American Heart Association: Some Kids & Teens at Risk for Premature CVD

INTRODUCTION: It is well known that adults are at risk of cardiovascular disease (CVD) due to having obesity and Type 2 Diabetes, but it is now known that children and adolescents are also at risk of premature coronary artery disease and stroke for the same reasons.



According to a new scientific statement from the American Heart Association (AHA) published in the Association’s journal Circulation this past Monday (February 25, 2019) [1], obesity and severe obesity in childhood and adolescence have been added to the list of conditions that put kids and teenagers at increased risk for premature heart disease, including coronary artery disease (CAD) and stroke and are considered at high risk of cardiovascular disease simply by having Type  2 Diabetes, whether or not they are overweight.

Childhood overweight is defined as a Body Mass Index (BMI) between the 85th to 94th percentile for age and sex, and childhood obesity is defined as having a Body Mass Index (BMI) ≥ 95th percentile for age and sex.

Youth with obesity are now considered at-risk of heart disease and stroke
and those with severe obesity are now considered at moderate risk of heart disease and stroke based on a large-scale study from 2016 that followed 2.3 million people for over 40 years and found the risk of dying from a cardiovascular disease were 2-3 times higher if people’s body weight as adolescents had been in the overweight or obese category, compared to youth with normal weight [2].

Obesity,  specifically the ectopic fat  (fat in the organs) is considered an independent risk factor for cardiovascular disease (CVD) and is associated with other CVD risk factors such as high triglycerides, low levels of HDL cholesterol, high blood pressure,  high blood sugar (hyperglycemia),  insulin resistance, inflammation and oxidative stress.

It Is estimated that in 2014 ~6% of all youth 2 to 19 years old in the United States were severely obese [3] and 2015 Canadian data indicates that obesity in children aged 5-17 years of age averaged around 12% (14.5% for boys and ~9.5% in girls) [4].

Given these children are 2-3 times more likely to have premature cardiovascular disease as adults, the time to successfully address their overweight and obesity is when they are still young.

Cardiovascular Disease -a leading cause of death

Cardiovascular disease is the leading cause of death for people of all ages and both genders in the United States [5] and the second leading cause of death in Canada [6] and a large percentage of these deaths are entirely preventable with appropriate dietary and lifestyle habit changes whether they are implemented as children, youth or adults.

Proposed Mechanism – inflammation

The American Heart Association scientific statement states that the exact mechanism by which these contribute to cardiovascular disease remains to be fully understood and explained, they believe that the cardiovascular risk is brought about by a combination of insulin resistance and oxidative stress (free radical damage), but that inflammation comes first.

“Insulin resistance, oxidative stress, and
inflammation are linked multidirectionally, but emerging
evidence supports a mechanism by which inflammation
comes first.”

SIDE-NOTE: This idea that inflammation precedes insulin resistance is something I've been coming across recently. Some propose that insulin resistance itself may be a protective mechanism against high levels of circulating glucose (sugar) in the blood [a], in much the same way as the ability to produced more and more subcutanous fat (the fat directly under the skin) may be protective against the accumulation of fat around the organs (called visceral fat) or fat in the organs or even the bone (called ectopic fat). That is, excess energy (calories) seen as high levels of glucose in the blood may be the result of storage problems in fat cells (the body's inability to make new subcutaneous fat cells), and the subsequent overflow of fat may drive excess high glucose production in the liver.

a. Nolan CJ, Prentki M, insulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shift, Diabetes and Vascular Disease Research, Feb 15, 2019

The American Heart Association (AHA) suggests that inflammation may increase cardiovascular risk through a combination of these three factors;

(1) high triglycerides (TG)
(2) low high-density lipoprotein cholesterol (HDL)
(3) high small low-density lipoprotein (LDL) particles (LDL-s)

NOTE: Studies on LDL-particle size indicate that people whose LDL  is mostly the small, dense sub-particles have a 3x greater risk of coronary heart disease than those with mostly the large, fluffy sub-particle type, which is thought to be protective."

The American Heart Association suggests that it’s the inflammatory process itself that triggers insulin resistance as a mechanism to keep blood sugar high in order to meet the needs of an  immune system that has become activated, as would occur when the body is fighting a significant infection. 

