycemia. Sucrose also results in much lower release of GLP-1 from the L-cells, lower down in the intestine which results in some release of insulin, but a much smaller decreases glucagon so that at the level of the brain, there is less of a decrease in appetite and less of an increase satiety (feeling full).  As a result, eating foods sweetened with sucrose results in higher glucose, higher insulin, very little decrease in appetite, less feeling full and less decreased food intake, compared with isomaltulose.

As a result, sustained feeding with sucrose in mice results in insulin resistance and fatty liver.

Differential Effect of eating Sucrose with a Meal or Alone – Gabor Erdosi – Food News 2018

If these sugars are eaten with a meal, instead of alone, the effect on blood glucose and insulin is removed, but GIP release is still triggered to be released to a large extent compared with isomaltulose, and fatty liver persists in the mice in the sucrose group.

The Effect of Combining Refined Carbohydrates with Fat

As can be seen from the graph on the left hand side at the bottom, when refined carbs are combined with fat, there is a huge response of GIP.

Effect of having Fat with Carbohydrate-based Food – Gabor Erdosi – Food News 2018

Eating boiled potato and low-fat veal didn’t result in this effect but the addition of butter to the potato dramatically changed this.

From an evolutionary perspective it makes sense, because there are no naturally occurring cases where a food has both high carbohydrates and high fat at the same time.  Our body’s have not evolved to see these two macronutrients together.

The following is from a recent overview from May 2018 which provides a summary of GIP actions in response to a high Glycemic Index meal.

Summary of actions of GIP in response to a high Glycemic Index meal – Gabor Erdosi – Food News 2018

When high GI carbohydrate food is eaten and passes through digestion in the stomach and then as it enters the upper small intestine, the K-cells release GIP which has several actions, including decreasing lipolysis, increasing insulin secretion in the pancreas, decreasing fat oxidation, increasing the AKT-mTOR pathway in the brain, and increasing fat storage in the liver.

How Does Bariatric Surgery / Gastric Bypass Work

Many people assume that the reason gastric bypass works is because the stomach is made smaller, so that the person cannot overeat, but this is not primarily what makes it effective.

Bariatric Surgery / Gastric Bypass – Gabor Erdosi – Food News 2018

But what occurs within a week of the Roux-en-Y gastric bypass surgery is that there is a dramatic change in the balance of the incretin hormones.

Effect of Roux-en-Y Bypass Surgery on Incretin Hormones; first two weeks – Gabor Erdosi – Food News 2018

After only a week, GIP release is ½ what it was before the surgery and GLP-1 is almost doubled.

These changes in only a week are not a result of weight loss, but of the surgery’s impact on correcting the imbalance in the incretin hormones – essentially causing an ‘opposite imbalance’ which corrects the defect cause by the Type 2 Diabetes and overeating of ultra-refined carbs.

There are other types of surgical interventions, such as the Duodenal-Jejunal bypass liner tube that impact incretin hormones, as well as numerous medications. There are selective sodium-dependent glucose transporter 1 inhibitors that block glucose absorption and impair GIP release in the same way that a roux-en-Y gastric bypass does.

“Gastric Bypass in a Pill” – Gabor Erdosi – Food News 2018

There are also numerous other medications such as sodium-glucose co-transporter 2 inhibitors, Glucagon-like Peptide 1 Agonists, and Dipeptidyl Peptidase 4 Inhibitors that impact the incretin hormones to varying degrees (and even some that claim to and do nothing!).

Numerous Other Medications Used to Impact Incretin Hormones – Gabor Erdosi – Food News 2018

…and there are low carbohydrate diets that significantly reduce the release of GIP from the K-cells, because there are low levels of carbohydrate consumed at any one time to trigger it’s release.  As a result, significantly less insulin is release, which is how LCHF diets followed over time lower insulin resistance.

Effect of a Low Carbohydrate Diet on GIP – Gabor Erdosi – Food News 2018

Summary of Part 1 and Part 2 of the Perils of Food Processing

  • Speed and location of intestinal nutrient absorption is crucial in determining metabolic response to a food
  • The greatest effect in incretin hormone response is seen with carbohydrate rich plant processing, therefore retaining the plant or grain structure as much as possible is crucial
  • Diets high in ultra-refined, quick absorbing food plausibly results in altered intestinal hormonal profile, altered hunger / satiety signalling and as a result higher food intake and increased meal frequency
  • The above effect is exaggerated when ultra-processed carbohydrates are consumed in combination with significant amounts of fat (the “doughnut effect”).
  • GIP may be part of a “thrifty mechanism” in mammals; easily digestible, high energy density foods overstimulate it (think “honey” to hunter-gatherers).

Practical “Takeaways”

  • Processing of food that are high in fat and protein has little effect on intestinal hormone levels, so prioritize food items in terms of desired amount of macronutrients
  • Plant or grain foods (carbohydrate containing) should be carefully selected based on their most dense, undisturbed structure. Processing, whether grinding, pureeing or cooking disrupts the plant / grain structure and accelerates absorption of the carbohydrate, which triggers an intestinal hormonal response which results in reduced satiety. Excluding most carbohydrate-based foods also solves this problem
  • Consume carbohydrate foods at the end of the meal (after protein and fat foods)
  • Have fewer, larger meals vs small, frequent ones. Avoid “snacking” between meals
  • Eat meals slowly to maximize the satiety effect and increase the release of the lower intestinal hormones.

Perhaps you wonder what all this information means for you. How should this information change the way you eat and what you eat?  What does this mean in practical terms when planning dinner, or eating dinner – especially if you have Type 2 Diabetes or insulin resistance and also if you are well now, but have a family history with many common metabolic disorders.  How can you change how you eat to stay well?

I can help.

Please send me a note using the “Contact Me” form located on the tab above to find out information about the services I offer (in-person or via Distance Consultation using telephone or Skype) and I will reply shortly.

To your good health!

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


The full lecture can be watched here:

References

(continued from Part 1)

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17. Bligh, H. Frances J., Ian F. Godsland, Gary Frost, Karl J. Hunter, Peter Murray, Katrina MacAulay, Della Hyliands, et al. “Plant-Rich Mixed Meals Based on Paleolithic Diet Principles Have a Dramatic Impact on
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18. Desmarchelier, Charles, Tobias Ludwig, Ronny Scheundel, Nadine Rink, Bernhard L. Bader, Martin Klingenspor, and Hannelore Daniel. “Diet-Induced Obesity in Ad Libitum-Fed Mice: Food Texture Overrides the Effect of Macronutrient Composition.” British Journal of Nutrition 109, no. 08 (2013): 1518–27.

19. Vilsbøll, T., T. Krarup, J. Sonne, S. Madsbad, A. Vølund, A. G. Juul, and J. J. Holst. “Incretin Secretion in Relation to Meal Size and Body Weight in Healthy Subjects and People with Type 1 and Type 2 Diabetes
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20. Alsalim, Wathik, Bilal Omar, Giovanni Pacini, Roberto Bizzotto, Andrea Mari, and Bo Ahrén. “Incretin and Islet Hormone Responses to Meals of Increasing Size in Healthy Subjects.” The Journal of Clinical
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21. Koopman, Karin E., Matthan W.A. Caan, Aart J. Nederveen, Anouk Pels, Mariette T. Ackermans, Eric Fliers, Susanne E. la Fleur, and Mireille J. Serlie. “Hypercaloric Diets with Increased Meal Frequency, but Not Meal Size, Increase Intrahepatic Triglycerides: A Randomized Controlled Trial.” Hepatology 60, no. 2 (2014): 545–53.

22. Stote, Kim S., David J. Baer, Karen Spears, David R. Paul, G. Keith Harris, William V. Rumpler, Pilar Strycula, et al. “A Controlled Trial of Reduced Meal Frequency without Caloric Restriction in Healthy, Normal-Weight, Middle-Aged Adults.” The American Journal of Clinical Nutrition 85, no. 4 (April 1, 2007): 981–88.

23. McQuaid, S. E., L. Hodson, M. J. Neville, A. L. Dennis, J. Cheeseman, S. M. Humphreys, T. Ruge, et al. “Downregulation of Adipose Tissue Fatty Acid Trafficking in Obesity: A Driver for Ectopic Fat Deposition?” Diabetes 60, no. 1 (2010): 47–55.

24. Kokkinos, Alexander, Le Roux, Carel W, Kleopatra Alexiadou, Nicholas Tentolouris, Royce P. Vincent, Despoina Kyriaki, et al. “Eating Slowly Increases the Postprandial Response of the Anorexigenic Gut
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25. Rigamonti, A. E., F. Agosti, E. Compri, M. Giunta, N. Marazzi, E. E. Muller, S. G. Cella, and A. Sartorio. “Anorexigenic Postprandial Responses of PYY and GLP1 to Slow Ice Cream Consumption: Preservation in
Obese Adolescents, but Not in Obese Adults.” European Journal of Endocrinology 168, no. 3 (March 1, 2013): 429–36.

26. Llewellyn, Clare H., Van Jaarsveld, Cornelia Hm, David Boniface, Susan Carnell, and Jane Wardle. “Eating Rate Is a Heritable Phenotype Related to Weight in Children.” The American Journal of Clinical Nutrition
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27. Chapter 1. in “Sweeteners and Sugar Alternatives in Food Technology”, 2nd Edition Kay O’Donnell (Editor), Malcolm Kearsley (Editor) ISBN: 978-1-118-37397-2 Jul 2012

28. Wiley-Blackwell Gross, Lee S., Li Li, Earl S. Ford, and Simin Liu. “Increased Consumption of Refined Carbohydrates and
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29. Scazzina, Francesca, Susanne Siebenhandl-Ehn, and Nicoletta Pellegrini. “The Effect of Dietary Fibre on Reducing the Glycaemic Index of Bread.” British Journal of Nutrition 109, no. 07 (2013): 1163–74.
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30. Nguyen, Nam Q., Tamara L. Debreceni, Jenna E. Bambrick, Bridgette Chia, Judith Wishart, Adam M. Deane, Chris K. Rayner, Michael Horowitz, and Richard L. Young. “Accelerated Intestinal Glucose Absorption in Morbidly Obese Humans: Relationship to Glucose Transporters, Incretin Hormones, and Glycemia.” The Journal of Clinical Endocrinology &amp; Metabolism 100, no. 3 (2015): 968–76.

31. Foster-Schubert, Karen E., Joost Overduin, Catherine E. Prudom, Jianhua Liu, Holly S. Callahan, Bruce D. Gaylinn, Michael O. Thorner, and David E. Cummings. “Acyl and Total Ghrelin Are Suppressed Strongly by Ingested Proteins, Weakly by Lipids, and Biphasically by Carbohydrates.” The Journal of Clinical Endocrinology & Metabolism 93, no. 5 (2008): 1971–79.

32. Lomenick, Jefferson P., Maria S. Melguizo, Sabrina L. Mitchell, Marshall L. Summar, and James W. Anderson. “Effects of Meals High in Carbohydrate, Protein, and Fat on Ghrelin and Peptide YY Secretion in
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33. Rizi, Ehsan Parvaresh, Tze Ping Loh, Sonia Baig, Vanna Chhay, Shiqi Huang, Jonathan Caleb Quek, E. Shyong Tai, Sue-Anne Toh, and Chin Meng Khoo. “A High Carbohydrate, but Not Fat or Protein Meal Attenuates Postprandial Ghrelin, PYY and GLP-1 Responses in Chinese Men.” PLOS ONE 13, no. 1 (January 31, 2018): e0191609.

34. Shukla, Alpana P., Elizabeth Mauer, Leon I. Igel, Wanda Truong, Anthony Casper, Rekha B. Kumar, Katherine H. Saunders, and Louis J. Aronne. “Effect of Food Order on Ghrelin Suppression.” Diabetes
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35. Hägele, Franziska A, Franziska Büsing, Alessa Nas, Julian Aschoff, Lena Gnädinger, Ralf Schweiggert, Reinhold Carle, and Anja Bosy-Westphal. “High Orange Juice Consumption with or In-between Three
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36. García-Martínez, Jose Manuel, Ana Chocarro-Calvo, Antonio De la Vieja, and Custodia García-Jiménez. “Insulin Drives Glucose-Dependent Insulinotropic Peptide Expression via Glucose-Dependent Regulation of
FoxO1 and LEF1/β-Catenin.” Biochimica et Biophysica Acta (BBA) – Gene Regulatory Mechanisms 1839, no. 11 (November 1, 2014): 1141–50.

37. Pfeiffer, Andreas F.H., and Farnaz Keyhani-Nejad. “High Glycemic Index Metabolic Damage – a Pivotal
Role of GIP and GLP-1.” Trends in Endocrinology & Metabolism, 2018.

38. Collier, G., and K. O’Dea. “The Effect of Coingestion of Fat on the Glucose, Insulin, and Gastric Inhibitory Polypeptide Responses to Carbohydrate and Protein.” The American Journal of Clinical Nutrition 37, no. 6 (June 1, 1983): 941–44.

39. McClean, P. L., N. Irwin, R. S. Cassidy, J. J. Holst, V. A. Gault, and P. R. Flatt. “GIP Receptor Antagonism Reverses Obesity, Insulin Resistance, and Associated Metabolic Disturbances Induced in Mice by Prolonged
Consumption of High-Fat Diet.” AJP: Endocrinology and Metabolism 293, no. 6 (October 23, 2007):E1746–55.

40. Ceperuelo-Mallafré, Victòria, Xavier Duran, Gisela Pachón, Kelly Roche, Lourdes Garrido-Sánchez, Nuria Vilarrasa, Francisco J. Tinahones, et al. “Disruption of GIP/GIPR Axis in Human Adipose Tissue Is Linked
to Obesity and Insulin Resistance.” The Journal of Clinical Endocrinology & Metabolism 99, no. 5 (May 2014): E908–19.

41. Gögebakan, Özlem, Martin A. Osterhoff, Rita Schüler, Olga Pivovarova, Michael Kruse, Anne-Cathrin Seltmann, Alexander S. Mosig, Natalia Rudovich, Michael Nauck, and Andreas F. H. Pfeiffer. “GIP Increases Adipose Tissue Expression and Blood Levels of MCP-1 in Humans and Links High Energy Diets to Inflammation: A Randomised Trial.” Diabetologia 58, no. 8 (August 2015): 1759–68.

42. Mohammad, S., R. T. Patel, J. Bruno, M. S. Panhwar, J. Wen, and T. E. McGraw. “A Naturally Occurring GIP Receptor Variant Undergoes Enhanced Agonist-Induced Desensitization, Which Impairs GIP Control of
Adipose Insulin Sensitivity.” Molecular and Cellular Biology 34, no. 19 (2014): 3618–29.

43. Nie, Y., R. C. Ma, J. C. N. Chan, H. Xu, and G. Xu. “Glucose-Dependent Insulinotropic Peptide Impairs Insulin Signaling via Inducing Adipocyte Inflammation in Glucose-Dependent Insulinotropic Peptide
Receptor-Overexpressing Adipocytes.” The FASEB Journal 26, no. 6 (2012): 2383–93.

44. Timper, K., J. Grisouard, N. S. Sauter, T. Herzog-Radimerski, K. Dembinski, R. Peterli, D. M. Frey, et al. “Glucose-Dependent Insulinotropic Polypeptide Induces Cytokine Expression, Lipolysis, and Insulin
Resistance in Human Adipocytes.” AJP: Endocrinology and Metabolism 304, no. 1 (2012): E1–13.

45. Miyawaki, Kazumasa, Yuichiro Yamada, Nobuhiro Ban, Yu Ihara, Katsushi Tsukiyama, Heying Zhou, Shimpei Fujimoto, et al. “Inhibition of Gastric Inhibitory Polypeptide Signaling Prevents Obesity.” Nature
Medicine 8, no. 7 (2002): 738–42.

46. Boylan, Michael O., Patricia A. Glazebrook, Milos Tatalovic, and M. Michael Wolfe. “Gastric Inhibitory Polypeptide Immunoneutralization Attenuates Development of Obesity in Mice.” American Journal of
Physiology – Endocrinology And Metabolism 309, no. 12 (2015): E1008–18.

47. Nasteska, D., N. Harada, K. Suzuki, S. Yamane, A. Hamasaki, E. Joo, K. Iwasaki, K. Shibue, T. Harada, and N. Inagaki. “Chronic Reduction of GIP Secretion Alleviates Obesity and Insulin Resistance Under High-Fat
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48. Althage, M. C., E. L. Ford, S. Wang, P. Tso, K. S. Polonsky, and B. M. Wice. “Targeted Ablation of Glucose-Dependent Insulinotropic Polypeptide-Producing Cells in Transgenic Mice Reduces Obesity and
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49. Calanna, S., F. Urbano, S. Piro, R. M. Zagami, A. Di Pino, L. Spadaro, F. Purrello, and A. M. Rabuazzo. “Elevated Plasma Glucose-Dependent Insulinotropic Polypeptide Associates with Hyperinsulinemia in
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50. Chia, Chee W., Juliana O. Odetunde, Wook Kim, Olga D. Carlson, Luigi Ferrucci, and Josephine M. Egan. “GIP Contributes to Islet Trihormonal Abnormalities in Type 2 Diabetes.” The Journal of Clinical Endocrinology & Metabolism 99, no. 7 (July 2014): 2477–85.

51. Chen, Shu, Fumiaki Okahara, Noriko Osaki, and Akira Shimotoyodome. “Increased GIP Signaling Induces Adipose Inflammation via a HIF-1α-Dependent Pathway and Impairs Insulin Sensitivity in Mice.” American
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52. Cavin, Jean-Baptiste, André Bado, and Maude Le Gall. “Intestinal Adaptations after Bariatric Surgery: Consequences on Glucose Homeostasis.” Trends in Endocrinology & Metabolism 28, no. 5 (May 2017):
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53. Xiong, Shao-Wei, Jing Cao, Xian-Ming Liu, Xing-Ming Deng, Zeng Liu, and Fang-Ting Zhang. “Effect of Modified Roux-En-Y Gastric Bypass Surgery on GLP-1, GIP in Patients with Type 2 Diabetes Mellitus.”
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54. Falkén, Y., P. M. Hellström, J. J. Holst, and E. Näslund. “Changes in Glucose Homeostasis after Roux-En-Y Gastric Bypass Surgery for Obesity at Day Three, Two Months, and One Year after Surgery: Role of Gut
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Why Carbs and Fat Together are Irresistible

A study that is due to be published on July 3, 2018 in the scientific journal Cell Metabolism is the first to demonstrate that compared to foods high in carbs or fat, foods with both carbs and fats together result in much more dopamine being released from the striatum, which is the reward-center of our brain [1]. Dopamine is the same neurotransmitter that is released during sex and that is involved in the addictive “runner’s high” familiar to athletes. This is one powerful neurotransmitter!