They propose that this process of inflammation leads to;
(1) defective activity of an enzyme that is responsible for breaking down triglycerides (i.e. lipoprotein lipase) which would normally be used by the body as energy or stored in fatty tissue for later use
(2) blocking of normal fat cell creation (adipogenesis)
(3) an increase in triglycerides in order to deal with infectious toxins and
(4) an overproduction of smaller LDL particles* and HDL particles

*The ADA suggests that the formation of small LDL particles may perform some important function in this situation of high inflammation, as small LDL particles can easily penetrate the blood vessels to deliver cholesterol to damaged tissue and that oxidation of these small LDL particles make athlerosclerosis even worse.

The decrease in HDL cholesterol which is frequently seen on a standard cholesterol test (lipid panel) in the context of inflammation is thought to be associated with a decrease in reverse cholesterol transport which promotes the building up of cholesterol in the tissues, where it is used for the synthesis of cortisol for the cell membranes that have become damaged by what the body sees as an ‘infection’.

Recommended Dietary Changes

The AHA recommends different dietary and lifestyle changes for each of the risk factors

High Triglycerides(TG)

The AHA recommends a diet low in simple carbohydrates and added sugars, high in dietary fiber from fruits* and vegetables**, moderate amounts of complex carbohydrates, and high in polyunsaturated*** and  monounsaturated fats, without specific restriction of saturated fats.

NOTES:

* fructose, the sugar in fruit is a simple carbohydrate and can be a major contributor to high TG. 

** there is no distinction between starchy vegetables such as potato and sweet potato (which accounts for a large percentage of overweight children and adult's 'vegetable' servings) and non-starchy vegetables such as leafy greens and cruciferous vegetables, such as broccoli and cauliflower, as well as a whole host of other low carbohydrate non-starchy vegetables. 

*** it is well established that omega 6 polyunsaturated fats contribute to the inflammation process yet the recommendation doesn't indicate that there should be a decrease in omega 6 polyunsaturated fats such as from soybean oil, canola oil, etc. and an increase in anti-inflammatory omega 3 fats from fatty fish such as tuna, salmon, sardines, etc even though the paper itself proposes inflammation at the heart of the issue.  This makes no sense to me.

Total LDL Cholesterol

Diet high in fiber from fruits* and vegetables**, whole grains, high in polyunsaturated*** and monounsaturated fats, low in saturated
fat and devoid of trans fats.

See Notes above for * , ** and ***.

NOTE: The body of the AHA paper elaborates on the detrimental effect of the small LDL subparticle (LDL-s), yet no such differentiation from total LDL cholesterol (LDL-c) is made in the Dietary Recommendations. Why is that?

Particle size of LDL can be established by testing, using Apo B:Apo A ratio (Apo B is a component of lipoproteins involved in atherosclerosis and cardiovascular disease) and by proxy using a TG:HDL ratio. 

It makes no sense to me that the dietary recommendations focus on total LDL cholesterol when the paper makes it clear that it is the small LDL subparticle that is the risk factor.

Blood glucose (without diagnosis of
Type 1 or Type 2 diabetes)

Low glycemic diet limiting intake of added sugar to ≤5% of total
calories, high in fruits* and vegetables**, encouraging intake of
polyunsaturated*** and monounsaturated fats, and without specific limitation to dietary saturated fats.

See Notes above for * , ** and ***.

Some final thoughts…

The dietary recommendations in this paper that focus on lowering simple carbohydrate and added sugars are very sound, as are recommending moderate amounts of complex carbohydrate and high in monounsaturated fat. However, to me it makes no sense for the AHA to recommend a diet high in fruit when fruit is the primary source of the simple sugar fructose and it also makes no sense to me for the dietary recommendations not to differentiate between starchy vegetables like potatoes, sweet potatoes and corn (which is actually a grain that is counted as a vegetable) that raise blood sugar and the non-starchy vegetables such as salad greens,  broccoli and cauliflower and the abundance of other low carbohydrate vegetables.

Furthermore, given that the AHA proposes an inflammatory mechanism at the root of the cardiovascular disease process, it makes no sense to me for the dietary recommendations to fail to differentiate between pro-inflammatory omega 6 polyunsaturated fatty acids (such as those found in soybean and canola oil) and anti-inflammatory omega 3 polyunsaturated fatty acids, such as those found in fatty fish.

Finally, when the body of the paper makes it very clear that it is the small LDL cholesterol subparticle that contributes to athlersclerosis and that oxidization of it in particular is an additional risk factor, why do the dietary recommendations not focus on lowering the small LDL subparticle, rather than total LDL cholesterol?

Eating a lower carbohydrate intake will both reduce triglycerides (TG) and increase high density lipoproteins (HDL), resulting in an improved TG:HDL ratio, which would indicate a reduction in the small, dense LDL subfraction, and reduced risk of cardiovascular disease.   Recommending a reduction in saturated fat intake will likely reduce any increase in HDL cholesterol with no consistent evidence that lower total LDL cholesterol will result in lower cardiovascular rates.

On one hand, the paper provides a good explanation about the risks of the small, dense LDL subparticle yet recommends lowering dietary intake of saturated fat, in order to lower total LDL cholesterol.

Why the avoidance of consistent dietary changes that would reduce the small, dense LDL subparticle and increase protective HDL? 

If you would like to know about the services that I offer for lowering body weight in adults as well as youth as well as bringing high blood sugars under control, then please click on the Services tab to learn more. If you have questions related to my services then please send me a note using the Contact Me form located on the tab above and I will reply as I am able.

To your good health!

Joy

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Copyright ©2019 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. American Heart Association, Cardiovascular Risk Reduction in High-Risk Pediatric Patients – a scientific statement from the American Heart Association, Circulation. 2019;139:00-00
  2. Twig G, Tirosh A, Leiba A, Levine H, Ben-Ami Shor D, Derazne E, Haklai
    Z, Goldberger N, Kasher-Meron M, Yifrach D, Gerstein HC, Kark JD.
    BMI at age 17 years and diabetes mortality in midlife: a nationwide cohort
    of 2.3 million adolescents. Diabetes Care. 2016;39:1996–2003.
  3. Skinner AC, Perrin EM, Skelton JA. Prevalence of obesity and severe obesity
    in US children, 1999–2014. Obesity (Silver Spring). 2016;24:1116–
    1123. doi: 10.1002/oby.21497
  4. Statistics Canada. 2015 Canadian Community Health Survey, Measured children and youth body mass index (BMI) (World Health Organization classification), by age group and sex, Canada and provinces, Canadian Community Health Survey.
  5. Benjamin EJ, Virani SS, Callaway CW et al (on behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee). Heart disease and stroke statistics—2018 update: a report from the American Heart Association [published correction appears in Circulation. 2018;137:e493]. Circulation. 2018;137:e67–e492
  6. Statistics Canada, Leading causes of death, total population, by age group, https://www150.statcan.gc.ca/t1/tbl1/en/tv.action?pid=1310039401

There’s Something About Real Life Personal Stories

NOTE: This article is an editorial but is cross-posted under Science Made Simple to make it easy to find.

Critics of the use of a low carbohydrate diet for weight loss and for putting the symptoms of Type 2 Diabetes into remission will often say that there are no randomized control trials (RCTs) showing that this diet is safe and effectiveness over the long-term, but what they often don’t realize is that there were no randomized controlled studies demonstrating safety and efficacy underlying the recommendation that people consume 45-65% of their daily calories as carbohydrate, while limiting their fat intake. What we do have in both Canada and the US since 1977 (when the Dietary Guidelines in both countries changed) is 40+ years of epidemiological data showing a massive increase in the incidence and prevalence of obesity and Type 2 Diabetes that shows no sign of letting up, and a millions of people that are fed-up of feeling “sick and tired”. Is it simply that people stopped “moving” as much or could it be the diet?

Recently, the therapeutic use of a low carbohydrate diet as a dietary option for reducing blood sugar, use of blood-sugar lowering medications and for weight loss has been recognized by the American Diabetes Association  (ADA) in the release their 2019 Standards of Medical Care in Diabetes (you can read more about that here. In addition, in October 2018 the ADA and the European Association for the Study of Diabetes (EASD) released a joint position paper that classifies a low carbohydrate diet as Medical Nutrition Therapy for the treatment of Type 2 Diabetes in adults (more about that here). This means that physicians and healthcare professionals in Europe and the United States can recommend a low carbohydrate diet as one of the treatment options for their patients.  This moves a low carbohydrate diet from the realm of popular lifestyle choice to Medical Nutrition Therapy for the purpose of disease management.

You can get a one-page downloadable summary (with references) of both the American Diabetes Association (ADA) 2019 Standards of Medical Care in Diabetes and the ADA and the European Association for the Study of Diabetes (EASD) joint position paper here.