It is thought that there are separate areas of the brain that evaluate carb-based foods and fat-based foods and both are involved in the release of dopamine, but when carbs and fat appear in the same food together, this results in what the researchers called a “supra-additive effect“. That is, both areas of the brain get activated at the same time, resulting in much more dopamine being released and a much bigger feeling of “reward” being produced.

This combination of carbs and fat in the same food is why we find foods such as French fries, donuts and potato chips irresistible.

In fact, the study found that people were willing to pay more for foods that combine both carbs and fat than for foods that were only high in carbs but not fat such as candy, or only high in fat but not carbs, such as cheese.

This powerful reward-system involving dopamine is why we will choose the fries over the baked potato and why we have no difficulty wolfing back a few donuts, even when we’ve just eaten a meal.

This “supra-additive effect” on the pleasure center of our brain, along with the fact that more insulin is released when both carbs and fat are eaten together[2] may help explain the roots of the current obesity epidemic and the metabolic diseases such as Type 2 Diabetes that go along with it.

Carbohydrate intake was high in the early 1900s and gradually decreased until about 1954, leveled off, then began to increase again[3]. What caused that to occur? At that time, ultra-refined carbohydrates began appearing in the market and these by their very nature were devoid of the whole, unprocessed grain that slows the release of insulin [3] (for more information on the mechanism, please see this article).  Excess release of insulin made worse by the constant eating of ultra-refined carbohydrate foods underlies the process of how insulin resistance develops and in time, how Type 2 Diabetes develops [3].

The early 1950’s was also when the “diet-heart hypothesis” proposed by Ancel Keys took root, along with the recommendation that Americans (and later, Canadians) reduce their consumption of saturated fat (more in this article).  With the recommendation to decrease saturated fat was the necessity to create fats to replace them, which is when and why both soybean oil and later, canola oil were created (see this article for more information). These industrial seed oils began to replace natural fats such as butter, lard and tallow in home and restaurant cooking, frying and baking.

With the creation of "polyunsaturated vegetable oils", French fries were now a healthy food - after all, they were vegetables fried in "healthy polyunsaturated fat". 

What could possibly go wrong?

This new study provides the missing link as to the mechanism by which the “perfect storm” was created. That “perfect storm” was the simultaneous appearance in the late 1950s and early 1960s of ultra-refined carbohydrates and industrial seed oils (promoted as “heart healthy” by the American and Canadian Dietary Guidelines) that literally hijacked the reward system of our brain!

Is there little wonder why rates of overweight and obesity began rising at in the early 1960s and have continued to rise dramatically ever since?

As far as our brains are concerned, French fries are much more desirable than a baked potato and donuts and pastry much more desirable than toast because they literally make us feel good!  Eating French fries and pastry results in considerably more dopamine being released than eating baked potato or plain toast. Eating these foods produce something comparable to a “runner’s high” in people that have never run a block or have even gotten off the couch!

While discovery of the dopamine-centered mechanism is new to this study, the food industry has known for some time that processed foods containing both carbohydrate and fat will result in people coming back and buying more and more of their product. Carbs and fat is why Pringles® chips could boast “betcha can’t eat just one!“, but it’s not just Pringles®. This combination of carbs and fat is in all processed foods; from so-called “junk food” such as chips and Cheezies® to foods that are perceived as “healthy foods”, such as granola bars and commercial peanut butter.

Carbs and fats together are the essence of “fast food” – from Big Macs® dripping with cheese and mayo sandwiched between several buns, to French fries of all types, super-sized or not.  People may joke about “junk food being addictive”, however understanding the “supra-additive” effect of carbohydrate combined with fat makes these foods as addictive to our brains as a “runner’s high” is to an athlete, or what makes people seek out sex. Addictive? Maybe not in the truest sense of the word except in cases of food addiction, but certainly in the rest of us there is a powerful draw to want to eat them.

Knowing and understanding this mechanism is of no small consequence! It should inform our food choices.

We need to be aware of foods that we eat that “hijack” our appetites. They could be “healthy foods” like cashews that are both high in fat and high in carbohydrate.  Given what we know about the triggering of the reward system in the brain, should those of us with current or past weight problems have them around?

Another way this knowledge should inform our food choices is around the concept of “cheat days”.  People who see me seeking weight loss often ask me about whether they can have one day a week, or one day a month where they eat “cheat foods”.  Knowing the very potent chemically-mediated reward system involved with eating foods such as pizza or French fries or ice cream, do you think these are foods that are helpful to eat once a week or once a month? How much will eating those foods cause you to crave them later, after your “cheat day”? Is it worth it?

From a purely academic perspective, knowing the mechanism also helps explains why metabolically healthy people can lose weight either following a low-fat diet or a low-carb diet, because it is the combination of both carbs and fats that stimulate the reward centers.

Note: a low-carb approach is preferable for people who have have already become insulin resistant or diagnosed with Type 2 Diabetes because they are no longer able to handle more than small amounts of carbohydrate at a time without it significantly impacting their blood sugar (and insulin) levels.

So, knowing that eating carbs and fat together result in a huge release of dopamine and light up the reward-centers of our brain, how should we choose foods differently? What do we do if we eat carbs and fat at the same meal; does it matter which we eat first? Does how we process and prepare our carb-based foods make a difference on our blood sugar?

The answer to these questions is easy.  Yes, based in this study and many others, how we eat meals that have carbs, fat and protein (called “mixed meals”) matters and how quickly or slowly our blood sugar rises depends on when we eat them as well as how we process and prepare them.

This is where I can help.

I can explain in a very easy to understand way how to eat in such as ways as to minimize the impact on blood sugar, and beyond that, how to lower insulin release and insulin resistance which keeps blood sugar levels high.

If you would like information about my services or about having me design a Meal Plan for you, please send me a note using the “Contact Me” tab above and I will reply as shortly.

To our good health,

Joy


 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Di Feliceantonio et al., 2018, Supra-Additive Effects of Combining
    Fat and Carbohydrate on Food Reward, Cell Metabolism 28, 1–12
  2. Carrel, G., L. Egli, C. Tran, P. Schneiter, V. Giusti, D. D’Alessio, and L. Tappy. “Contributions of Fat and Protein to the Incretin Effect of a Mixed Meal.” American Journal of Clinical Nutrition 94, no. 4 (2011):997–1003.
  3. Gross, Lee S., Li Li, Earl S. Ford, and Simin Liu. “Increased Consumption of Refined Carbohydrates and the Epidemic of Type 2 Diabetes in the United States: An Ecologic Assessment.” The American Journal of Clinical Nutrition 79, no. 5 (2004): 774–779.
  4. O’Dea, K., Nestel, P.J., and Antonoff, L. “Physical Factors Influencing Postprandial Glucose and Insulin Responses to Starch” 33, no. 4 (April 1, 1980): 760–65. https://doi.org/10.1093/ajcn/33.4.760.

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Ten Common Low Carb Myths

In my time interacting on social media (Facebook, Twitter) as the LCHF-Dietitian (@lchf-RD) I keep coming across many of the same misconceptions about eating a low carb diet, so I decided to write an article dispelling 10 of the most common myths.

Myth 1: “A low carb diet will cause clogged arteries and heart attacks because it is too high in saturated fat.”

Firstly, as elaborated on in a previous article, a recent study published at the end of March 2018 in Nutrients looked at health and nutrition data from 158 countries worldwide and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease, so even if someone following a low carb diet chose to eat foods high in saturated fat, it does not mean they are necessarily at higher risk of heart attacks or strokes.

Secondly, a low carb diet does not necessarily have to be high in saturated fat. In fact,  it may have very little added fat at all such as when people are aiming to lose weight, so that they burn more of their own body fat.

While there is no increased risk with eating the saturated fat that is naturally found in meat (chicken, beef, pork, etc.), except for specific clinical requirements (for example, a ketogenic diet for epilepsy) there is no reason anyone has to add additional saturated fat. There are other sources of fat that are delicious and have beneficial properties, such as monounsaturated fats found naturally in olive oil and avocados and their oils.

Myth 2: “A low carb diet has way too much protein in it!”

There are different types of low carb diets and a low carb diet may not necessarily have a lot of protein – whether as eggs, cheese, meat, or fish.

In a very low carb (ketogenic) diet used for epilepsy, the diet is mostly fat and has low protein, however in a low carb diet used for weight loss and improving metabolic conditions such as Type 2 Diabetes or high blood pressure, the amount of protein will be moderate.

How much protein is “too much”?

The RDA for Protein is set at 56 gm per day (based on 0.8 g protein per kg of body weight) is the minimum amount to prevent deficiency.  This is not the optimal amount, but the absolute minimum amount. So, whether a given person is eating 1200 calories a day or 2500 calories per day they have an absolute requirement for 56 gm of protein per day.

The maximum amount of protein per day is set at ~200 g / day and is calculated based on >2.5 g protein per kg of body weight, and the range from 56 g to 200 g of protein per day is referred to as the range of safe intake.

According to Dr. Donald Layman, Professor Emeritus of Human Nutrition from the University of Illinois, a high protein diet doesn’t start “until well above 170 g / day”.  You can read more about this here.

Everybody’s needs for protein is different and many people, especially adults and older adults are either not getting enough protein or it is mostly at dinner, with little at breakfast and lunch, which is a concern in older adults, as it puts them at risk for sarcopenia, the muscle wasting often seen in older adults eating a Westernized diet.  You can read more about that here.

In any case, most low carb diets aren’t anywhere near the level of what is considered a “high protein diet”, let alone “too high in protein”.

Myth 3: “Low Carb Diets involve eating lots of meat”.

While there are some, especially those involved in the body-building or body-sculpting world that choose to follow a variation of a low-carb diet which involves eating lots of meat (and protein, in general), there are some variations of a low-carb diet that don’t involve eating meat at all.  As mentioned above, ketogenic diets used for those with epilepsy or seizure disorder are mostly fat and ketogenic diets used as an adjunct therapy in treatment of specific types of cancer are often mostly fat, as well depending on the specific type of cancer.

Therapeutic low carb or ketogenic diets used for weight loss or improving metabolic conditions such as Type 2 Diabetes, high blood pressure and abnormal cholesterol may be based on a moderate amount of protein, with some of that as meat if the individual eats it and enjoys it. To eat low-carb,  there is no requirement to eat meat at all.

A low carb diet can be designed to accommodate pescatarians (those that only eat fish), as well as vegetarians. There are even some vegans that choose to follow a low carb diet for a variety of reasons, although getting enough of all nutrients is a major challenge, just as it is for those following a Standard American/Canadian Diet.

I’ve written an article about the range of foods that can be eaten on a low carb diet which can be read here.

Myth 4: “Low carb diets are dangerous because the brain needs a certain amount of carbohydrate”.

Except for erythrocytes (red blood cells) every cell in the body has mitochondria (the so-called “powerhouse of the cell”). The mitochondria can use a variety of fuel sources and turn it into Acetyl-CoA, which then enters the Kreb’s Cycle and generates Adenosine Triphosphate (ATP) which is what every cell in the body requires for life. The brain is no different than any other cell in the body that has mitochondria, as it can efficiently and safely use Acetyl-CoA can be made from carbohydrate (e.g. glucose), ketone bodies (a byproduct of fatty acid breakdown) and amino acids from protein to generate Acetyl-Coa. Most parts of the brain have no requirement for dietary carbohydrate, as it can use ketones generated from fat breakdown.

Certain parts of the brain and red blood cells do need glucose (approximately 30 g a day) and that need is fulfilled by a process called gluconeogenesis where glucose is made by the liver and kidneys from substrates other than carbohydrate, including amino acids (from proteins) or glycerol  (from fat breakdown).

In fact, the human body doesn’t require any dietary carbohydrate provided the amount of protein and fat in the diet is sufficient (to be used as substrates, as mentioned above); from page 275 of Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005);

The lower limit of dietary carbohydrate compatible with life apparently is zero, provided that adequate amounts of protein and fat are consumed. 

Please see this article for more information.

This does not mean that low carb diets contain no carbohydrate! As mentioned above, some liberal low carb diets have enough carbohydrate such that the person does not go into ketosis, while therapeutic ketogenic diets (done under medical supervision) such as those used for the management of epilepsy or as an adjunct to cancer treatment may have < 30 g of carbohydrate.

Myth 5: “A Low carb diet is imbalanced and causes nutrient deficiencies”.

With the exception of a therapeutic ketogenic diet for epilepsy or as an adjunct to cancer treatment, eating a well-formulated low-carb diet provides adequate nutrients, even those such as thiamine (vitamin B1) and folate which are normally associated with grain products. There are many low-carb sources of thiamine, including pork, chicken liver, macadamia nuts and peanuts, flax-seed and asparagus and just 1 serving of each of these can meet an adult’s daily requirement.

Likewise, there are many low-carb sources of folate (vitamin B9), including the low carb leafy vegetables that are abundant in a well-formulated low carb diet, as well as other green vegetables such as asparagus, spinach, Brussels Sprouts and avocado.

Vitamin C is plentiful in foods outside of citrus fruit, including red and green bell pepper, broccoli, cauliflower and strawberries, as well as in lemon and lime that can be used as a seasoning for salad dressing, fish or to flavour water.

Calcium is easily obtained from well-designed meal plans that include cheese and yogurt, fish (such as sardines and canned salmon), almonds and leafy vegetables such as spinach, collards and kale.

A well-designed low carb diet provides a wide range of foods; from cheese and other dairy products, nuts, seeds, fruit, low carb vegetables and meat, fish and poultry and can provide the essential nutrients that a healthy body requires, including vitamins and minerals.

The only two nutrients that will likely be sub-optimal are vitamin D and magnesium– but are certainly not provided in lesser amounts than in the average Canadian or American diet. I advocate for supplementation of both of these nutrients, whether someone is following a Standard American or Canadian diet or a low-carb diet.

Myth 6: “Low carb diets are so restrictive”.

This is one of the two myths that I often joke about around the dinner table, because the food we eat is anything but restrictive.

People can eat a huge variety of vegetables and meat, fish and poultry which require the minimum of cooking and food preparation so even for someone with little or no cooking skill or time to prepare food, a well-designed low carb diet is entirely possible.  I design them for clients all the time, because many people fall into this category or live alone and don’t want to cook elaborate meals for themselves.

For those that enjoy cooking and have the time to do it there are very few, if any traditional foods that can not be made low carb – and made very tasty! 

As can be easily seen in the recipes on this web page, as well as the article I wrote on what people can eat on a low carb diet, there is almost no recipe that can be adapted for those that choose to eat low carb.  There is even rolls for sandwiches and several different types of pizza (to suit those who follow a higher fat low carb diet or a lower fat low carb diet).  I invent the recipes for myself and share them on my webpage because food should not only be healthy, but enjoyable.

Myth 7: “Low carb diets are not sustainable”.

This is the second myth that makes me chuckle, because I know of people that have been eating this way for 15 or 20 years which in and by itself demonstrates it is quite sustainable. There are one-year and two-years studies on this web page the also indicate that a well designed low carb diet is quite sustainable.

What is “not sustainable“ about eating fresh, healthy, whole foods that can be prepared with a minimum of cooking or as elaborate as one’s imagination allows?

Myth 8: “Low carb diets require you to constantly count carbs and check your ketone levels”.

First of all, a well-designed low carb Meal Plan does all the “carb counting” for you – all you need to do is decide what you want to eat. This is no different whether someone eats a moderate amount of carbs or a low amount of carbs. In fact, how foods are grouped on your Meal Plan, you’ll know how many carbs are in one serving any food in that group, should you want to add something to your Meal Plan.

As far as checking ketones, unless one is on a low level of carbohydrates (ketogenic diet) and either has certain health conditions or taking specific medications, there is no need.

Myth 9: “It doesn’t matter if you eat low carb or low fat, the only thing that matters is Calories In Calories Out”.

This answer may stir up some controversy, because there is a wide range of opinion on this.

Some advocates of a low-carb diet insist that Calories In Calories Out (CICO) is irrelevant because metabolism is different when one eats low carb. Some advocates of a low-fat diet will say that low-carb only works because in the end, people eat less calories.

I think it is “both / and not “either / or”.

Most low-fat diets are calorie-restricted diets and when calories are restricted, people’s metabolism slows down.  That is why people following a  carbohydrate-based low-calorie diet feel cold, tired and lethargic; because their body is conserving the calories it is getting for important metabolic functions. Because the body is primarily using carbohydrate as fuel, fat stores are only accessed when carbohydrate is restricted – which also slows down metabolism.

When people are eating a diet that is low in carbohydrate and which has sufficient protein, and is higher in a variety of fats, people’s bodies are mainly using fat as fuel. If their Meal Plan is designed for weight loss, then some of the fat they are using for fuel is their own fat stores – so ‘fuel’ is never restricted.  If the body needs more energy, it will take the “extra” it needs from fat stores. In this way, the body doesn’t have to slow metabolism to conserve energy, because there is always more fat in the person’s fat stores. Eating a diet based predominantly based on healthy fats and protein with much lower level of carbohydrates makes people feel full after eating much less, so the end result is that they generally eat less calories, which is why they are able to lose weight.

That is, a calorie is still a calorie but all fuels are not considered equal.

Myth 10: “Ketones are dangerous and you can die from them!”

Unfortunately, this is way too common a myth – even one in which some healthcare professionals are confused.

Ketones are naturally produced in our bodies during periods of low carb intake, in periods of fasting for religious or medical tests, and during periods of prolonged intense exercise. This state is called ketosis. It is normal and natural and something everyone’s body does when using fat as its main fuel source.

Once our glycogen levels are used up, fat is broken down for energy and ketone bodies are a byproduct of that. These ketones enter into the mitochondria of the cell and are used to generate energy (as ATP) to fuel our cells.

Ketosis is a normal, physiological state and we may produce ketones after sleeping all night, if we haven’t gotten up and eating something in the middle of the night.

Ketoacidosis on the other hand is a serious medical state that can occur inuntreated or inadequately treated Type 1 Diabetics, where the beta cells of the pancreas don’t produce insulin. It may also occur in those with Type 2 Diabetes who decrease their insulin too quickly or who are taking other kinds of medication to control their blood sugars.

In inadequate management of Type 1 Diabetes or in insulin-dependent Type 2 Diabetes, ketones production will be the first stage in ketoacidosis. This is not the case when the above medical issues are not present.

Final Thoughts…

There are a wide range of low-carb diets with various levels of carbohydrate, protein and fat. Some are high in meat, others low in meat, while others have no meat at all. Some are very high in protein and others are very high in fat. Some promote weight loss, others make it very difficult. There are different types of low carb diets because they are used for different purposes.