As covered in previous articles, there are ample studies showing that a well-designed low carbohydrate diet is both safe and effective for putting Type 2 Diabetes into remission and for weight loss.

In fact, there was a list compiled by Dr. Sarah Hallberg at the end of January 2018 of studies that involved a low carbohydrate diet which spanned  18 years, 76 publications involving 6,786 subjects, including 32 studies of 6 months or longer and 6 studies of 2 years or longer. Now, it is a year later and there are numerous other studies including very recent two-year data from the Virta Health study which demonstrates that a low carbohydrate diet is not only safe, but effective long term.

But there’s something about real-life, personal (n=1) accounts of ordinary people losing weight and putting their Type 2 Diabetes and other metabolic conditions into remission that people find very compelling.

Diet Doctor, a well-known website dedicated to a low-carb high fat / “keto” approach has a whole section of “success stories”, and a very popular ketogenic Facebook page from Nigeria which promotes a “keto” diet (mostly self-defined) does as well.

What about when the “ordinary people” that lose weight and put their own metabolic disorders into remission also happen to be healthcare professionals? It seems many find this particularly compelling because we know the full range of dietary options and have chosen the method we have after careful consideration.

As many of you know, I was recently the featured guest on the Low Carb MD Podcast which was hosted by Dr. Tro Kalajian and Dr. Brian Lenzkes. As outlined on the article at the link above, both of these doctors struggled with obesity their whole lives and both have lost weight and found improved metabolic health, and are now helping their patients to do the same.

Then there’s me, a Registered Dietitian in private practice who’s lost almost 50 pounds and put my Type 2 Diabetes of 10 years into remission.

The three of us are just ‘two Docs and a Dietitian’ who were sick of being sick, but there are many more healthcare practitioners just like us that have done similarly, including some of the more than 1500 that are part of the Canadian Clinicians for Therapeutic Nutrition (CCTN) Facebook group and members of CCTN.

We are ordinary people who as clinicians are knowledgeable about the therapeutic benefits of following a low carbohydrate diet and who have implemented it in our own lives. Our stories are not scientific case studies, nor are they part of a randomized controlled trials or research of any kind.  Our single subject (n=1) anecdotal stories and those of hundreds of thousands of ordinary people from all walks of life are powerful because they stand in sharp contrast to the large percentage of the population that are overweight or obese just like we were, but who keep eating the same way and getting sicker.

We offer people choices.

The choice of turning things around.

The option of getting healthy.

The ability to achieve a healthy body weight and in the process be able to have our doctors reduce or eliminate medications for metabolic diseases.

If you’re tired of being “sick and tired” then I’d encourage you to listen to the podcast above or to have a look through some of the “Science Made Simple” articles on this web page under the Food for Thought tab. There you can learn about the different types of “low carb” and “keto” diets and get a feel for what eating this way is like.

If you would like medical support in the US, be sure to check out Dr. Kalajian and Dr. Lenzkes, other physicians such as Dr. Eric Westman and Dr. Ted Naiman, as well as the Virta Health Clinic, as well as many others who are knowledgeable and experienced to provide you with support in this area. If you are in Canada and are looking for a therapeutic nutrition practitioner, you can search the list on the CCTN website (link above) and if you’d like to know how I can help (either in-person or from where you are via Distance Consultation) then feel free to send me a note using the Contact Me form above and I’ll reply as soon as possible.

To your good health!

Joy

You can follow me at:

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https://www.instagram.com/lchf_rd

 

Copyright ©2019 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.

Insulin Resistance, Hyperinsulinemia and Hyperglycemia

The distinction between insulin resistance and hyperinsulinemia is often unclear because these terms are frequently lumped together under “insulin resistance“, but they are separate concepts. Hyperinsulinemia (“too high insulin”) is when there is too much insulin secreted from the pancreas in response to high levels of blood sugar (hyperglycemia) and insulin resistance is where the taking in of that glucose into the cells is impaired.

Blood glucose is a tightly regulated process. A healthy person’s blood glucose is kept in the range from 3.3-5.5 mmol/L (60-100 mg/dl) but after they eat, their blood sugar rises as a result of the glucose that comes from the broken-down carbohydrate-based food. This triggers the hormone insulin to be released from the pancreas, which signals the muscle and adipose (fat) cells of the body to move the excess sugar out of the blood. What happens in insulin resistance is that the cells of the body ignore signals from insulin telling it to move glucose from broken down from digested food from the blood into the cells. When someone is insulin resistant, blood glucose stays higher than it should be for longer than it should be (hyperglycemia).

The Process of Moving Glucose Inside the Cell

A special transporter (called GLUT4) that can be thought of as a ‘taxi’ exists in muscle and fat cells and is controlled by insulin. This ‘taxi’ moves glucose from the blood and into the cells. GLUT4 ‘taxis’ are kept inside the cell until they’re needed. When ‘taxis’ are required, they go to the surface of the cell, bind with insulin and pick up their ‘passenger’ (glucose) and moves it inside the cell. Both the ‘taxi’ (GLUT4 receptor) and the insulin are also taken inside the cell and then replaced on the surface of the cell with new receptors. As long as there are GLUT4 ‘taxis’ available on the surface of the cell to transport glucose inside everything’s good, but when blood sugar is quite high, the pancreas keeps releasing insulin to bind with the GLUT4 ‘taxis’, but those ‘taxis’ may not appear fast enough on the cell surface to pick up the glucose. In this case, blood sugar remains higher then it should be for longer, a state called hyperglycemia. When there are insufficient receptors to move glucose into the cell, this is called insulin resistance. It may be temporary, as in the example above, or may be long-term. If it is temporary, the rise in blood sugar (hyperglycemia) is short but if the receptors don’t respond properly long-term, then blood sugar remains higher for a longer period of time, until the ones that do work can bring the glucose inside. In one case, the blood sugar may be quite high for a short time or may be moderately high for a long time. In both cases, the body is exposed to higher blood sugar than it should be, and this causes damage to the body. It isn’t known whether insulin resistance comes first or hyperinsulinemia does. It is believed that it may be different depending on the person.

What Triggers Hyperinsulinemia?

It is known that excessive carbohydrate intake can trigger hyperglycemia, as well as hyperinsulinemia. Eating lots of fruit, for example or foods that contain fructose (fruit sugar) will cause the body to move that into the body first in order to get it to the liver, before it deals with glucose. This causes glucose levels in the blood to rise, resulting in both hyperglycemia and hyperinsulinemia. Lots of processed foods contain high fructose corn syrup (HFCS) which contributes to problems with high blood sugar and hyperinsulinemia.

There are other things that can also trigger hyperglycemia and hyperinsulinemia include certain medications (like corticosteroids and anti-psychotic medication) and even stress. Stress causes the hormone cortisol to rise, which is a natural corticosteroid. It is thought that long-term stress may lead to hyperinsulinemia, which increases appetite by affecting neuropeptide Y expression. This may explain why people eat more when they’re stressed and are very often drawn to carbohydrate-based foods that are quickly broken down for energy.

Diseases Associated with Hyperinsulinemia

It is well known that hyperglycemia that occurs with Type 2 Diabetes contributes to problems with the eyes, kidneys and nerves of the extremities, especially the feet and toes. Less known are the diseases and metabolic problems that can occur due to hyperinsulinemia.

Hyperinsulinemia has a well-establish association to the development of Type 2 Diabetes and Gestational Diabetes (the Diabetes of pregnancy), but also to Metabolic Syndrome (MetS).

Metabolic Syndrome (MetS) is a cluster of symptoms that together put people at increased risk for cardiovascular disease, including heart attack and stroke.

These symptoms of MetS include having 3 or more of the following;

  1. Abdominal obesity (i.e. belly fat), specifically, a waist size of more than 40 inches (102 cm) in men and more than 35 inches (89 cm) in women
  2. Fasting blood glucose levels of 100 mg/dL (5.5 mmol/L) or above
  3. Blood pressure of 130/85 mm/Hg or above
  4. Blood triglycerides levels of 150 mg/dL (1.70 mmol/L) or higher
  5. High-density lipoprotein (HDL) cholesterol levels of 40 mg/dL (1.03 mmol/L) or less for men and 50 mg/dL (1.3 mmol/L) or less for women

Hyperinsulinemia is also an independent risk factor for obesity, osteoarthritis, certain types of cancer including breast and colon/rectum, Alzheimer’s Disease and other forms of dementia[1], erectile dysfunction[2] and polycystic ovarian syndrome (PCOS)[3].

The damage associated with hyperinsulinemia is due to the continuous action of insulin in the affected tissues[4].