Each person’s requirement for protein is different, so following a generic “low carb diet” downloaded from the internet will be based on an ‘average’ amount of protein for adults and not your needs . The amount of fat you will be encourage to eat will be based around the protein needs that are set by the web page. If you are wanting to lose weight, very often you may find that you lose a bit at first and then weight plateaus for extended periods of time.  Many of my clients come to me after trying this approach, feeling that a “low carb diet doesn’t work for me”.  The issue very often is that the plan wasn’t designed for “them” at all.

Most general types of “low carb diets or plans” allow people to select the level of carbohydrate they want to limit. Often, people will choose a ketogenic level because they want to lose weight quickly, with little regard for making sure they are getting sufficient nutrients.

For otherwise healthy young adults with no major risk factors and who are not taking any medications, this might work out fine however for adults with medical or metabolic conditions – and especially for those taking medications for Diabetes or high blood pressure, this can put them at significant risk. As outlined in more detail in a previous article, medical supervision is absolutely required before a person changes the level of  their carbohydrate intake if they are taking;

(1) insulin

(2) medication to lower blood glucose such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc.

(3) medication for blood pressure such as Ramipril, Lasix (furosemide), Lisinopril / ACE inhibitors, Atenolol / β₁ receptor antagonists

or

(4) mental health medication such as antidepressants, medication for anxiety disorder, and mood stabilizers for bipolar disorder and schizophrenia.

For everyone who does not fall into the above category, it’s important to realize that there is a very big difference between a generic meal plan downloaded from a “low-carb” website and one designed just for you, based on your physiological needs and ensuring that you get adequate nutrients based on your own medical history and family risk factors. For a low-carb style diet to provide the nutrients that you need for your age, gender and activity level, it needs to be designed for you; factoring in your need for specific nutrients.  It’s not simply a matter of choosing a level of “macronutrients”  (“macros”) such as carbohydrate, fat and protein, but ensuring adequate “micronutrients”, too. That is the difference between having an Individual Meal Plan designed specifically for you by a knowledgable Registered Dietitian and one that is based on general cutoff points.

For this to be a way of eating that is balanced in terms of overall nutrients and will meet specific health goals and which is healthy and interesting enough to be sustainable over the long term, it needs to be carefully designed for each individual.

Do you have questions about how I can help design a Meal Plan for you? Or for you and your partner?

Please send me a note using the Contact Me form located on the tab above and I will reply shortly.

To your good health!

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

CBC Interview with a Low Carb Physician – 5 minutes and all the basics

Dr. Miriam Berchuk is a Calgary-area physician and an active member of the Canadian Clinicians for Therapeutic Nutrition who was interviewed today (June 11, 2018) on CBC Radio (Calgary Eyeopener) about her personal use and promotion of a Low Carb diet for weight loss and specific metabolic conditions related to insulin resistance.

While the interview lasts just a touch over 5 minutes, everything that one needs to know to understand what a low carb diet is (and isn’t!) is clear, as well as when medical supervision should be sought.

If you want to know the basics or are having a difficult time explaining it to others, Dr. Berchuk’s interview should be very helpful.

The Perils of Food Processing – Part 1

This article is based on a lecture given by Gabor Erdosi, MSc, MBA– Food News Conference, May 19, 2018 – Prague, Czech Republic

Introduction – Gabor Erdosi, MSc, MBA is a Molecular Biologist from Debrecen, Hungary who is employed in the Food Industry but whose hobby is reading scientific publications and analyzing the available information. The talk that this article is based on was given at the Food News Conference, May 19, 2018 – Prague, Czech Republic  and is the condensation of approximately 4 years worth of Gabor’s studying of the literature.

Gabor founded and heads up the Lower Insulin group on Facebook which is dedicated to discussing the scientific basis of the relationship between metabolic diseases and food and lifestyle factors. At present, the group has ~5300 members.

This new series titled The Perils of Food Processing reflects Gabor’s conviction that what’s of primary importance in the interaction between food and our physiology (GI tract) is the speed and location of food absorption in the digestive system. This article is arranged according to the same principle.

The reason I am writing this series of articles is because I believe what Gabor Erdosi has come to understand about the effects of food processing on the speed and location of food absorption — especially carbohydrate, and which affects the very nature of hunger and satiety is absolutely crucial to understanding the current epidemic of metabolic diseases we now face.

This first article provides an overview of the gastrointestinal system and the so-called “incretin hormones” and how the amount a food is cooked or ground impacts how quickly it is absorbed and the energy stored.


When talking about Food Processing, the issue arises as to how to properly define the concept of ‘processing’.

How do we define ‘food processing’? Humans have been processing their food in one way or another for hundreds of thousands of years – be it cutting, cooking or grinding their food in some way.  These are all forms of food processing.

In terms of the effect of Food Processing on human physiology, a few main questions that this series of articles will address, arise;

(i) are all forms of food processing created equal?

(ii) does the food processing of different macronutrients and foods have different results?

(iii) could these changes in food processing over the last few hundred years or so have anything to do with the epidemic of metabolic diseases that we now face?

1. Overview of Gastrointestinal Physiology

Before getting into the topic of the effect of different types of food processing on the speed and place of absorption, it’s necessary to provide an overview of the gastrointestinal physiology and how the digestive system works and what hormones are released in response to different nutrients.

1. Overview of Gastrointestinal Physiology – Gabor Erdosi – Food News 2018

The important concept here is that we have “sensor cells” (K-cells, L-cells) within our gastrointestinal tract and these cells release different hormones in response to different nutrients.

K-cells release an incretin hormone called GIP and the L-cells release an incretin hormone called GLP-1, as well as GLP-2, PYY and Oxyntomodulin (OXM).

What is important to note is that the distribution of these cells is not uniform.

The K-cells are more abundant in the upper part of the small intestine and other cells, the L-cells are more abundant in the lower part of the small intestine. This uneven distribution of these incretin-hormone-releasing sensor-cells has profound implications, as will be seen later.

Uneven distribution of the K-cells and L-cells in the small intestine – Gabor Erdosi – Food News 2018

2. Nutrient Sensing, the Incretin Effect and Hunger-Satiety Signalling in the Gut

Nutrient-Sensing

So, what happens when we eat foods that we have evolved to see for millennia? As the food goes through the small intestine, it triggers hormonal release from these incretin-hormone-releasing sensor-cells.

If you eat meat and berries, for example, which are foods we have evolved to see for hundreds of thousands of years, they have a fairly balanced stimulatory effect on these sensor cells. These incretin hormones will be released in a more or less balanced manner.

However, as will be shown later on, when we eat food products that we have not evolved to see – relatively new food products on an evolutionary scale, these patterns are completely disrupted.

There are several nutrient-sensing hormones in the small intestine, but the one to focus on with respect to the effect of food processing is SGLT1 –  which is a glucose sensor. Both the K-cells and the L-cells contain this nutrient-sensing receptor, and most others, as well.

Keep in mind for the next articles that the distribution of these cells is uneven; with more in the K-cells higher up in the small intestine and increasing numbers further down in the L-cells.

The Incretin Effect

When we eat glucose, such as in an oral glucose tolerance test or when someone gets intravenous glucose in a hospital, the difference in the insulin response is called the “incretin effect”.

As you can see from the diagram below, the response to an oral or intravenous glucose load is very large and can be 50-70% of the insulin response.

The “Incretin Effect” to oral or intravenous glucose – Gabor Erdosi – Food News 2018

The majority of the insulin response is stimulated by these incretin hormones (GIP, GLP-1, etc.) secreted by the K-cells and L-cells and not directly via glucose.

The Physiological Effects of the Incretin Hormones

In addition to the insulin-stimulating effect, these incretin hormones have very different effects.

The K-cells, which are more abundant in the upper small intestine, secretes Glucose-dependent Insulinotropic Polypeptide (GIP) which acts on the pancreas – not only to result in insulin release, but also increase glucagon. At the level of the fat cells, the adipose tissue, it increases increases triglyceride storage, resulting in weight gain. In this way, GIP supports insulin’s effect on storing lipids. This is an anabolic-type of hormone and if it is very high, it can cause inflammation in adipose tissue.

The L-cells, which are more abundant in the lower small intestine, secrete Glucagon-like Peptide-1 (GLP-1) which also acts on the pancreas to increase insulin, but decreases glucagon. This GLP-1 at the level of the brain, acts to decrease appetiteincrease satiety (feeling full) and decrease food intake.

  1. Hunger-Satiety Signalling in the Gut
Effects of Intestinal hormones on hunger-satiety signaling – Garbor Erdosi – Food Net 2018

It is important to note that there is only one hormone that can increase hunger and that is ghrelin which is synthesized in the stomach.

All the other hormones, including CCK, PP, PYY, GLP-1 and OXM (Oxyntomodulin) decrease hunger. That is, all of these hormones promote satiety; the feeling of being ‘full’. It is very important to note that four of these hormones, CCK, PYY, GLP-1 and OXM are all synthesized in the small intestine L-cells.

The above is the all the basic physiology that is needed to understand the effects of food processing on the speed and location of nutrient absorption, the nature of hunger and satiety and how the current epidemic in metabolic diseases we now face is a result of disregulation of this system.

3 a. The Effect of Cooking Foods on Body Weight

One of the most ancient forms of food processing is cooking, and there are studies which indicate that there is an association between how many raw foods people eat and their body weight.  There is a generally tendency that the more raw foods a person eats, the lower their body weight. That does not mean that eating a vegetarian diet is more desirable, it is only to point out that with more and more processing – in this case, cooking, the higher body mass tends to be.

The Effect of Cooking Foods on Body Weight – Gabor Erdosi Food News 2018

3b. The Effect of Cooking Foods on Nutrient Availability

Carbohydrate-rich Foods

The relationship between cooking foods and body weight is particularly important with respect to carbohydrate-rich foods. For example, when grains are cooked they become much more digestible – meaning that more of the nutrients in the grain is available to be absorbed. In the case of potatoes, there is double or triple the amount of energy (calories) available to the body when they are cooked versus when they are raw. When a potato is cooked, the digestible starch increases 2-3 times, which means that these calories are now available to the body where they weren’t when they were raw.

The Effect of Cooking Carbohydrate on Nutrient Availability – Gabor Erdosi – Food News 2018
Lipid and Protein-rich Foods
The Effect of Cooking Lipid (fat) and Protein-rich Foods on Nutrient Availability – Gabor Erdosi Food News 2018

When foods that are high in lipids (fats) such as peanuts are cooked, the amount of energy the body is able to derive from the food, increases. As well, significantly more amino acids in protein-rich foods such as egg make it to the large intestine (where their nutrients are absorbed) when the protein-rich food is cooked.

3c. The Effect of Non-Thermal Food Processing on Nutrient Availability

Mechanical processing, such pounding food is also an ancient form of food processing which has an effect on how many nutrients are available to be digested. The nutrients available to the body when food is eaten raw and whole versus raw and pounded is significant, and this holds true whether the food is animal protein such as meat or a starchy vegetable such as sweet potato.

In a study with mice, one group of mice was fed meat either raw and whole or raw and pounded and then the group was crossed over to cooked and whole or cooked and pounded. The other group of mice was fed sweet potato eaten raw and whole or raw and pounded and then crossed over to cooked and whole or cooked and pounded.

When the meat or starchy vegetable (sweet potato) was eaten raw and whole, it was associated with lower body mass than the same foods eaten raw and pounded because the mice lost weight. As expected from what is known about the effect of cooking on nutrient availability (see above), when the mice ate the cooked meat or cooked sweet potatoes, they either didn’t lose as much weight (in the case of the meat) or actually gained weight (in the case of the sweet potato).

The conclusion of this study was worth noting;

“Our results indicate that human dieters who count calories and eat similar mixed diets but cook them to different extents would experience different weight gain outcomes at comparable levels of physical activity. This prediction is consistent with recent long-term data indicating that preparation-specific factors affect the relationship between caloric consumption and weight gain in humans.”

3 d. The Effect of Hydrolyzing Protein on Hormonal Response in the Small Intestine

Hydrolyzed protein, is essentially pre-digested protein and this process has an impact on which hormones are released in the small intestine when it is eaten.

In a 2010 study, comparing soy protein with soy protein hydrolysates and whey protein with whey protein hydrolysates, it was found that significantly more insulin compared to glucagon is released with the hydrolysates versus the intact protein. This means that the insulin to glucagon ratio is higher and insulin is the hormone which signals the body to store energy.  A higher insulin to glucagon ratio means that the body is storing energy rather than responding to glucagon which signals the body to use glucose and fat for energy.

4 a. The Effect of Mechanical Processing on the Blood Glucose Response of a Carbohydrate Food

Grinding / Juicing Fruit

Mechanical processing of a food doesn’t change the amount of carbohydrate that is in it. That is, when we compare 60g of whole apple with 60 g of pureed apple or 60g of juiced apple, there is the same amount of carbohydrate each. When we compare the Glycemic Index of these three, the results are very similar so this isn’t very helpful to tell us about the blood glucose response to actually eating these different foods.

When these foods are eaten, the blood glucose response 90 minutes later, is significantly  different.

Note: It’s not relevant to the outcome, but on this graph, slow and quick puree and juice as just differences in the amount of time it took for the liquid to be drunk.
The Effect of Mechanical Processing of Fruit on Blood Glucose Response – Gabor Erdosi – Food News 2018

As can be seen by the graph on the right, in healthy individuals blood insulin level goes very high with the juiced apple and in response, blood glucose then goes very low, below baseline.

The response that we see with the juiced apple is typical of what is seen with ultra-processed carbohydrates.

Grinding Grains

Grinding grains is another type of ancient food processing which changes the hormonal response in the small intestine.

The Effect of Mechanical Processing of Wheat on Blood Glucose Response – Gabor Erdosi – Food News 2018

When healthy individuals eat grain-based meals, the plasma insulin response increases the smaller the particle size of the grain.  That is, a specific amount of whole grain releases less insulin than the same amount of cracked grains, which is less than the same amount of course flour. The highest amount of insulin is released in response to eating the same amount of fine flour.

What was true for wheat in this study was true for rice as well and what was of interest, is there wasn’t a big difference between the insulin response with brown rice versus white rice.

The Effect of Mechanical Processing of Rice on Blood Glucose Response – Gabor Erdosi – Food News 2018

There is no difference in the Glycemic Index or Glycemic Load of whole wheat versus ground wheat or whole rice versus ground rice, but there is a huge difference in the insulin response with difference types of mechanical processing.

It’s also important to note that the amount of  fiber that was in the grain did not make a difference in the amount of insulin released, only the amount of mechanical processing of the grain. So, eating brown rice versus white rice won’t change the amount of insulin that is released – and insulin is a hormone that signals the body to store energy (calories).

In this next study, the same response that we saw with the pureed and juiced apples (above) is also seen with finely ground wheat bread. We see plasma glucose rise rapidly and then it drops below baseline at 120 minutes (circled).

Plasma glucose rises rapidly with bread made with wheat flour, then drops below baseline at 120 minutes

We know that the difference wasn’t due to the amount of fiber, because in this study they added back the fiber and it didn’t make a difference.

The difference had to do with the amount of disruption to the structure of the grain. So, eating whole wheat bread versus eating white bread — which is just adding the fiber that was taken out back won’t help much in terms of the insulin response.

The disruption of the structure of the grain had very adverse effects on the hormonal response; both the insulin response and GIP response, which can be seen in the next graph;

Disruption to structure of grain has adverse effect on insulin response and GIP response – Gabor Erdosi – Food News 2018

The bread made with flour resulted in a much larger insulin response and plasma GIP response than those made with whole kernel grains

Recall from the first article in this series, that GIP is released from the K-cells, which are dominant in the upper part of the small intestine. Bread made from ground flour results in a much greater and earlier hormonal response than bread made from whole grains.

The same researchers did another study a year later, this time with wheat bread, rye bread with the endosperm, traditional rye bread and high-fiber rye bread. As can be seen from these graphs (whether wheat or rye bread), it is the structural difference of the bread that explains the insulin response after a meal, not the total amount of fiber.

Note: Gabor Erdosi made a table comparing the Area Under the Curve (AUC) of the hormonal response of GIP (from the K-cells in the upper part of the small intestine) and GIP-1 (from the L-cells in the lower part of the small intestines) for the different breads which was very telling.
Area Under the Curve (AUC) of the hormonal response of GIP and GIP-1 for the different breads – Gabor Erdosi – Food News 2018

As can be seen from this table, there was almost double the GIP/GLP-1 ratio in the refined wheat bread (5.02) than the traditional rye bread (2.75) and this difference was largely due to significantly more GIP being released from the K-cells high up in the small intestine with the refined wheat bread than with the traditional rye bread.

It wasn’t due to fiber, because there was less GIP released with the traditional rye bread than even with the high fiber rye bread.

4 b. In-Vitro Hydrolysis of Starch Highly Correlates to Starch Digestion in the Small Intestine

This study shows a striking ability to predict how starch is hydrolyzed (broken down) in the small intestine with how it is broken down in a petri-dish in a lab using alpha-amylase. A perfect correlation would be = 1 and in this case it is 0.95.

Glycemic Response and Insulin Response to Starch Hydrolysis in-vitro and In-vivo – Gabor Erdosi – Food News 2018

As can be seen from these graphs, the glycemic response (blood sugar response) and the insulin response in the body can be accurately predicted using this method.

In this article we considered the effect of various kinds of ‘food processing’ on the speed and location of food absorption of individual macronutrients (such as protein, fat and carbohydrate), but we rarely eat meals that are only carbohydrate, or only protein or only fat.

How does the presence of protein and fat-rich foods influence the hormonal response in the small intestine and how do these affect the hormonal response to carbohydrate? How does fiber content or addition of fiber affect the hormonal response, or does it? These will be the topic of the next article where we’ll look at the hormonal response of the body to mixed meals (meals with different combinations of fat, protein and carbohydrate.

Perhaps you wonder what all this information means for you.

Maybe, like many you’ve become metabolically unwell with Type 2 Diabetes or high blood pressure or high cholesterol despite eating a diet rich in whole wheat bread, whole grain rice and lots of cooked vegetables and are beginning to realize that how your food is processed is as important a factor as the nutrients it contains in it’s unprocessed form.

I can help.

Feel free to send me a note using the “Contact Me” form located on the tab above to find out information about the services I offer, both in-person in my office or via Distance Consultation (using telephone or Skype).

To your good health!

Joy


 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


Part 2 (conclusion) of The Perils of Food Processing can be read here.