Risk factors for developing insulin resistance include a family history of Type 2 Diabetes, in utero exposure to Gestational Diabetes (i.e. an unborn child whose mother had Gestational Diabetes), abdominal obesity (fat around the middle) and detection of hyperinsulinemia.  Assessors of insulin resistance using blood tests such as the Homeostatic Model Assessment (HOMA2-IR) test which estimates β-cell function and insulin resistance (IR) from simultaneous fasting blood glucose and fasting insulin or fasting blood glucose and fasting C-peptide[1]. As well, incorporation of some forms of exercise including resistance training may lower insulin resistance in the muscle cells and weight loss – even when people are not very overweight can increase uptake of glucose, due to lowered insulin resistance of the liver.

Detection of hyperinsulinemia can occur using an Oral Glucose Sensitivity Index (OGIS), which is similar to a 2-hr Oral Glucose Tolerance Test (2-hr OGTT) which is a test where a fasting person drinks a known amount of glucose and their blood sugar is measured before the test starts (baseline, while fasting) and at 2 hours. In the OGIS, both blood glucose and blood insulin levels are measured at baseline (fasting), at 120 minutes and at 180 minutes [5].

Glucose and insulin response patterns that result after people take oral glucose can also be used to determine hyperinsulinemia status. Between 1970 and 1990, Dr. Joseph R. Kraft collected data from almost 15,000 people which showed five main glucose and insulin response patterns; with one being the normal response. Kraft’s methodology was to measure both glucose and insulin response over a 5-hour period, noting the size of both the glucose and insulin peaks, as well as the rate that it took the peaks to come back down to where it started from. Kraft concluded that a 3-hour oral glucose tolerance test with both glucose and insulin measured at baseline (fasting), 30, 60 120 and 180 minutes was as accurate as a 5-hour test. Most striking about the original study and recent re-analysis of this data found that up to 75% of people with normal glucose tolerance have carrying degrees of hyperinsulinemia [9]. You can read more about that in this recent article.

Hyperinsulinemia and insulin resistance together are the essence of carbohydrate intolerance; the varying degrees to which people can tolerate carbohydrate without their blood sugar spiking. This is not unlike other food intolerance such lactose intolerance or gluten intolerance which reflect the body’s inability to handle specific types of carbohydrate in large quantities.

Some final thoughts…

Insulin resistance and hyperinsulinemia are present long before a diagnosis of pre-diabetes and are now are considered an entirely separate stage in the development of the disease (you can read more about that here). A recent study reported that abnormal blood sugar regulation precedes a diagnosis of Type 2 Diabetes by at least 20 years [6] which means that long before blood sugar becomes abnormal, the progression to Type 2 Diabetes has already begun. Knowing how to recognize the symptoms of insulin resistance and hyperinsulinemia and to have them measured or estimated, as well as to detect the abnormal spike in blood glucose that often occurs 30 to 60 minutes after eating carbohydrate-based food is essential to avoiding progression to Type 2 Diabetes as well as the complications associated with hyperglycemia and hyperinsulinemia.

If you would like my help in lowering your risk to developing Type 2 Diabetes and the chronic disease risks associated with hyperinsulinemia or in reversing their symptoms, please send me a note using the Contact Me form on the tab above. I provide both in-person consultations as well as by Distance Consultation,using Skype and phone.

To your good health!

Joy

You can follow me at:

       https://twitter.com/lchfRD

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References

  1. Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.
  2. Knoblovits P, C.P., Valzacci GJR,, Erectile Dysfunction, Obesity, Insulin Resistance, and Their Relationship With Testosterone Levels in Eugonadal Patients in an Andrology Clinic Setting. Journal of Andrology, 2010. 31(3): p. 263-270.
  3. Mather KJ, K.F., Corenblum B, Hyperinsulinemia in polycystic ovary syndrome correlates with increased cardiovascular risk independent of obesity. Fertility and Sterility, 2000. 73(1): p. 150-156.
  4. Crofts CAP, Z.C., Wheldon MC, et al, Hyperinsulinemia: a unifying theory of chronic disease? Diabesity, 2015. 1(4): p. 34-43.
  5. 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.
  6. Sagesaka H, S.Y., Someya Y, et al, Type 2 Diabetes: When Does It Start? Journal of the Endocrine Society, 2018. 2(5): p. 476-484.

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.