 

Gabor’s full lecture can be watched here:

References

  1. Gribble, Fiona M., and Frank Reimann. “Enteroendocrine Cells: Chemosensors in the Intestinal Epithelium.” Annual Review of Physiology 78, no. 1 (2016): 277–99.
  2. Reimann, Frank, and Fiona M Gribble. “Mechanisms Underlying Glucose-Dependent Insulinotropic Polypeptide and Glucagon-like Peptide-1 Secretion.” Journal of Diabetes Investigation 7 (2016): 13–19.
  3. Nauck, Michael A., and Juris J. Meier. “Incretin Hormones: Their Role in Health and Disease.” Diabetes, Obesity and Metabolism 20 (2018): 5–21.
  4. Perry, B., and Y. Wang. “Appetite Regulation and Weight Control: The Role of Gut Hormones.” Nutrition & Diabetes 2, no. 1 (January 2012): e26.
  5. Groopman, Emily E., Rachel N. Carmody, and Richard W. Wrangham. “Cooking Increases Net Energy Gain from a Lipid-Rich Food.” American Journal of Physical Anthropology 156, no. 1 (2015): 11–18.
  6. Evenepoel, Pieter, Dirk Claus, Benny Geypens, Martin Hiele, Karen Geboes, Paul Rutgeerts, and Yvo Ghoos. “Amount and Fate of Egg Protein Escaping Assimilation in the Small Intestine of Humans.”
  7. American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 5 (November 1999): G935–43.
  8. Carmody, R. N., G. S. Weintraub, and R. W. Wrangham. “Energetic Consequences of Thermal and Nonthermal Food Processing.” Proceedings of the National Academy of Sciences 108, no. 48 (2011):
    19199–203.
  9. Morifuji, Masashi, Mihoko Ishizaka, Seigo Baba, Kumiko Fukuda, Hitoshi Matsumoto, Jinichiro Koga, Minoru Kanegae, and Mitsuru Higuchi. “Comparison of Different Sources and Degrees of Hydrolysis of
    Dietary Protein: Effect on Plasma Amino Acids, Dipeptides, and Insulin Responses in Human Subjects.” Journal of Agricultural and Food Chemistry 58, no. 15 (August 11, 2010): 8788–97.
  10. Haber, G.B., K.W. Heaton, D. Murphy, and L.F. Burroughs. “Depletion and Disruption of Dietary Fiber” The Lancet 310, no. 8040 (1977): 679–82.
  11. Heaton, K.W., S.N. Marcus, P.M. Emmett, and C.H. Bolton. “Particle Size of Wheat, Maize, and Oat Test Meals: Effects on Plasma Glucose and Insulin Responses and on the Rate of Starch Digestion in Vitro” 47,no. 4 (1988): 675–82.
  12. O’Dea, K., Nestel, P.J., and Antonoff, L. “Physical Factors Influencing Postprandial Glucose and Insulin Responses to Starch” 33, no. 4 (April 1, 1980): 760–65.
  13. Juntunen, Katri S., Leo K. Niskanen, Kirsi H. Liukkonen, Kaisa S. Poutanen, Jens J. Holst, and Hannu M. Mykkänen. “Postprandial Glucose, Insulin, and Incretin Responses to Grain Products in Healthy Subjects.”The American Journal of Clinical Nutrition 75, no. 2 (2002): 254–262.
  14. Juntunen, K.S., D.E. Laaksonen, Leo K Niskanen Karin Autio Jens J Holst, Kari E Savolainen, Kirsi-Helena Liukkonen, Kaisa S Poutanen, and Mykkänen, H.M. “Structural Differences between Rye and Wheat Breadsbut Not Total Fiber Content May Explain the Lower Postprandial Insulin Response to Rye Bread” 78, no. 5(2003): 957–64.
  15. Bornet, F R, A M Fontvieille, S Rizkalla, P Colonna, A Blayo, C Mercier, and G Slama. “Insulin and Glycemic Responses in Healthy Humans to Native Starches Processed in Different Ways: Correlation with in Vitro Alpha-Amylase Hydrolysis.” The American Journal of Clinical Nutrition 50, no. 2 (1989): 315–23.

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

Evolving Theory of Obesity – a combination of refined carbs and industrial seed oils

Three years ago, my theory about the roots of the current obesity and Diabetes epidemic was simple. I believed that it was largely a matter of us eating too many carbs while having reduced the amount of healthy fat we ate. I now think it is a little more subtle than that, and that it is specifically the combination of a diet too high in refined carbs while high in industrial seed oils (such as soybean and canola oil) that underlies the issue.

When I first started reading and writing about the current obesity and Diabetes epidemic, my thoughts were summarized in two articles written in May and June of 2015. In the first article, I documented how in 1970-72 only 6% of men and 11.7% of women were considered obese (Body Mass Index > 30) in Canada, but by 2013 obesity in men had tripled to 20.1% in men and to  17.4% in women. In the second article, I explained how the changes in the obesity rates coincided with the changes in the Dietary Recommendations that began in 1977 and continued in 1982, 1992 and 2005 and which encouraged people to eat considerably more carbs and a lot less fat coincided with the increased obesity rates, and that the increasing rates of Type 2 Diabetes (9.4% in 2014 in Canada) was just a natural outworking of the higher obesity rates.

The problem was, I really didn’t know of any specific mechanisms that related one to the other.

Now I know of several.

This article summarizes my current theory of obesity, as it relates to previous articles and a brand new study published last week.

Correlation is not Causation

There’s an expression in science is that “correlation is not causation“.

That is, the fact that a dramatic increase in obesity rates correlates (or coincides) with the changes in the Dietary Recommendations doesn’t mean that the Dietary Recommendations ’caused’ the obesity epidemic or the Diabetes epidemic.

One can hypothesize that there is a relationship between these two things, but without some understanding of the mechanism and more data, we don’t know what this relationship might be.

From the reading I have been doing the last number of years, I have some ideas of some of what may be involved.

Evolution of the Theory

A presentation at a conference at the beginning of March (documented in  two previous articles) got me thinking that the picture was bigger than just “too many carbs” and a “decrease in the satiety effect of saturated fat” from full fat milk, cheese and butter. I was challenged by the fact that in the late 1960s and early 1970s, people in the US and Canada were generally slim, despite eating carbohydrates at just about every meal;

“They ate cereal or toast for breakfast and just about every household had a toaster. Lunch was often sandwiches, as there were no microwaves to heat food up in. Potatoes were a mainstay at dinner, sometimes pasta – yet the majority of young adults and adults were slim. Of course there were always some people that were overweight. Most elementary school classes had one ‘chubby’ kid, but when one looks around the classes of today or on public transit or in stores and supermarkets, most people are considerably heavier than people in the 1950’s and 1960’s”

(from A New Hypothesis for Obesity Part 1)

The question was raised ‘what resulted in overweight and obesity all of a sudden exploding in the 1970’s and just keep rising?’

What changed?

We knew that (based on US data) people began eating ~240 calories a day more as carbohydrate but what was causing them to do this? Was it just because the Dietary Recommendations were encouraging us to eat more carbohydrate or was there something else going on?

Not More Fat but the Type of Fat

While people were eating more carbohydrate, neither people in Canada nor the US were eating more fat, but the type of fat we’ve been eating since the 1970s has changed substantially. This tweaked my interest.

We’d reduced our intake of saturated fat (because the “Diet-Heart Hypothesis” had told us they were the “cause of cardiovascular disease”) and we dutifully ate more and more of ‘polyunsaturated fats’ / vegetable oils  which as I wrote about previously are more appropriately called “industrial seed oils“.  These oils, including soybean, corn oil and canola oil contain high amounts of linoleic acid which is at the very top of the omega 6 (n-6) pathway and these fats which elongate to arachidonic acid are pro-inflammatory products in nature.

There is nothing inherently ‘bad’ about linoleic acid which is found naturally in nuts and seed oils, including walnut, macadamia and sesame oil, but it is the sheer amount of these industrial seed oils which suddenly became excessive in our diet, which I think may be a significant factor.  These fats are in our bread, pastries, salad dressing, margarine and even our peanut butter.  Canned fish is packed in it, our mayonnaise is made from it and everything we eat that is fried from a restaurant is bathed in these industrial seed oils. On top of that, many of us use it our own homes to cook with.

So many of the foods we now eat are prepared with soybean or canola oil and as a result, we consume a much greater amount of linoleic acid than our body ever evolved to handle.

As outline in previous articles, these oils are much more unstable than the saturated fats they were created to replace. What I mean by ‘unstable’ is that they are more easily oxidized – that is, when industrial seed oils are heated in the making of commercial foods using them or in cooking, they react with oxygen in the air to form toxic substances including  aldehydes  and lipid peroxides.  When these oils are heated, they produce oxidized metabolites which have been also been implicated in the development of a variety of conditions, including non-alcoholic fatty liver disease (NAFLD), cardiovascular disease and cancer and it has been proposed that inflammation is involved in the development of Type 2 Diabetes and metabolic syndrome, as well.

Also as written about previously, cardiolipin  is an important component of the inner membrane of the mitochondria (the so-called “powerhouse of the cell”) and the fats that make up cardiolepin change, depending on the types of fats in the diet. That is, the fatty acid composition of cardiolepin is altered by us eating a diet high in linoleic acid, such as soybean and canola oil. This past week a study about cardiolepin was published that added a very interesting piece to my evolving theory of the obesity and Type 2 Diabetes epidemic.

In this new study, researchers at the University of Copenhagen found that when large amounts of cardiolipin are produced in ‘brown fat’ cell mitochondria, there is much stronger calorie-burning. Conversely, when there are low amounts of cardiolepin in brown fat, there is much less calorie-burning. Low amounts of cardiolepin and less calorie-burning in brown fat was reported to be associated with obesity and Type 2 Diabetes [1].

Note: "Brown fat" is a specialized type of fat that burns fat, rather than stores it and cardiolepin acts like a kind of on-off switch for the activity in our brown fat.

This study got me thinking that since it is known that the fatty acid composition of cardiolepin changes according to the fatty acid composition of the diet (covered in previous blogs), what effect has the massive increase in linoleic acid intake in the diet in both Canada and the US had on the function of the cardiolipin? 

Could it be that a shift in the types of fats that make up cardiolepin in brown fat stemming from a very high linoleic acid intake from industrial seed oils has had a similar effect as an absolute decrease in cardiolepin – and that this is somehow related to the increase in obesity and Type 2 Diabetes?

Type of Fats and Refined Carbohydrates

My theory of obesity has evolved and will likely continue to evolve. I don’t think that increased carbohydrate consumption based on changes in the Dietary Recommendations in the late 1970s / early 1980s in and by itself resulted in the obesity epidemic and huge increase in Type 2 Diabetes we see now.

I currently believe that the introduction of these manufactured industrial seed oils (soybean, canola, corn) that were created in the 1970s and meant to replace saturated fat in the diet (presumably to protect people from heart disease!) may be part of the initiation of the disease process.

As documented in earlier articles, we know that these fats are easily oxidized, have a direct impact on increasing inflammation and triggering the disease generation process in several health conditions and on acting on the endo-cannibinoid receptors in the body, in much the same way as cannabis (marijuana).  Could it be that these created oils that are very high in the average Western diet actually lead people to consuming more and more carbohydrate-based foods; foods that often comes liberally bathed in more industrial seed oils?

The mechanism of how the above might work was presented in an earlier article and had to do with how energy is generated in the electron transport chain of the mitochondria being different for saturated fats and unsaturated fats.

There are several possible mechanisms that may link consumption of these novel fats to obesity and development of Type 2 Diabetes (oxidation, inflammation, food cravings) and now based on this new study, the possibility of an increase in linoleic acid content in cardiolepin and it’s effect on fat burning.

It will take years more research before we have a fuller picture, so what do we do in the meantime?

Sensible Recommendations based on the Current Knowledge

For someone who is metabolically healthy (i.e. does not have Type 2 Diabetes or Insulin Resistance, hypertension or high cholesterol), it would seem that a whole-foods approach combined with avoiding omega – 6 industrial seed oils such as soybean, canola and corn oil combined with being mindful of the amount and type of carbohydrate in the diet may be sufficient to avoid developing these chronic diseases. Such a scenario would not be unlike the diet of the average American or Canadian in the 1950s and 60s. Not that that diet was that healthy, when compared with a classic Mediterranean diet, Japanese or Okinawan-style diet, or a whole food low-carbohydrate diet. These, it would seem offer a much healthier alternative.

For those who are already are insulin resistant or been diagnosed with Type 2 Diabetes, avoiding industrial seed oils would prudent and eating naturally-obtained vegetable fats such as olive oil or avocado oil instead. Since it does not seem that studies clearly support that saturated fat causes heart disease and not simply increase in surrogate markers of heart disease such as higher LDL (which LDL subfraction?), it would seem that using modest quantities of real butter is preferable to eating margarine made from industrial seed oils. It would also seem that at least initially, eating a diet where the amount and type of carbohydrate is kept to a quantity that does not trigger large amounts of insulin release or spike blood glucose makes good sense. As I wrote about recently, with the availability of Continuous Glucose Monitoring (CGM), this approach can be tailored to each individual person’s response to specific foods. We are no longer reliant on Glycemic Index or Glycemic Load, which are derived from healthy people’s response to foods, not those with Type 2 Diabetes. A suitable diet could be expressed as a variety of different lifestyles (just as for the healthy individual) including a Mediterranean diet, Okinawan-style diet, or whole food low-carbohydrate diet – with carbohydrate levels tailored on an individual basis, based on glycemic response and insulin levels.

Whether a person is healthy or metabolically unwell, based on the studies I have read and some of the mechanisms that have come to light, I can see no benefit in people eating either industrial seed oils or refined, processed carbohydrates. There is every reason to believe that both of these may have been part of the underlying cause of the current obesity and Type 2 Diabetes epidemic.

Unrefined Carbohydrates and Healthy Fats

If someone is metabolically healthy, I recommend eating minimally processed carbohydrates as they reduce the ‘incretin effect‘ of hormones such as GIP, GLP-1 and GLP-2 that are released in the intestine and trigger the release of insulin from the pancreas beta-cells. Eating minimally processed carbs would result in less triggering of the release of insulin, thus reducing the likelihood of developing either insulin resistance or Type 2 Diabetes.

If someone is already insulin resistant or has Type 2 Diabetes, it seems from recent studies that minimizing carbohydrate initially, along with weight loss and some forms of activity may be at least as good if not more beneficial than a low-fat calorie-restricted diet. Certainly, many people find they are a lot less hungry eating a low carbohydrate whole foods diet and are easily able to stick with it long term (a year or two in studies), allowing for a period of improving insulin sensitivity and lower overall blood sugar levels. It certainly has been demonstrated to be safe and effective in periods up to two years.

For both those that are metabolically healthy or insulin resistant or have Type 2 Diabetes, avoiding industrial seed oils makes good sense, for all the reasons outlined above.

What about your specific situation?

Do you have questions about the type and amount of carbohydrates that are most suitable for you based on your health and family history? What about which fats are are the best choices given your lifestyle?

I can help.

Please feel free to send me a note using the “Contact Me” form located on the tab above to find out how I can support your needs and I will reply as soon as possible. Remember, I provide both in-person services and am experienced providing services via Distance Consultation (telephone or Skype).

To your good health!

Joy


 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Reference

Sustarsic EG, Ma T, Lynes MD et al, Cardiolipin Synthesis in Brown and Beige Fat Mitochondria Is Essential for Systemic Energy Homeostasis,
Cell Metabolism (2018), https://doi.org/10.1016/j.cmet.2018.05.003

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

 

 

 

How Much Does Your Type 2 Diabetes Cost per Year?

The most recent data available from 2011 indicates that the cost per person per year of having Type 2 Diabetes in Canada ranges from $1611 (Quebec) to $3427 (New Brunswick) based on an average income of $43,000 per year. Necessary medications, devices and supplies are expensive – costing more than 3% of income. While those with extended health benefits may not consider this cost now, a change in employment circumstances can affect this overnight.

As Type 2 Diabetes progresses, more medications are often added and the number of times blood sugar needs to be taken each day often increases, as well.  Job loss or retirement suddenly results in Canadians being faced with bearing the burden of their disease, along with the chronic, progressive nature of poorly managed blood sugars.

A per-province breakdown using the 2011 figures from the Canadian Diabetes Association appears below;

Cost of Type 2 Diabetes per person per year by province (2011 figures) – from Canadian Diabetes Association

It doesn’t have to be so.

Long term studies that have been published in the last couple of years (reviewed in previous articles on this site) which demonstrate that a well-designed low carbohydrate or ketogenic diet can and does enable a significant improvement in Type 2 Diabetes symptoms.

After as little as 10 weeks, glycosylated Hemoglobin (HbA1C) has been reported to drop a full percentage point; from 7.6% to 6.6%. After a year, the average HbA1C was 6.3%, which is below the diagnostic criteria for Type 2 Diabetes.  That is, in just a year of following a well-designed low carbohydrate diet, it has been demonstrated that people can get their average blood glucose in the non-Diabetic range.

Medication use drops substantially when people are able to control their blood sugar by limiting the amount and types of carbohydrates they eat.  At the start of the study mentioned above published in Feb of 2018, 87% of people were taking at least one medication for Diabetes and at just 10 weeks, almost 57% had one or more Diabetes medications reduced or eliminated. After one year, Type 2 Diabetes medication prescriptions other than Metformin declined from 57% to below 30%. Insulin injections were reduced or eliminated in 94% of users and sulfonylurea medication was entirely eliminated.

For each one of these individuals, a simple change to a low carbohydrate diet resulted not only in significantly improved health and a reduction in Diabetes symptoms, but in significantly reduced cost, as well.

According to Virta Health who conducted the study referred to above, cost savings are as indicated in this diagram below.

The cost of "Diabetes Reversal" below reflects the estimated cost of an individual being cared for by the Virta Health multi-disciplinary team program, which appears to be an excellent program given the methods used in the studies they have published. 

It should be noted that the cost of working one-on-one with me over the course of a year (and as overseen by your GP) is substantially less. In fact, getting started by being assessed and having me design an individual Meal Plan just for you is significantly less than the yearly cost of achieving better blood sugar control in the graphic below.
Average Per Person Per Year Saving Potential (US dollars, 2018) – from Virta Health

Sometimes people are hesitant to invest in the cost of seeing a Registered Dietitian who can help them adopt a low carbohydrate lifestyle that can enable them to achieve significantly improved blood sugar control – even though the yearly costs of Diabetes supplies is far greater than the cost of being assessed and getting a Individualized Meal Plan. Such an estimate is at the level of health they are today, but waiting a few years, with longer Type 2 Diabetes, more medications, possibly including insulin injections, and the cost is closer to $3500 in 2011 Canadian dollars / $4000 in 2018 (US) dollars.

Does this make any sense?

The sooner someone changes their diet and lifestyle upon being diagnosed with Type 2 Diabetes, the more likely it seems they may be able to achieve full remission of symptoms. If you’ve followed my own story on “A Dietitian’s Journey” then you know how much harder it is for me, after being diagnosed 10 years ago.

If you have extended benefit coverage, then now is the time to invest some time in learning how to make lifestyle changes that will benefit your health and your finances for the years to come.  Even for those without such coverage, the cost of an assessment package which will provide you with a  Meal Plan designed specifically for you is substantially less than you are already paying for your medications, devices and supplies. I provide both in-person services in my Coquitlam, British Columbia office and via Skype Distance Consultations.

If you have questions about this package entails or about the flexible payment options that are available, why not send me a note using the “Contact Me” form located above? I’ll be happy to reply.

To your good health,

Joy


 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

Canadian Diabetes Association, The Burden of Out of Pocket Costs for Canadians with Diabetes, 2011, http://www.diabetes.ca/CDA/media/documents/publications-and-newsletters/advocacy-reports/burden-of-out-of-pocket-costs-for-canadians-with-diabetes.pdf


Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

CVD Risk Improves By Use of Ketogenic Diet in Type 2 Diabetes at 1 year

One of the concerns raised by opponents of a very low carb or ketogenic diet is that it increases risk of cardiovascular disease such as heart attack and stroke, but does it?

Results of a peer-reviewed study of cardiovascular outcomes of people with Type 2 Diabetes (T2D) that was published at the beginning of May in the Journal of Cardiovascular Diabetology[1] found that those that followed a ketogenic diet significantly improved in 22 of 26 cardiovascular disease risk factors, including biomarkers of cholesterol / lipoproteins, blood pressure, inflammation, and carotid intima media thickness (cIMT).

Previous published results from the same researchers and published in February of 2018 demonstrated that reversal of T2D symptoms was able to be achieved and sustained long term using a ketogenic diet[2,3].

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was not only a significant decrease in blood sugar and weight, but a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

The results of this most recent study do much to dispel the myth that a therapeutic ketogenic diet puts individuals at increased risk for heart attack and stroke. In fact, it reduces their risk.

Methods

Continuous Care Intervention (CCI) Group Participants

At the beginning of the study, there were 238 participants enrolled in the continuous care intervention (CCI) group and all had a diagnosis of Type 2 Diabetes (T2D) with an average HbA1c of  7.6%  ±1.5%.  They ranged in age from 46 – 62 years of age, 67% were women and 33% were men. Weight of the subjects ranged from 200 pounds to 314 pounds (117±26 kg) with an average weight of 257 pounds (117 kg) and Average Body Mass Index (BMI) was 41 kg·m-2 (class III obesity) ±9 kg·m-2, with 82% categorized as obese.  The majority of participants (87%) were taking at least 1 medication for glycemic control medication.

At the end of a year, 218 participants (83%) remained enrolled in the  continuous care intervention (CCI) group.

Intervention and Monitoring of CCI Group

Each participant in the CCI group received an Individualized Meal Plan which enabled them to attain and maintain nutritional ketosis. They also received behavioral and social support, biomarker tracking tools, and ongoing care from a health coach with medication management by a physician.

Subjects typically required <30 g·day−1 total dietary carbohydrates.

Daily protein intake was targeted to a level of 1.5 g·kg−1 based on ideal body weight and participants were coached to incorporate dietary fats until they were no longer hungry.

Other aspects of the diet were individually tailored to ensure safety, effectiveness and satisfaction, including consumption of 3-5 servings of non-starchy vegetables and sufficient mineral and fluid intake.

Participants ability to achieve and maintain nutritional ketosis was determined by subjects monitoring their blood ketone level of β-hydroxybutyrate (BHB) using a portable, handheld device. Blood glucose and β-hydroxybutyrate (BHB) levels were initially tracked daily using a combination blood glucose and ketone meter and frequency of tracking was modified by the care team based based on each individual’s needs and preferences.

Participants with high blood pressure (hypertension) were provided with an automatic home blood pressure machine (sphygmomanometer) and they were instructed to record their readings daily to weekly in the supplied app, depending on recent blood pressure control. Antihypertensive medication prescriptions were adjusted based on home blood pressure readings and reported symptoms.

Downward Adjustment and/or Discontinuation of Medications

As blood pressure came down, diuretic medication was the first antihypertensive medication to be discontinued. This was followed by beta blockers (unless the participant had a history of coronary artery disease).

Angiotensin-converting-enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) were generally continued due to their known protective effect on the kidneys in those with Type 2 Diabetes.

Statin medications were adjusted to maintain a goal of LDL-P under 1000 nmol L−1 (or based on participant preference after full risk/benefit discussion with the physician).

The Usual Care (UC) Group

For comparison purposes, an independent group of patients with Type 2 Diabetes were also recruited for the study and were referred to Registered Dietitians that provided dietary advice according to the American Diabetes Association Guidelines [4].

Laboratory Assessors

Since an abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) is a known risk factor for CVD [5] and is very common in people with Type 2 Diabetes, a number of laboratory tests were conducted at the beginning of the study and the end to determine if they improved, stayed the same or got worse.

Most common in people with Type 2 Diabetes is where there are increased triglycerides (TG), decreased high-density lipoprotein cholesterol concentration (HDL-C) and increased small low-density lipoprotein particle number (small LDL-P).

The authors of this study state that evidence suggests that increased very low-density lipoprotein particle number (VLDL-P) and a large VLDL-P in particular may be one of the key underlying abnormalities in this abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) associated with T2D.

The authors also outline how higher concentrations of small LDL are often associated with increased total LDL particle number (LDL-P) and increased ApoB which is the main protein constituent of  very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL). The authors provide previous study evidence that demonstrates that in people with insulin resistance and T2D, increased total LDL particle number (LDL-P) and increased ApoB may exist even with normal to low LDL-C concentrations values. For this reason, LDL-C alone was not relied on as a measure of abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) in this study as it could miss the impact of increased total LDL particle number (LDL-P) and/or ApoB.

The authors mentioned that in previous studies with carbohydrate restriction of up to 1 year, while triglycerides (TG) usually decrease and HDL-C often increase, LDL-C sometimes increased and other times decreases. The authors note that although higher LDL-C is a known risk factor for CVD, low LDL-C may also reflect higher small, dense LDL, total LDL particle number (LDL-P) or ApoB and thus be a risk factor, as well.

Since inflammation is involved at all stages of the atherosclerotic process, higher high-sensitivity C-reactive protein (CRP) and/or higher white blood cell count (WBC) were assessed as risk factors for CVD.

Finally, since high blood pressure (hypertension) is also an added risk factor for CVD in people with T2D, tighter blood pressure control was deemed to reduce the risk of DVD, stroke and other microvascular events.

Continuous Care Intervention (CCI) Group

Standard laboratory fasting blood draws of the CCI group were obtained at the start of the study (baseline), at 70 days (3 months) and at ~ 1 year follow-up.

Lipid/cholesterol-related tests included ApoB, ApoA1, total cholesterol, triglycerides, direct HDL-C concentrations and LDL was calculated using the Friedewald equation.

The LipoProfile3 algorithm was used to determine relationship of lipid subfractions to cardiovascular (CVD) risk – specifically the number of HDL particles (HDL-P) previously reported  to be associated with death, Myocardial Infarction (MI), stroke and hospitalization, HDL-C (HDL cholesterol) which is the amount of cholesterol those particles are carying, which is not associated with these negative outcomes and HDL-P subclasses [6].

Risk was also determined using the lipoprotein insulin resistance score (LP-IR) which was proposed to be associated with the homeostasis model assessment of insulin resistance (HOMA-IR) and glucose disposal rate (GDR) [7].

Finally, risk was also determined using the 10-year atherosclerotic  cardiovascular disease (ACSVD) risk score of the American College of Cardiology [8].

Carotid ultrasonography (cIMT) measure was performed at baseline and 1 year to characterize atherosclerotic risk.

The Usual Care (UC) Group

Body measurements, vital signs and fasting blood draws for the Usual Care (UC) group were obtained at the start of the study (baseline) and at 1 year using the same clinical facilities and laboratory and data collection methods. Carotid ultrasonography (cIMT) measure was also performed at baseline and 1 year to characterize atherosclerotic risk.

Results

There were no significant difference in the baseline characteristics of the two sub groups of CCI participants (web-based on onsite-based) and no significant difference at 1 year, so for the purpose of analysis, data from both groups were combined.

As well, there were no significant difference in the baseline characteristics of the Usual Care (UC) group (which served as an observational comparison group) and the Continuous Care Intervention Group (CCI) except mean body weight and BMI were higher in the CCI versus the UC group.

The within-Continuous Care Intervention group changes in the following lipids and lipoproteins were all statistically significant and were as follows;

ApoA1  [a component of high-density lipoprotein (HDL)] increase by + 9.8%)

ApoB / ApoA1 ratio decreased by − 9.5%

Triglycerides (TG) decreased by − 24.4%

LDL-C increased by + 9.9% but LDL-particle size also increased by + 1.1% (that is, large fluffy LDL increased compared with small, dense LDL)

HDL-C increased by + 18.1%

total HDL-P increased by + 4.9%

large HDL-P increased by 23.5%

Triglyceride/ HDL-C ratio decreased by − 29.1%

large VLDL-P decreased by − 38.9%

small LDL-P decreased by − 20.8%

There were no significant changes in total LDL-P or ApoB.

These results are impressive!

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

In addition, the Continuous Care Intervention group had a significant reduction in;

systolic blood pressure decreased − 4.8%

diastolic blood pressure decreased − 4.3%

C-Reactive Protein (CRP) decreased almost 40% (i.e. − 39.3%) 

white blood cell (WBC) count decreased − 9.1%

Below are graphs of the changes in biomarkers for the Continuous Care Intervention (CCI) group (figure 1) and the Usual Care (UC) Group;

FIGURE 1: changes in biomarkers for the Continuous Care Intervention (CCI) group

 

FIGURE 2: changes in biomarkers for the Usual Care (UC) group

Below is a comparative graph of the two groups, the Continuous Care Intervention (CCI) Group and the Usual Care (UG) Group

FIGURE 3: changes in biomarkers for the Continuous Care Intervention (CCI) group compared to the Usual Care (UC) group

Some Final Thoughts…

This study demonstrates that a therapeutic ketogenic diet followed over the course of 1 year significantly improved 22 of 26 cardiovascular disease risk markers in those with Type 2 Diabetes. This is huge!

The size of the study group was large and had an 83% retention rate over the course of the year – which in and by itself demonstrates that the intervention diet was one that people had no difficulty staying with in their day-to-day lives, without the use of meal replacements (shakes or bars).

While not a randomized control trial between CCI and UG groups, this study supports that a ketogenic diet is both safe and effective for periods of up to a year (and in other studies has been documented to be safe and effective for up to two-years). Not only can a well-designed ketogenic diet reverse many of the symptoms of Diabetes (documented in this earlier article) it can also significantly improve risk markers for cardiovascular disease.

Do you have questions about how a carefully-designed low carbohydrate or ketogenic diet can help you improve symptoms of Type 2 Diabetes and lower markers of risk factors for cardiovascular disease?

Please send me a note using the “Contact Me” form above to find out more about how I can provide you with in-person or Distance Consultation services (via Skype or long distance telephone).

To our good health,

Joy


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References

  1. Bhanpuri NH, Hallberg SJ, Williams PT et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  2. McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD, A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, JMIR Diabetes 2017;2(1):e5, URL: http://diabetes.jmir.org/2017/1/e5, DOI: 10.2196/diabetes.6981
  3. Hallberg SJ, McKenzie AL, Williams, PT et al. Diabetes Ther (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.
  4. America Diabetes Association, Lifestyle management. Diabetes Care. 2017;40 (Suppl 1):S33–S43
  5. Fruchart J-C, Sacks F, Hermans MP, Assmann G, Brown WV, Ceska R, et al. The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in patients with dyslipidemia. Am J Cardiol. 2008;102:1K–34K.
  6. May HT,  Anderson JL, Winegar DA, Utility of high density lipoprotein particle concentration in predicting future major adverse cardiovascular events among patients undergoing angiography, Clinical Biochemistry, 2016;49(15): 1122-1126
  7. Shalaurova I, Connelly MA, Garvey WT, Otvos JD. Lipoprotein insulin resistance index: a lipoprotein particle-derived measure of insulin resistance. Metabol Syndr Relat Disord. 2014;12:422–9.
  8. Goff DC, Lloyd-Jones DM, Bennett G, Coady S, D’Agostino RB, Gibbons R, et al. ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;2014:S49–73 (tool: http://tools.acc.org/ASCVD-Risk-Estimator-Plus/#!/calculate/estimate/)

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Two More Good Indicators of Cardiovascular Risk

In a recent article about why Waist Circumference and Waist-to-Height Ratio is so important, I explained that a meta-analysis from 2012 which pooled data from 300,000 adults of different races and ages found that the lowest risk of cardiovascular disease and shorter lifespan was associated with a Waist to Height Ratio (WHtR) of 0.5. That is, we are at lowest risk when our waist circumference is less than half our height (even if our BMI is in the normal range). I also explained exactly how to take waist circumference, so that the results are accurate.

There are other measures of cardiovascular risk that I think are worth considering.

  1. A 2015 study of 3200 adults found that Waist-to-Hip Ratio (WHR) is more accurate in predicting 10-year cardiovascular risk than Waist to Height Ratio (WHtR), however whether this relationship would hold up in a sample as large as the meta-analysis above is unknown. I feel it is worth mentioning Waist-to-Hip Ratio (WHR) as an indicator of cardiovascular risk, as it is easy to do.
  2. Another index this 2015 study found to accurately predict 10-year  cardiovascular risk was something called Conicity Index which I will touch on even though it is not as easily determined as Waist-to-Hip Ratio (WHR) or Waist to Height Ratio (WHtR).

Determining Waist to Hip Ratio

As mentioned in the previous article, to use these indices requires waist measurements and hip measurements to be done accurately and at a specific place on the body.  To make it easier, I will repeat how to measure waist circumference here and below, how to measure hip circumference.

Measuring Waist Circumference

For the purposes of calculating risk associated with increase abdominal girth, waist circumference needs to be measured at the location that is at the midpoint (i.e. half way) between the lowest rib and the top of the hip bone (called the “iliac crest”). Below is a picture that should help.

Where to measure waist circumference

This measurement should be taken with a flexible seamstress-type tape measure, being sure that the tape measure is at the same height in the front and the back, when looking in front of a mirror. That is, the tape measure should be perpendicular to the floor (not higher in the back or the front).

It’s also important that the person’s abdomen (belly) is completely relaxed when taking the measurement, not sucked in.  One way to do that is to taking a deep breath and let it out fully just as the measurement is taken.

If your Waist to Height ratio is greater than 0.5, then you are at increased risk for cardiovascular events and a shortened lifespan. Looking at the graph above, one can see that for every little bit over 0.5, the risk rises steeply.

Measuring Hip Circumference

Hip circumference needs to be measured at the widest portion of the buttocks (butt) and as with waist circumference, the tape measure needs to be parallel to the flood (same height in the front and the back, when looking in front of a mirror).

For both the waist and hip measurement, the tape measure should be snug around the body, but not pulled so tight that it is constricting and it is best if a stretch‐resistant but flexible seamstress-type tape measure is used.

Assessing Waist-to-Hip Ratio

If the waist circumference is measured in inches, then the hip circumference needs to be as well – same if the measurement is in centimeters; both need to be in the same units.

To calculate the Waist-to-Hip Ratio take the waist circumference and divide it by the hip circumference.

Waist-to-Hip Ratio and Risk of Cardiovascular Disease

The following ratios are associated with low, moderate and high risk of cardiovascular risk;

Low Risk: For men, if the ratio is 0.95 or less, for women if the ratio is 0.80 or less

Moderate Risk: For men, if the ratio is 0.96 – 1.0, for women if the ratio is 0.81 – 0.85

High Risk: For men, if the ratio is 1.0 or more, for women if the ratio is 0.85 or more.


The Waist-to-Hip Ratio can also be thought of as people being shaped like “apples” or “pears“.

“Apples” versus “Pears”

People who carry most of their excess weight around their middle (“apples”) have more visceral fat and this type of fat is much more dangerous than the fat under our skin (called “sub-cutaneous fat”) because it is found around the heart, liverpancreas and other organs and increases the risk not only of cardiovascular disease, but also Type 2 Diabetes and hypertension.

People who’s hips are much wider than their waist (so-called “pears”) have less visceral fat and therefore lower risk of these weight-related health problems.

Conicity Index

Conicity Index(CI) is a little more cumbersome a calculation than either Waist-to-Hip (WHR) Ratio or Waist-to-Height (WHtR), but was found in the 2015 study mentioned above with 3200 subjects to be a strong predictor of cardiovascular risk.

Conicity literally means “cone-shaped” and determines how much our  body fat distribution like two end-to-end cones.

In the first figure below, body weight is distributed evenly, however when someone has a conical distribution, their weight is more heavily distributed around the abdomen. As a result, it has increased conicity and is more highly correlated to increased cardiovascular disease (as well as Type 2 Diabetes and hypertension).

For those who are interested in calculating Conicity Index (CI), the formula is below along with the formula for Waist-to-Hip (WHR) Ratio, Waist-to-Height (WHtR).

Indices of central adiposity

Final Thoughts…

Given the sample size of the data on which Waist-to-Height (WHtR) is based (300,000 adults) and that it is an easy to determine and robust measure of cardiovascular risk, this is the one I tend to favour.  That said, Waist-to-Hip (WHR) Ratio was previously used for years and found to be a simple and accurate predictor of risk. From that point of view, either could be used, but why not both?

In my clinical experience, I have encountered many people with much wider hips than waist (so-called “pears”) but whose Waist-to-Height (WHtR) is considerably greater than 0.5, and for this reason I tend to put more credence on Waist-to-Height (WHtR) than Waist-to-Hip (WHR) Ratio as a measure of visceral fat and increased cardiovascular risk.

Since both Waist-to-Height (WHtR) and Waist-to-Hip (WHR) Ratio are very easy to determine, for those with a family risk of cardiovascular disease, Type 2 Diabetes or hypertension, I think it makes sense to aim for a waist measurement that is within both of these easily obtained measures.

Do you have questions about how I can help you lower your risk of cardiovascular disease, Type 2 Diabetes or hypertension? I provide both in-person and Distance Consultation services via Skype or telephone (and remember, many extended benefits plans will reimburse for visits with a Registered Dietitian).

Please feel free to send me a note using the “Contact Me” form on the tab above to find out more.

To our good health,

Joy

References

  1. Rabiee B,  Motamed N, & Perumal D, et al. Conicity index and waist-hip ratio are superior obesity indices in predicting 10-year cardiovascular risk among men and women. Clin. Cardiol. 38, 9, 527–534 (2015)

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Importance of Waist Circumference & Waist to Height Ratio

Most of us know that obesity is where a person has high levels of body fat, but at what point does overweight become obese? There are different ways of determining this and one way that many people are familiar with is the Body Mass Index.

Body Mass Index (BMI) classifies whether a person is overweight or obese by looking at their weight to height ratio. It is calculated by taking a person’s weight (in kilograms) and dividing it by their height (in meters squared).

BMI= weight (kg) / height (m) x height (m).

People are considered overweight if their BMI is between 25 and 29.9 and obese if it is above 30.

There are different levels of obesity, too.

Class I obesity is a BMI between 30 and 34.9.

Class II obesity is a BMI between 35 and 39.9.

Class III obesity (also called morbid obesity) is a BMI is greater than 40.

In recent years, research has determined that waist-to-height ratio is a much better predictor of cardiovascular health risk and a shorter lifespan due to illness than BMI, which is weight to height ratio.

A meta-analysis from 2012 pooled data from multiple studies, and examined Waist to Height Ratio (WHTR) in more than 300, 000 adults from several different ethnic groups and found that was a far better predictor of cardiovasular of metabolic risk factors in both men and women, than BMI [1].

A 2014 study found a correlation between Year of Life Lost (YLL) for different values of Waist to Height Ratio (WHtR) and found that YLL increased dramatically in both males and females when above 0.52 – a waist circumference of just over half one’s height [2].

Waist-to-Height Ratio Is More Predictive of Years of Life Lost than Body Mass Index [2]
These two studies found that the least amount of years of life lost is associated with a Waist to Height Ratio of 0.5That is, our waist circumference should be less than half our height, even if our BMI is in the “normal range”*.

*Both males and female non-smokers have a slightly increased Years of Life Lost at waist circumference > 0.50, even when their BMI was in the normal range (18.5 to to 22) - which means that waist circumference is a more important predictor of shortened lifespan due to cardiovascular disease, than BMI. 

Determining Waist to Height Ratio

If you’re a male and 5’10” tall (70″ tall), then to be in the lower risk category, your waist circumference should be 35 inches or less.

If you’re a female and 5’6″ tall (66″ tall), then your waist circumference should be 33 inches or less.

Waist to Height Ratio

But where should we measure waist circumference?

Is it where we wear our pants? Is it at the smallest part of our belly, where it dips in? Is it where our navel (belly button) is? Each one of these will produce very different results.

Measuring Waist Circumference

For the purposes of calculating risk associated with increase abdominal girth, waist circumference needs to be measured at the location that is at the midpoint (i.e. half way) between the lowest rib and the top of the hip bone (called the “iliac crest”). Below is a picture that should help.

Where to measure waist circumference

This measurement should be taken with a flexible seamstress-type tape measure, being sure that the tape measure is at the same height in the front and the back, when standing in front of a mirror. That is, the tape measure should be perpendicular to the floor (not higher in the back or the front).

It’s also important that the person’s abdomen (belly) is completely relaxed when taking the measurement, not sucked in.  One way to do that is to taking a deep breath and let it out fully just as the measurement is taken.

If your Waist to Height ratio is greater than 0.5, then you are at increased risk for cardiovascular events and a shortened lifespan. Looking at the graph above, one can see that for every little bit over 0.5, the risk rises steeply.

How Much Should I Weigh?

People often ask me “how much should I weigh” – wanting me to provide them with a specific weight in pounds or kilos.

While I can give people a ball-park figure based on their height and weight, how much we should weigh is when our waist circumference is half our height. At this weight, we have the lowest risk of heart attack and stroke (cardiovascular disease) and the lowest amount of Years of Life Lost.

Health is not a number on the scale.  Its the measurement of the amount of fat in our abdomen, around our liver, kidneys, pancreas and heart.

If your waist circumference is greater than 0.5 you are at risk.

If you have been diagnosed with Type 2 Diabetes or pre-Diabetes, high blood pressure or high cholesterol, then this risk is compounded.  Add to that a family history of these, and your risks are even higher.

While we can’t change our family history, we can change our diet and lifestyle and lower our risk.

Attaining a waist to height ratio of 0.5 is often associated with lower blood sugars, lower blood pressure and better cholesterol – even more so when the diet to achieve the weight loss is intentionally designed for these outcomes.

If you would like help getting on your own road to better health, please send me a note using the Contact Me form on this web page, and let me know how I can help. Remember, I provide both in-person and Distance Consultation services via Skype and many extended benefits plans will reimburse for visits with a Registered Dietitian.

Please send me a note if you have questions.

To our good health,

Joy


 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Ashwell M, Gunn P, Gibson S (2012) Waist-to-height ratio is a better screening tool than waist circumference and BMI for adult cardiometabolic risk factors: systematic review and meta-analysis. Obes Rev 13: 275–286
  2. Ashwell M, Mayhew L, Richardson J, Rickayzen B (2014) Waist-to-Height Ratio Is More Predictive of Years of Life Lost than Body Mass Index. PLoS ONE 9(9)

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Don’t Try This at Home – the need for medication supervision

There are some things that people should not do on their own and one of them is to begin a low carb or ketogenic diet without first consulting with their doctor, especially if they take certain types of medication. Medical supervision is absolutely required before a person changes the level of  their carbohydrate intake if they are taking;

(1) insulin

(2) medication to lower blood glucose such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc. and other types of glucose lowering medication such as Victoza, etc.

(3) medication for blood pressure such as Ramipril, Lasix (furosemide), Lisinopril / ACE inhibitors, Atenolol / β₁ receptor antagonists

(4) mental health medication such as antidepressants, medication for anxiety disorder, and mood stabilizers for bipolar disorder and schizophrenia.

I don’t provide low carbohydrate dietary services those taking insulin (either Type 1 Diabetes or Type 2 Diabetes), but encourage those considering adopting this type of lifestyle to first consult with a healthcare professional with CDE certification, as well as their family doctor. This is very important because clinical studies indicate that insulin levels need to be adjusted downward very soon after beginning a low carbohydrate or ketogenic diet and this must be medically supervised.

I also recommend to those taking medication for mental health conditions that they consult with their psychiatrist and/or family practice physician before changing their diet. A low carb or ketogenic diet may have an effect on the dosage of medication required, especially with mood stabilizing medications such as Lithium. (A recent article written by Psychiatrist Georgia Ede, MD related to a ketogenic diet appeared in Psychology Today and appears here.)

Why do I advise people coming to me to implement a low carbohydrate or ketogenic lifestyle and taking medication to control their blood sugar or blood pressure first consult with their doctor before changing how they eat? It is because eating less carbohydrate can result in blood sugar levels and blood pressure coming down fairly soon afterward and this can have serious consequences if dosages of these medications are not monitored and adjusted downward (and often being discontinued entirely).  For example, a sudden drop in blood pressure could result in people becoming dizzy or confused and could even result in injury to themselves or others if they ‘blacked out’ while walking or driving a car.

Some medications which lower blood sugar such as sodium glucose co-transporter 2 (SGLT2) medication including Invokana, Forxiga, Xigduo, Jardiance, etc. can result in life-threatening and even fatal cases of a very serious condition called “Diabetic ketoacidosis (DKA)” even with no change in diet, but these risks can be increased for patients on a very low carbohydrate diet as the combination of the medication and the low carb diet may increase the amount of ketone production (see Health Canada’s Safety Review here).

Those with significant alcohol consumption who are taking these medications are at risk for DKA, so it is very important that if you drink alcohol on a regular basis and take these medications to tell your doctor. If you are taking any of these medications and come to me, I will ask you about your alcohol consumption because alcohol and these medications together could potentially result in this serious and potentially life-threatening condition.

People taking any of the above medications (or any medications for other conditions) should not adopt a low carb or ketogenic lifestyle on their own without first checking with their doctor.

Another thing that people should never do on their own is adjust the dosage of any of their prescribed medication without first discussing it with their doctor. The consequences of doing so can be very serious, even life-threatening. For example, people taking SGLT2 inhibitors such as Invokana or Jardiance who decrease their insulin dosage suddenly are at increased risk for DKA. This is very serious. Medication dosages and timing must be adjusted by a doctor.

Another condition which is less common than DKA but is very serious is Hyperosmolar Hyperglycemia State (HHS).  It is life-threatening and has a much greater death rate than DKA, reaching up to 5-10%. It is most commonly seen in people with Type 2 Diabetes (T2D) that have some illness which results in reduced fluid intake, and them becoming seriously dehydrated. Being sick with an infection is one such situation where it is very important for you to see your doctor if you have T2D, so they can monitor you for HHS. You can read more about HHS here.

If you come to see me to adopt a low carb or ketogenic diet, I will work with you to coordinate dietary and lifestyle changes with your doctor, as they monitor your health and adjust the levels of prescribed medications. In more complex cases, I may ask for written consent to coordinate care with your doctor because depending on those medications, your doctor may need to know in advance what level of carbohydrates you have been advised to eat so that they can monitor your health and make adjustments in your medication dosage.

Your health is important and your diet and the medications need to be coordinated and overseen by your doctor. The potential risks are too great to attempt to do this on your own.

Do you have questions as to how I could work with you and your doctor as they oversee you adopting a low carb lifestyle?  Feel free to drop me a note using the Contact Me form on the tab above.

To your good health!

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

 

 

 

Keto 153 – Interview with Joy Kiddie, the LCHF-Dietitian from Ketovangelist

For those who are curious about my background and how I came to practice and support the use of a therapeutic low carb and ketogenic diet, here is the interview that was done by Brian Williamson, from Ketovangelist just this past week (May 1 2018).

The interview lasts just over an hour (there’s a short commercial at the beginning and end of the interview) and begins with discussing my research, findings and publication in a peer-reviewed journal in the area of mental health nutrition (specifically micronutrient intake and dietary intake in ADHD) and how that research background contributed to my approach to using a low carbohydrate and ketogenic diet in therapeutic nutrition.

During the interview, Brian and I discussed several areas, including the politics of nutrition, changes in Dietary Guidelines in both the US and Canada in 1977, the obesity epidemic and the role that I see for individual nutrition in helping those with Type 2 Diabetes and insulin resistance and many of the associated conditions of high blood pressure, high triglycerides / abnormal cholesterol levels and obesity.

Special thanks to Brian Williamson for inviting me and to Chris, his editor for his post-production work.

I hope you enjoy the interview, and feel free to drop me a note through the Contact Me form, if you have any questions on how I can help you, either in-person or via Distance Consultation on Skype.

To our good health!

Joy

Keto 153 – Joy Kiddie interview on Ketovangelist

Please click the MP3 player bar above to listen to the interview.


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References

Here is the link to the interview on Ketovangelist https://www.ketovangelist.com/keto-153-joy-kiddie-shares-her-story-and-how-shes-changing-the-world-as-a-lchf-dietitian/

 

A Therapeutic Low Carb Diet

When people are diagnosed with Type 2 Diabetes they are often sent for Diabetes education which teaches them, among other things to “choose starchy foods such as whole grain breads and cereals, rice, noodles, or potatoes at every meal” and that “good management of diabetes includes healthy eating, staying active and taking required medication [1].  There is certainly a need for medication when blood sugar levels are not being controlled but what if in other cases, as Hippocrates has said food could be our medicine?

Food As Medicine

A therapeutic diet is involved in the management and treatment of many diseases and conditions. When someone is diagnosed with Celiac disease, for instance  they are taught by a Dietitian to avoid gluten-containing foods because these cause damage to their intestines. A therapeutic diet for someone with Celiac disease involves them avoiding gluten-containing foods and beverages because eating them causes damage to their body.

A therapeutic diet for someone that is diagnosed with a food allergy often involves them avoiding eating that food and related foods that may also cause an adverse reaction.  If a person is allergic to banana, for instance they may also react to pineapple, papaya or chestnuts. Except in the case of serious (anaphylactic) allergies, after a person has avoided those foods for a long time, a “food challenge” may be done to determine whether the person is later able to tolerate the foods in question, or not. Sometimes foods are able to be reintroduced later and other times, such as the case of Celiac disease, they cannot because to do so will result in damage to their body.

A therapeutic diet in someone diagnosed with Type 2 Diabetes involves limiting foods that result in too much insulin being released and/or that results in their blood sugar rising too high and too often. This may be for a period of time – after which something that can be likened to a ‘food challenge’ can be performed to determine whether there has been significant improvement or not and if so, which kinds of carbohydrate may be able to be re-introduced, in what quantities and with what frequency.  More on that below.

Evidence Base for Using Dietary Carbohydrate Restriction in Diabetes Management

A Critical Review Article written by 26 authors and researchers appeared in the Journal of Nutrition in 2015 provided 12 points of evidence to support the use of low-carbohydrate diets as the first approach to treating Type 2 Diabetes. The summary of these points include that;

  1. Hyperglycemia is the most salient feature of Diabetes and that dietary carbohydrate restriction has the greatest effect on decreasing blood glucose levels.
  2. During the epidemics of obesity and Type 2 Diabetes, caloric increases have been due almost entirely to increased carbohydrates.
  3. Benefits of dietary carbohydrate restriction do not require weight loss.
  4. Although weight loss is not required for benefit, no dietary intervention is better than carbohydrate restriction for weight loss.
  5. Adherence to low-carbohydrate diets in people with Type 2 Diabetes is at least as good as adherence to any other dietary interventions and is frequently significantly better.
  6. Replacement of carbohydrate with protein is generally beneficial.
  7. Dietary total and saturated fat do not correlate with risk for cardiovascular disease.
  8. Plasma saturated fatty acids are controlled by dietary carbohydrate more than by dietary lipids.
  9. The best predictor of microvascular and, to a lesser extent, macrovascular complications in patients with Type 2 Diabetes, is glycemic control (HbA1c).
  10. Dietary carbohydrate restriction is the most effective method (other than starvation) of reducing serum TGs and increasing high-density lipoprotein.
  11. Patients with Type 2 Diabetes on carbohydrate-restricted diets reduce and frequently eliminate medication (and people with Type 1 usually require lower insulin).
  12. Intensive glucose lowering by dietary carbohydrate restriction has no side effects comparable to the effects of intensive pharmacologic treatment.

The authors provided strong support of the 12 points, concluding that there is a need for “reappraisal of dietary recommendations” which stems from;

1. The general failure to halt the epidemic of Diabetes under current
guidelines,

2. The specific failure of low-fat diets to improve obesity, cardiovascular
risk, or general health (points 1 and 4),

3. Constant reports of side effects of commonly prescribed
Diabetes medications, some quite serious (points 12),

4. Most importantly, the continued success of low carbohydrate
diets to meet the challenges of improvement in the features of Diabetes and metabolic syndrome in the absence of side effects.

The authors underscore that

“the benefits of carbohydrate restriction are immediate and well-documented.”

and that

“Concerns about the efficacy and safety of carbohydrate restriction are long term and conjectural rather than data driven. Most objections stem from the proposed dangers of total or saturated fat embodied in the so-called diet–heart  hypothesis. At this point, the diet–heart hypothesis has had a record of very limited clinical or experimental success to support its position.”

As I’ve mentioned in past articles, a low carbohydrate diet is not new, but may in fact represent the diet followed by humans for much of our evolutionary history, prior to the rise of agriculture. Given the very positive outcomes of carbohydrate restricted diets, the authors conclude that people with Type 2 Diabetes should not be discouraged from following such a diet as is often the case, but rather that the strength of the evidence is that;

“current knowledge dictates that carbohydrate restriction should be a default treatment for Type 2 Diabetes and a default adjunct therapy for Type 1.”

The authors state that the insistent by those that object to the use of low carbohydrate diets on the basis that long-term randomized controlled trials are the only kind of data that will be accepted “is without precedent in science.”

“The seriousness of diabetes requires that we evaluate all of the evidence that is available. The 12 points are sufficiently compelling that we feel that the burden of proof rests with those who are opposed.’


Authors of this Review included:

  1. Richard D. Feinman Ph.D, Department of Cell Biology, State University of New York
  2. Wendy K. Pogozelski Ph.D, Department of Chemistry, State University of New York
  3. Arne Astrup M.D., Department of Nutrition, Exercise and Sports, Copenhagen University
  4. Richard K. Bernstein M.D., New York Diabetes Center, Mamaroneck, NY
  5. Eugene J. Fine M.S., M.D., Department of Radiology (Nuclear Medicine), Albert Einstein College of Medicine, Bronx, New York
  6. Eric C. Westman M.D., M.H.S., Duke University Medical Center, Durham, NC
  7. Anthony Accurso M.D., Department of Medicine, Johns Hopkins Bayview Medical Center, Baltimore, MD
  8. Lynda Frassetto M.D. Department of Medicine, University of California San Francisco, San Francisco, CA
  9. Barbara A. Gower Ph.D. Department of Nutrition Sciences, University of Alabama at Birmingham, Birmingham, Alabama
  10. Samy I. McFarlane M.D., Departments of Medicine and Endocrinology, State University of New York Downstate Medical Center, Brooklyn, NY
  11. Jörgen Vesti Nielsen M.D., Karlshamn, Sweden
  12. Thure Krarup M.D. Department of Endocrinology I, Bispebjerg University Hospital, Copenhagen, Denmark
  13. Laura Saslow Ph.D. University of California San Francisco, San Francisco, CA
  14. Karl S. Roth M.D. Department of Pediatrics, Creighton University, Omaha, NE
  15. Mary C. Vernon M.D. Private Practice, Lawrence, KS
  16. Jeff S. Volek R.D., Ph.D. Department of Human Sciences (Kinesiology Program) Ohio State University, Columbus, OH
  17. Gilbert B. Wilshire M.D. Mid-Missouri Reproductive Medicine and Surgery, Columbia, MO
  18. Annika Dahlqvist M.D. Hälsocentralen Centrum, Sundsvall, Sweden
  19. Ralf Sundberg M.D., Ph.D. Private Practice, Malmö, Sweden
  20. Ann Childers M.D. Private Practice, Lake Oswego, OR
  21. Katharine Morrison M.R.C.G.P., Ballochmyle Medical Group, Mauchline, East Ayrshire, Scotland
  22. Anssi H. Manninen M.H.S. Metabolia Oulu, Oulu, Finland
  23. Hussain M. Dashti M.D., Ph.D., F.A.C.S., F.I.C.S., Faculty of Medicine, Department of Surgery, Kuwait university, Kuwait
  24. Richard J. Wood Ph.D. Springfield College, Springfield, MA
  25. Jay Wortman M.D. First Nations Division, Vancouver, BC, Canada
  26. Nicolai Worm Ph.D. German University for Prevention and Health Care Management, Saarbrücken, Germany

Blood Sugar Response in Healthy People vs Actual Responses in Individual Diabetics

We have the Glycemic Index  (GI) which tells us how easily specific foods raise blood sugar in healthy people; specifically how much blood sugar will rise when a healthy person eats 50 g of that food and Glycemic Load (GL) tells us how healthy people respond to the carbohydrate in one serving of that food.

As outlined in the previous two articles titled “Not All Carbs Are Created Equal“, while brown rice and whole grain spaghetti may have a lower GI or GL than their white counterparts, they still result in a rapid rise in blood sugar even in healthy people. Would we expect brown rice or whole grain spaghetti to have any better a response in those with Type 2 Diabetes? Of course not, yet the recommendations are for those with Type 2 Diabetes to eat “starchy foods such as whole grain breads and cereals, rice, noodles, or potatoes at every meal“.

Given that the symptom of Type 2 Diabetes is that body can’t properly use the insulin that is released and as a result “sugar builds up in the blood instead of being used as energy” [1] – how does it make sense to recommend to someone with Type 2 Diabetes to “eat starchy foods such as whole grain breads and cereals, rice, noodles, or potatoes at every meal” because these “starchy foods are broken down into glucose, which your body needs for energy”[1]? Either the body can’t use the food as energy because of the dysfunction in insulin or it can.

In Type 2 Diabetes, the mechanism in which the body effectively uses carbohydrates for energy is ‘broken’ and body keeps making and releasing more and more insulin to try and bring glucose into the cells. Common sense would indicate that a therapeutic diet for someone with an intolerance to more than very small amounts of carbohydrate would be to limit foods that are high in carbohydrate, particularly those that cause a rapid spike in blood glucose even in healthy people.

We don’t need to guess how much a person with Type 2 Diabetes’ blood sugar is going to rise when they eat a food based on the GI or GL (which is based on healthy people) because we can test it in THEM!

As mentioned in the previous article, without spending any additional money on testing equipment, someone with Type 2 Diabetes can eat 25 g or 50 g of a carbohydrate-based food, test their blood sugar every half hour and know exactly how their body responds to it!  They can see their blood sugar rise to 11 mmol/L (200 mg/dl) or 14 mmol/L (250 mg/dl) or 16.5 mmol/L (297 mg/dl) or higher in the first hour and KNOW. No guess work is required! 

With the availability of relatively inexpensive Continuous Glucose Monitors (CGM) such as the  FreeStyle Libre ($50 CDN) and one sensor worn for 2 weeks ($90), someone with Type 2 Diabetes can test 25 g or 50 g of specific carbohydrate-based food and KNOW exactly how their body responds!

Continuous Glucose Monitor (CGM) readings

People with Type 2 Diabetes can KNOW that 1/2 cup of whole grain rice or 1/2 of a baked potato (or some other food) resulted in their blood sugar spiking to 16.5 mmol/L (297 mg/dl) and know that this is not a food they tolerate even when eaten with a mixed meal that includes protein-based foods and non-starchy vegetables.  

Guess work based on Glycemic Index or Glycemic Load – the blood sugar response of healthy people is no longer needed. 

Role for a Therapeutic Low Carb Diet

Just as there is a role for a therapeutic diet in other food-related conditions such as food intolerance and Celiac disease, there is a role for a therapeutic diet in Type 2 Diabetes.

A person diagnosed with Type 2 Diabetes has (1) the inability to handle more than a very small carbohydrate load and (2) has cells which are insulin resistant, therefore it makes good clinical sense to design a therapeutic diet which enables them to lower their overall blood glucose response in order to enable the pancreatic beta cells that remain to begin to recover (these are the cells that produce insulin) and to allow their body cells which have become insulin resistant to become insulin sensitive again.

A Dietitian is knowledgeable to design such an  therapeutic diet in such a ways as to include a wide variety of foods that supplies all the essential amino acids, fatty acids, vitamins and minerals that a person requires while containing only small amounts of carbohydrate at any given time

Lab test results such as fasting insulin and fasting blood glucose (to calculate HOMA-IR) and tests of insulin response to a known glucose load (3 hour challenge) could be performed in time to monitor the degree of improvement in insulin sensitivity and pancreatic function or simply use existing routine lab tests such as TG:HDL ratio as a proxy, along with HbA1C and fasting blood glucose. This way, once a person’s body has begin to heal and restore some beta-cell function, a Dietitian can then design a customized therapeutic diet around each individual’s actual tolerance or intolerance to specific carbohydrates!  We don’t need to rely on glycemic response data such as the GI or GL (which are based on healthy people) but can use an individual’s own blood sugar response! 

We do this in other types of food intolerance by means of a “food challenge” and it is time we do this in Type 2 Diabetes as well.

With the advent of relatively inexpensive Continuous Glucose Monitors, we have the technology for individuals to do this easily with the help of a Dietitian, such as myself. It is more labour-intensive, but it can certainly be done using the standard blood glucose monitor that Diabetics already own and use by standardizing the size of the test food and testing blood sugar every 1/2 an hour for 3 hours.

It is long overdue for those with Type 2 Diabetes to be able to have therapeutic diets which are designed to improve their symptoms, rather than to expect them to eat carbohydrate loads they can’t handle, getting worse in time, then turning to medication to manage the disease. Type 2 Diabetes does not have to be “a chronic, progressive disease”.

Do you have questions how a low carb diet may be able to help you manage and improve the symptoms of Type 2 Diabetes?

Please send me a note using the “Contact Me” form on this web page and I will respond shortly.

To our good health!

Joy


 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Diabetes Canada, Diabetes and You, Basic Meal Planning, https://www.diabetes.ca/diabetes-and-you/healthy-living-resources/diet-nutrition/basic-meal-planning
  2. Richard D. Feinman, Wendy K. Pogozelski, Arne Astrup, Richard K. Bernstein, Eugene J. Fine, Eric C. Westman, Anthony Accurso, Lynda Frassetto, Barbara A. Gower, Samy I. McFarlane, Jörgen Vesti Nielsen, Thure Krarup, Laura Saslow, Karl S. Roth, Mary C. Vernon, Jeff S. Volek, Gilbert B. Wilshire, Annika Dahlqvist, Ralf Sundberg, Ann Childers, Katharine Morrison, Anssi H. Manninen, Hussain M. Dashti, Richard J. Wood, Jay Wortman, Nicolai Worm,

Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base,
Nutrition,
Volume 31, Issue 1,
2015,
Pages 1-13,

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

 

 

 

 

 

Some Carbs are Better than Others (for Diabetics) – Part 3

INTRODUCTION: In the first article in this series on carbohydrates, I explained that Glycemic Index (GI) is a way to rate carbohydrates based how easily they raise the blood sugar of healthy people and that some carbohydrates are better than others when they cause much less of a rise in blood sugar. I wanted to know how would I react to carbohydrate-based foods now that I have been eating low carb for so long (>1 year) and have seen a partial reversal of symptoms of the Type 2 Diabetes that I’ve had for more than 10 years.

I decided to conduct some impromptu ‘experiments’ and the results led to some reading in the literature. The information I discovered is VERY exciting for me and for others with Type 2 Diabetes or Insulin Resistance.

Once people have achieved significant reversal of symptoms following a therapeutic low carb or ketogenic diet, there is a way to begin to re-introduce carb-based foods in a way that does not cause their blood sugar to spike.


As you may recall from the first article in this series on Carbohydrates, the Glycemic Index of a food is determine by having healthy people eat 50 grams of digestible carbohydrate of a given food, and then measure their blood glucose response over a 2 hour period (30 minutes, 60 minutes, 90 minutes, 120 minutes), plotting the curve then measuring the area under the curve (AUC) and comparing it to the AUC of pure glucose, the reference food.

The problem with the Glycemic Index or even the Glycemic Load (based on individual serving sizes) is that this data does not apply to those with Diabetes or Insulin Resistance.

Since I have been Diabetic for a long time, I decided to go about conducting my own sample-set-of-one (n=1) ‘experiment’, and one thing led to another…

The ‘Test Food’

I ate 1/2 cup of chickpeas (cooked from dried) which has 25 g of carbohydrate and measured my blood sugar response with the same meter at 30 minutes, 60 minutes, 90 minutes, 120 minutes, 180 minutes and 210 minutes.

blood glucose response to 25 g of chickpeas, cooked from dried

At the time I did this, I hadn’t eaten in 8 hours (considered a fasted state) and my starting blood sugar was 4.8 mmol/L (86 mg.dl). The chickpeas were part of a mixed meal with some chicken (high biological value protein) and a cucumber salad with olive oil.

At the highest point, my blood sugar went up to 5.8 mmol/L (105 mg/dl),  stayed there, then started to drop at 2 hours.

I was amazed.

When I first began changing my lifestyle a year ago, even eating low GI foods such as chickpeas caused my blood sugar to jump dramatically. I recall the first few months when I would eat 1 cup of hummus, which is chickpeas with tahini (ground sesame seeds) and has even more fiber than chickpeas alone and also has only 25 g of carbs, my blood sugar would always go up to ~ 8.6 – 8.9 mmol/L (155- 160 mg/dl).

This was a HUGE improvement after not eating more than 30 g of carbohydrate per day (i.e. a ketogenic diet) for the last 6 months!

The ‘Reference Food’

Two weeks ago, I was at a social occasion where a milk-chocolate covered cracker was served and I decided (in the interest of science, of course!) to read the nutritional label, measure out exactly 25 g of carbohydrate of this food and eat it, measuring my blood sugar at 0 minutes, 60 minutes, 90 minutes120 minutes, and 180 minutes.

This ‘reference food’ (high GI) was eaten after a dinner that had a fair amount of high biological value protein (steak) as well as some healthy fats (olive oil on vegetables) and fiber in the vegetables, and my starting blood sugar was 6.7 mmol/L (121 mg/dl).

Just look at the blood sugar spike!

When I ate 25 gm of carbohydrate as the cracker and chocolate, my blood glucose went from 6.7 mmol/L to 9.8 mmol/L (121 mg/dl -177 mg/dl)! That is, I had eaten the SAME amount of carbohydrate (25 g of carbs) as when I ate the cooked chickpeas and had THREE TIMES the blood sugar response!!

Both the meals I ate just before the ‘reference food’ (high GI, highly refined cracker with chocolate) and the ‘test food’ (low GI, intact chickpeas) had a high biological value protein (chicken, steak) which slows the blood sugar response of the body, and both had the same amount of fiber (the exact same salad).

Below is a graph of the two responses (chickpeas in blue, chocolate covered cracker, orange) over 3+ hours.

It is quite evident that 25 g of carbs as white flour with milk chocolate (refined carbs) is processed VERY differently by my body than 25 g of carbs such as whole, intact chickpeas!!
Comparison of blood glucose response of 25 g of carbohydrate as chickpeas and white flour cracker with chocolate (special thanks to Phil Thompson of the “Lower Insulin” Facebook group for the graph and calculations of area under the curve)

The area under the curve (AUG) was determined by lowering the cracker and chocolate curve down to sit just above the chickpea curve (grey curve) and then assessing where the respective points were and running the AUG formula relative to baseline.

The AUG of 25 g of carbs as chickpeas was 129.

The AUG of 25 g of carbs as white flour cracker with chocolate was 381.

The difference was 2.95.

The blood sugar response of the cracker with chocolate was THREE TIMES GREATER than the blood sugar response of the chickpeas – and both contained 25 g of carbs!

Some carbs are quite clearly better than others for this Type 2 Diabetic.*

* As I will elaborate on below, people's blood sugar response to different carbohydrate-based food is quite individual.

Objective Data

Facsimile for Glycemic Index of Cracker with Chocolate

I was able to find for purposes of estimation, that 25 g of carbohydrate as white bread with 5 g of margarine (a pretty good facsimile for 25 g of carbohydrate as white flour cracker covered with milk chocolate made with palm oil) has a GI of 70.1 when compared to the reference which was 25 g glucose in 125 ml water [1].

Studies of Effect of Eating Legumes (Pulses) Alone

A meta-analysis of 10 studies on the effect of pulses (legumes) eaten alone on blood sugar control in people with and without Diabetes [2] provided some helpful information. The pulses in the meta-analysis included chickpeas, black-eyed peas and various other beans (including red and white kidney, black, pinto, fava and white navy).

Seven of the 10 trials that looked at the effect of eating pulses alone had a crossover design (five had a washout period), studied a total of 253 participants, of which only 21 had Type 2 Diabetes, and 232 that had normal blood sugar.

Background diets were largely high-carbohydrate, low-fat diets (carbohydrate 52% of energy, protein 18% of energy, fat 29% of energy).

Due to the length of time I have had Type 2 Diabetes and the very high degree of persistent insulin resistance over the first 6 months of eating low carb but not ketogenic, the last 6 months my diet has been very low in carbohydrate (5-10% of energy), moderate in protein ~23% and 67-77% healthy fats.

It was found that fasting blood glucose following the eating of pulses alone was decreased by 0.82% (95% CI ), but there was no long term effect on HbA1C (3 month average blood sugar) or on HOMA-IR (fasting blood glucose: fasting insulin).

[Of interest, in low GI diets, eating of pulses lowered HbA1C (3 month average blood sugar) by 0.28% but had no change on fasting blood sugar or HOMA-IR. The average GI of the pulse-containing low-GI diets was 67 and as compared to the GI value of bread alone.]

The conclusions of the meta-analysis found that the strongest modifiers of benefit were in Type 2 Diabetes and that the legumes that modified blood sugar the most were black beans, white/navy beans, pinto beans, red and white kidney beans, chickpeas and fava beans.

“Specific to the pulses alone analysis, pulse species including Phaseolus vulgaris (black, white, pinto, red and white kidney beans), Cicer arietinum (chickpeas) and Vicia faba (fava beans) were also identified as significant modifiers.” [2]

Individual Glycemic Response  – role for personalized nutrition

A 2015 study from Israel[3] with 800 people who were monitored with continuous glucose monitors indicates that there isn’t a ‘universal’ blood sugar response to low GI foods or high GI carbs – that glycemic (blood sugar) response is very individual. 

“We continuously monitored week-long glucose levels in an 800-person cohort, measured responses to 46,898 meals, and found high variability in the response to identical meals, suggesting that universal dietary recommendations may have limited utility.

The study also found that an individual’s blood sugar response to different foods was able to be predicted by type and amounts of bacteria in their intestines (the ‘gut biome’ / ‘microbiome’ / ‘microbiota’) . 

Based on the data they collected, the team has since created and validated a machine-learning algorithm that combines blood parameters, dietary habits, anthropometrics (height, weight data), physical activity and gut microbiota  data that they say accurately predicts a person’s individual post meal blood sugar response to actual meals.

Applications in Dietetic Practice for Personalized Nutrition

There is a tremendous opportunity for Dietitians such as myself to help individuals with Type 2 Diabetes or pre-diabetes determine which carbohydrate-based foods cause the lowest, most gradual rise in blood sugar.

This is huge!

This means that after individuals have had significant reversal of Type 2 Diabetes / Insulin Resistance following a therapeutic low carb or ketogenic diet for a period of time, I can help them re-introduce carb-based foods into their diet by selecting ones that have the least impact on their blood sugar!

There are two ways this can be done;

  1. USING EXISTING BLOOD GLUCOSE METER – I can help those with Type 2 Diabetes eat a specific amount of a ‘test food’ that contains 50 g of carbohydrate (I will calculate this for them) and have them test their blood sugar every 30 minutes for 2 or 3 hours with the blood glucose meters they already have.  Then, I can take that data, enter it into an Excel sheet just as was done with my data above, and determine their blood sugar response.

  2. USING A CONTINUOUS GLUCOSE MONITOR – continuous glucose monitors (CGMs) such as the FreeStyle Libre have become relatively inexpensive and would be ideal for this kind of testing. Test strips for most standard home blood glucose monitors are $1 a piece, so testing every 30 minutes for 3 hours costs $6. The FreeStyle Libre costs $50 for the unit, and while test patches are $90 and last only two weeks, huge varieties of carbohydrate-based foods can be tried and measured in a short time, with no effort.

As a Dietitian I can not only help individuals carry out this kind of individual testing of carbohydrate-based foods, I can help them interpret the results as we begin to re-introduced some foods back into the diet once significant reversal of insulin resistance has been accomplished through the therapeutic use of a low carbohydrate or ketogenic diet.

Have questions how I can help you reverse insulin resistance by following a therapeutic low carb diet? Have you been following a low-carb or ketogenic diet for a while and want to begin determining which carb-based foods don’t spike your blood sugar? I can help.

Please send me a note using the “Contact Me” form on this web page and I will respond shortly.

To our good health!

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


References

  1. Aston LM, Gambell JM, Lee DM, Bryant SP, Jebb SA. Determination of the glycaemic index of various staple carbohydrate-rich foods in the UK diet. European journal of clinical nutrition. 2008;62(2):279-285.
  2. Sievenpiper, J.L., Kendall, C.W.C., Esfahani, A. et al. Effect of non-oil-seed pulses on glycaemic control: a systematic review and meta-analysis of randomised controlled experimental trials in people with and without diabetes. Diabetologia (2009) 52: 1479.
  3. Zeevi D, Korem T, Zmora N, et al. Personalized Nutrition by Prediction of Glycemic Responses. Cell. 2015 Nov 19;163(5):1079-1094.

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.


 

Some Carbs Are Better Than Others – Part 2 – Glycemic Load

In the introduction to this series on Carbohydrates, I explained that Glycemic Index (GI) is a way to rate carbohydrates based how easily they raise blood sugar. If you recall, low GI foods (those with a value of 55 or less) are more slowly digested, absorbed and metabolized and cause a lower and slower rise in blood glucose levels and very high GI foods (>70) are digested very rapidly, casing a large spoke in blood sugar. High GI foods (>55) are result in a fairly rapid rise in blood sugar.

The GI value of a food is determined comparing how healthy people‘s blood sugar responds over a two hour period to a food containing 50 grams of digestible carbohydrate from that food compared to 50 grams of glucose (pure sugar). The drawback to this rating scale is that the values are only known for a serving that has 50 grams of carbs in it.  That is, they compare the ability for different foods containing the SAME amount of carbohydrate it (50 g) to raise blood sugar. The problem with the Glycemic Index is that its hard to compare foods because a serving size may have considerably less than 50 g of carbs in it.  For example, the Glycemic Index of watermelon is 76, which is as high as the Glycemic Index of a doughnut, but one serving of watermelon (1/2 a cup) has 11 g of carbohydrate in it, while a medium doughnut (one serving) has 23 g of carbs.

This is where the concept of Glycemic Load (GL) is much more helpful, because it tells us how a healthy person’s body will respond to the carbs in one serving of a foodOne usual serving of a food would be considered to have a very high Glycemic Load if it is ≥20, a high Glycemic Load if it is between 11-19 and a low Glycemic Load if it is ≤10.

How to Determine Glycemic Load

To determine Glycemic Load  (GL) of a serving of a food, what needs to be known is:

The Glycemic Index (GI) of that food (found by referring to a table of Glycemic Indexes)

The number of grams of carbohydrate in the quantity of food considered to be one serving.

  • GL  = GI x (amount of carbohydrate per serving) / 100

For purposes of comparison,  let’s look at the Glycemic Load of the same foods we looked at the Glycemic Index for in the first article.

One slice of white bread has a Glycemic Load of 10 and so does one slice of whole wheat bread, which is considered low. Both have 15 g of carbs per slice.

 

One 1 cup of cooked white spaghetti has a Glycemic Load of 25 which is considered very high and while 1 cup of whole grain spaghetti only has a Glycemic Load of 14, this is still not low, just lower than white spaghetti.

A cup of boiled white rice has 53 g of carbs in it and has a very high Glycemic Load = 35. A cup of white spaghetti has 44 g of carbs in it and also has a very high Glycemic Load at 25. These foods are high in carbohydrate and will cause a rapid rise in blood sugar in healthy people. To those who are already Diabetic or pre-Diabetic this is a big problem.

One cup of cooked whole grain spaghetti has a Glycemic Load of 14 which is still not low and has 37 g of carbs in it.

 

A cup of boiled brown rice has a Glycemic Load of 20 which is still considered very high and has 42 g of carbs.  These foods are high in carbohydrate and will cause a fairly rapid rise in blood sugar in healthy people, let alone those who are already having problems.

So what’s the problem?

Eating a high Glycemic Load diet over a period of years and years will result in blood sugar after meals (called post prandial blood glucose) to be high. This puts a huge demand on the body to keep releasing insulin to try to move all that glucose into the body’s cells and get it out of the blood. Over time, a high Glycemic Load diet causes the body’s pancreas β-cells (beta cells) to decrease in function or in many cases, to die, resulting in a diagnosis of Type 2 Diabetes. As can be seen above, even eating the “whole grain” version of favourite foods does not necessarily reduce the insulin demand on our pancreas. Our  β-cells are under continual pressure to release insulin every time we eat – from our breakfast toast or cereal, to our mid-morning muffin, to our pasta lunch. Eating a low carb diet is a very effective way to lower the demand on our pancreas to keep producing and releasing insulin to deal with the constant spikes in our blood sugar from carbohydrate containing foods. But does that mean we need to remain eating a low carb diet forever? More on that in future articles in this series.

Glycemic Load will tell us how much a serving of food will increase our blood sugar but it doesn’t tell us how much insulin our body releases as a result of eating a food – that is, the demand we are putting on our pancreatic βcells.

For those that have been eating a high carbohydrate diet for years and years or have a family history of Type 2 Diabetes, knowing how much insulin is needed to process the carb -based foods we eat is hugely important, because we need to eating foods that do not put a large demand on our pancreatic β-cells.  For those that already have Type 2 Diabetes, it is especially important to eat in such a way as to preserve whatever β-cell function we have left!  Referring to the Insulin Index enables us to choose between carb-based foods based on the demand they put on our β-cells.

If you have questions as to how I can help you choose foods that result in much less glucose being released and also put much less demand on your  β-cells to keep producing and releasing insulin, please send me a note using the “Contact Me” form located on the tab above.

To our good health!

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


Reference

Oregon State University, Linus Pauling Institute, Micronutrient Information Centre, Glycemic Index and Glycemic Load http://lpi.oregonstate.edu/mic/food-beverages/glycemic-index-glycemic-load#glycemic-index


Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Some Carbs Are Better Than Others – Part 1 – Glycemic Index

INTRODUCTION: Not all carbs are created equal; some are broken down very quickly into simple sugars and others are broken down very slowly. In the past the terms “simple sugar” and “complex carbohydrate” were used to imply this concept there are newer terms that enable us to know how much eating these foods will raise blood glucose in healthy people. The “in healthy people” is important, as the ability to tolerate carbohydrate in those with insulin resistance (“pre-diabetes”) or Type 2 Diabetes is significantly affected.

This is the first article in a new series on carbohydrate.

Glycemic Index

The Glycemic Index (GI) is a way of rating carbohydrates based on their ability to raise blood sugar.

Low GI foods (those with a value of 55 or less) are more slowly digested, absorbed and metabolized and cause a lower and slower rise in blood glucose levels and very high GI foods (>70) are digested very rapidly, casing a large spoke in blood sugar. High GI foods (>55) are result in a fairly rapid rise in blood sugar.

Many of the foods people eat lots of in our society, such as bread, rice, pasta and cereal, even vegetables, are high GI foods. As once healthy people continue to eat these foods on a regular basis, they put a high demand on their body to produce and release insulin, which brings all that glucose into their cells. This insulin is released from the beta cells in the pancreas and people eating these high GI foods means that their beta cells have to release insulin over and over all day long and this constant demand on the beta cells, over time, results in the cells throughout their body becoming insulin resistant (no longer responding to insulin’s signal) or burning out their beta cells, resulting in Type 2 Diabetes.

Many people don’t realize that by the time they are diagnosed with Type 2 Diabetes, they already have beta cell dysfunctionbeta cell death and/or a decrease in beta cell mass. Once beta cells die, they’re gone. Our once healthy body is no longer healthy.  When we eat foods with significant carbohydrate – especially high GI carbohydrates, our ability to release insulin is significantly impacted and as a result, we can no longer tolerate carbs like we used to.  While the mechanism is different, it’s similar to someone that becomes intolerant to gluten; once they’re celiac, they can no longer tolerate foods that contain gluten without causing damage to their body.  Depending how long someone had Type 2 Diabetes when they were finally diagnosed, or how long they had it before they changed their eating habits will all factor in to how much carbohydrate they can process. For this reason, each person is different.

It’s not that carbs are inherently “bad”. It’s that our bodies are no longer able to process some of them they way we could when we were still healthy – so in those cases the sugar stays in our blood, damaging tissues throughout our body.

Knowing which carbs are high GI is important, because these are the foods that tax our already overtaxed beta cells if we are not Diabetic and limiting these foods significantly, or avoiding may be the best way for healthy people to remain healthy.

The good news is that there are some types of carbohydrates that some people can not only tolerate, but may actually improve their blood sugar control, and that’s the topic of an upcoming article.

How the GI of a Food is Determined

GI Graph

The GI value of a food is determined by feeding a group of healthy people the amount of a food that contains 50 grams of digestible (available) carbohydrate and then measuring the effect on their blood glucose levels over the next two hours. The area under their two-hour blood glucose response (glucose AUC) for this food is then measured.

At another time, the same group of healthy people eat 50 grams of glucose, (which is the reference food) and their two-hour blood glucose response is also measured.

The GI value for the test food is calculated for each person in the group by dividing their glucose AUC for the test food by their glucose AUC.

The final GI value for the test food is the average GI value all the people in the group.

In summary to determine the Glycemic Index of a food healthy (non-diabetic) people;

(a) eat 50 grams of digestible  carbohydrate of a particular food

(b) measure their blood glucose response over a 2 hour period

(c) plot the curve and measure the area under the curve (AUC)

(d) compare that AUC of the test food to the AUC of pure glucose (i.e. produced when the same people eat 50 g of glucose, which is the reference food.

Too Much of a ‘Good’ Thing

Many of the foods that people in the West enjoy and eat a lot such as bread, rice and noodles are High GI foods – these are ones that are rated at  ≥ 55 (compared to pure glucose, which is rated at 100).

White bread has a GI of 75 ± 2 and whole wheat bread isn’t much better, at 74 ± 2.

 

Boiled white rice is high GI at 73 ± 4, and while somewhat better boiled brown rice is still high GI at 68 ± 4.

White spaghetti has a GI of 49 ± 2 and whole grain spaghetti has a GI of 48 ± 5.

 

Rice noodles, such as those in Pho (Vietnamese Beef Noodle soup) are even higher, at 53 ± 7.

 

Breakfast cereals, whether boxed or cooked are also high GI.  Here is a table that summarizes some of these [1];

REAKFAST CEREALS  Glycemic index (glucose = 100)
Cornflakes 81 ± 6
Wheat flake biscuits 69 ± 2
Porridge, rolled oats 55 ± 2
Instant oat porridge 79 ± 3
Muesli 57 ± 2

Many people include vegetables such as potato, sweet potato and squash such as pumpkin in their “vegetable quota” for the day, but let’s look at the Glycemic Index for these;

VEGETABLES  Glycemic index (glucose = 100)
Potato, boiled 78 ± 4
Potato, instant mash 87 ± 3
Potato, french fries 63 ± 5
Carrots, boiled 39 ± 4
Sweet potato, boiled 63 ± 6
Pumpkin, boiled 64 ± 7

People in our culture eat a lot of bread, rice, pasta, starchy vegetables and cereal but one of the things we know is that eating them with good source of protein slows down how quickly they affect blood sugar. Oftentimes bread and cereal form the basis of breakfast, perhaps with a high GI glass of juice and frequently, people eat pasta with a tomato sauce for supper (or leftovers for lunch), and this kind of meal will spike their blood sugar. We also know that the fiber content of a mixed meal will also slow down the rate at which blood sugar rises from these carbs, so there are ways to ‘tone down’ the response.

Some Final Thoughts…

If you have a family history of Type 2 Diabetes, are overweight or have high blood sugar, it’s important to understand that what you eat matters and to eat in a way that does not put high demand on your beta cells to keep releasing insulin to process all that glucose.

The time to consider the effect on your body is now – before you get sick by having overtaxed your pancreas’ beta cells and experience beta cell death or mass loss and are diagnosed with Type 2 Diabetes.

Once we’ve crossed that threshold; once our once healthy body is no longer healthy, we need to learn to eat in a way that does not put high demand on our beta cells, that does not require our body to process large amounts of glucose at a time, in order to preserve whatever beta cell mass and function we have left.

Determining which carb-containing foods we can tolerate and in what quantities will enable us to eat in a way that keeps us from getting worse and keeps us from developing the very serious consequences of not doing so, which can include blindness, toe and food amputations and more.

In coming articles, I’ll explain Glycemic Load and the Insulin Index and I’ll also touch on a role for legumes (pulses) such as chickpeas and sources of “resistant starch” in a moderate carb ‘Mediterranean-style’ diet.


If you just found out you are pre-diabetic, now is the time to do something about it. Waiting will not make it better.

If you’ve been recently be diagnosed with Type 2 Diabetes, it’s not too late.  Studies have shown that changing eating habits and lifestyle soon after diagnosis makes it possible for some people to reverse their symptoms and to have their Diabetes go into remission. One thing is known, that doing nothing will bring needless firsthand understanding to the phrase that “Diabetes is a chronic, progressive disease”.  It doesn’t have to be.

If you want to know how I can help you, please send me a note using the “Contact Me” form located on the tab above.

To our good health!

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


References

  1. https://www.health.harvard.edu/diseases-and-conditions/glycemic-index-and-glycemic-load-for-100-foods

Also see: Atkinson FS, Foster-Powell K, Brand-Miller JC, “International tables of glycemic index and glycemic load values”, Diabetes Care 31(12); 2281-2283


Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

What is a Mediterranean Style Diet?

The recently released 2018 Clinical Practice Guidelines (CPG) Guidelines of Diabetes Canada recommend that those with Diabetes continue to eat 45% to 65% of their daily calories as carbohydrate, 10% to 35% of their daily calories as protein and only 20% to 35% of their daily calories, yet affirm that there is “evidence to support a number of other macronutrient-, food- and dietary pattern-based approaches” and that “evidence is limited for the rigid adherence to any single dietary approach”[1] .

One of the dietary patterns they recommend is a “Mediterranean-style dietary pattern” in order to “reduce major cardiovascular events and improve glycemic (blood sugar) control.”

So what is a “Mediterranean-style dietary pattern“?

According to the Clinical Practice Guidelines,

A “Mediterranean diet” primarily refers to a plant-based diet first described in the 1960s. General features include a high consumption of fruits, vegetables, legumes, nuts, seeds, cereals and whole grains; moderate-to-high consumption of olive oil (as the principal source of fat); low to moderate consumption of dairy products, fish and poultry; and low consumption of red meat, as well as low to moderate consumption of wine, mainly during meals”

Countries with coastlines on the Mediterranean Sea include Albania, Algeria, Bosnia and Herzegovina, Croatia, Cyprus, Egypt, France, Greece, Israel, Italy, Lebanon, Libya, Malta, Morocco, Monaco, Montenegro, Slovenia, Spain, Syria, Tunisia and Turkey and the diets of these countries vary considerably, so there isn’t only ONE “Mediterranean Diet“.

What is the Mediterranean Diet that the Clinical Practice Guidelines are referring to?

It would seem that they are referring to dietary intake based of southern Italy from the 1960s from when rates of chronic disease were reported to be amongst the lowest in the world and adult life expectancy was reported to be amongst the highest. That is, the health benefits of “The Mediterranean Diet” came out of Ancel Keys’ Six Country Study (1953) and later his Seven Countries Study (1970).  More on that below.

One of the academic papers that the Guidelines cites as the basis for a “Mediterranean diet” makes the direct link to Ancel Keys clear;

“Ecologic evidence suggesting beneficial health effects of the Mediterranean diet has emerged from the classic studies of
Keys.” [2]

In 1953, Ancel Keys published the results of his “Six Countries Study“[3], where it is said he demonstrated that there was an association between dietary fat as a percentage of daily calories and death from degenerative heart disease.

Four years later, in 1957, Yerushalamy published a paper with data from 22 countries [4], which showed a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s six country data (see below).

from [3].Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y.20, 118–139 (1953).

from [4] Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343–54

Nevertheless, in 1970, Keys went on to publish his Seven Countries Study in which he maintained that there was an associative relationship between increased dietary saturated fat and Coronary Heart Disease – ignoring the data presented in Yerushalamy’s 1957 study and failing to study countries such as France, in which the relationship did not hold.

In Keys’ paper published in 1989 [5] which was based on food consumption patterns in the 1960s in the seven countries, he found that the average consumption of animal foods (with the exception of fish) was positively associated with 25 year Coronary Heart Disease deaths rates and the average intake of saturated fat was strongly related to 10 and 25 year CHD mortality rates. Keys published this study 32 years after Yerushalamy’s 1957 paper which showed a significantly weaker relationship, yet it seems that people only remember Key’s data.

Countries with coastlines on the Mediterranean Sea on which there was known dietary and disease data in 1957 and that Keys later ignored in 1970 included France (labelled #8 on Yerushalamy’s graph above) and Israel (labelled #11). France is known for the “French paradox” (a term which came about in the 1980s) because of their relatively low incidence of coronary heart disease (CHD) while having a diet relatively rich in saturated fats. According to a 2004 paper about the French Paradox, there was diet and disease data available from the French population that was carried out in 1986–87 and which demonstrated that the saturated fat intake of the French was 15% of the total energy intake, yet such a high consumption of saturated fatty acids was not associated with high Coronary Heart Disease incidence in France [6]. Nevertheless, Keys published his 1989 study [5] ignoring the French dietary and disease data that was available from 1986-1987 [6]. Was it because it didn’t fit his hypothesis?

The diet of the French in the 1960's was every bit a "Mediterranean Diet" as that of southern Italy, but since Ancel Keys ignored (or did not study) the French data in the 1960s, that "Mediterranean Diet" remains ignored in the guidelines of today.

According to the French Paradox paper, high saturated fat intakes combined with low Coronary Heart Disease rates were also observed in other Mediterranean countries, including Spain and that rates in other non-Mediterranean Europeans countries such as Germany, Belgium are similar [6].

Perhaps then, a ‘true’ Mediterranean Diet which is protective of Coronary Heart Disease ought not to be defined as being largely “plant-based” and “low in consumption of red meat and dairy” – which the French diet clearly is not, but rather should focus on being a diet high in consumption of specific types of vegetables and fruit, nuts and seeds, abundant in the use of olive oil and that includes regular consumption of wine with meals.

As outlined in a recent article, eight recent meta-analysis and systemic reviews which reviewed evidence from randomized control trials that had been conducted between 2009-2017 did not find an association between saturated fat intake and the risk of heart disease. As well, recently published results from the Prospective Urban and Rural Epidemiological (PURE) Study, the largest and most global epidemiological study carried out to date and published in the Lancet in December 2017 found that those who ate the largest amount of saturated fats had significantly reduced rates of mortality (death) and that low consumption of saturated fat (6-7% of calories) was actually associated with increased risk of stroke.

Also as described in a recent article, a study published at the end of March 2017 in Nutrients and which examined health and nutrition data from 158 countries worldwide found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease, and that high carbohydrate consumption, particularly as cereals and wheat was most associated with the risk of cardiovascular disease – with both of these relationships holding up regardless of a nation’s average national income.

Final Thoughts…

The 2018 Clinical Practice Guidelines continue to recommend the health benefits of a “Mediterranean style diet” defined based on the 60-year-old-data of Ancel Keys’ Six Countries Study / 50 year old Seven Countries Study- when we now know that Keys excluded data that was available from countries including France, which did not fit his hypothesis.

Given that there seems to be increasing evidence that Keys’ Diet-Heart Hypothesis (the belief that dietary saturated fat causes heart disease) has been significantly challenged by newer data, is it not time to study the factors in the diet of this region that ARE protective against cardiovascular disease, and to redefine a Mediterranean diet in these terms?

Would you like to have a Meal Plan that emphasizes the foods of this region, including meat and cheese, fish and seafood, vegetables and fruit, nuts and seeds, olive oil and wine and which may play a protective role in heart heath?

Please send me a note using the Contact Me form located on the tab above, and I will reply as soon as possible.

To our good health!

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


References

  1. Sievenpiper JL, Chan CB, Dwortatzek PD, Freeze C et al, Nutrition Therapy – 2018 Clinical Practice Guidelines, Canadian Journal of Diabetes 42 (2018) S64–S79 http://guidelines.diabetes.ca/docs/CPG-2018-full-EN.pdf
  2. Trichopoulou A, Costacou T, Bamia C et al, Adherence to a Mediterranean Diet and Survival in a Greek Population, N Engl J Med 2003;348:2599-608.
  3. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y.20, 118–139 (1953).
  4. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343–54
  5. Kromhout D, Keys A, Aravanis C, Buzina R et al, Food consumption patterns in the 1960s in seven countries. Am J Clin Nutr. 1989 May; 49(5):889-94.
  6. Ferrières J. The French paradox: lessons for other countries. Heart. 2004;90(1):107-111.

Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.