When Normal Fasting Blood Glucose Results Aren’t Necessarily “Fine”

When people have a fasting blood glucose test and the results come back normal, they’re told (or assume) that everything’s fine. But is it? Certainly, a fasting blood glucose test is the least expensive test to find out if someone is already pre-diabetic, but for those wanting to avoid becoming Diabetic and to lower their risk of the other chronic disease associated with Type 2 Diabetes and high levels of circulating insulin (called hyperinsulinemia) noticing abnormalities in how we process carbohydrates is essential and these changes are estimated to take place a decade before our fasting blood sugar begins to become abnormal.

Our bodies have to maintain the glucose (sugar) in our blood at or below 100 mg/dl (5.5 mmol/L) but each time we eat or drink something other than water or clear tea or coffee, our blood sugar rises as our body breaks down the carbohydrate in the food from starch and complex sugars to glucose, a simple sugar.  Eating causes hormones in our gut, called incretin hormones to send a signal to our pancreas to release insulin, which moves the excess glucose out of our blood and into our cells. When everything is working properly, our blood sugar falls back down to a normal level within 2 hours after we eat (called 2 hours “postprandial”).

If we’re healthy and don’t snack after supper, our blood sugar falls to a lower level overnight but that too is maintained in a tightly regulated range between 60 mg/dl (3.3 mmol/l) and 100 mg/dl (5.5 mmol/l). During the night and as we approach morning, our body will break down our stored fat for energy and convert it to glucose in a process called gluconeogenesis.

When we have a fasting blood glucose test, it measures our blood sugar after we’ve fasted overnight and when we’re healthy, the results will be between 60-100 mg/dl (3.3-5.5 mmol/L). If it is higher than 100 mg/dl (5.5 mmol/l) but less than 125 mg/dl (6.9 mmol/L) we are diagnosed with impaired fasting glucose, but what if it’s normal? Is a normal fasting blood glucose test result enough to say that we’re not at risk for Type 2 Diabetes? No, because a fasting blood glucose doesn’t tell us anything about how our body responds when we eat.

A 2-hour Oral Glucose Tolerance Test (2 hr-OGTT) may be requested for people whose fasting blood glucose is impaired (higher than 100 mg/dl / 5.5 mmol/L) in order to see if it returns to normal after they consume a specific amount of glucose (sugar).

If their blood sugar returns to normal (less than100 mg/dl / 5.5 mmol/L) 2 hours after drinking a beverage containing 75 g of glucose (100 g if they’re pregnant) then the diagnosis remains impaired fasting glucose because it is only abnormal when fasting. However, if the results are greater than 140 mg/dl (7.8 mmol/L) but below 200 mg/dl (11.0 mmol/L), then they are diagnosed with impaired glucose tolerance which is called “pre-diabetes“.

If the 2-hour results are greater than 200 mg/dl (11.0 mmol/L), then a diagnosis of Type 2 Diabetes is made because their fasting blood glucose is > 7.0 mmol/L (126 mg/dl) and their 2-hour blood glucose is > 11.0 mmol/L (200 mg/dl).

But what if their fasting blood glucose is normal? Does that mean everything’s good? No, because we don’t know what happens to their blood sugar after they eat carbohydrate containing food, most notably between 30 minutes and 60 minutes.

A 2016 study looked at blood sugar and insulin response from almost 4000 men aged 20 years or older and 3800 women aged 45 years or older who had a 5-hour Oral Glucose Tolerance Test using 100 g of glucose. The study found that 53% had normal glucose tolerance; that is, they had normal fasting blood sugar and did not have impaired glucose tolerance (IGT) 2 hours after the glucose load. Of these people with normal glucose tolerance, 75% had abnormal blood sugar results between 30 minutes and 1 hour.

Normal Blood Glucose Pattern

A little less than 1000 people (990) out of the total with normal glucose tolerance (4030) had a normal glucose pattern (see graph below). It’s easy to see that the blood sugar rises to a moderate peak and then decreases steadily until it’s back to where it started from at 2 hours. This is what blood sugar is supposed to do.

Normal Glucose Curve (carbohydrate tolerance) – graph by Joy Y. Kiddie, MSc, RD (based on [1] 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.)

Abnormal Glucose Patterns

Almost the same number of people (961) as had normal glucose curves showed early signs of carbohydrate intolerance which can be seen most noticeably between 30 and 60 minutes. Keep in mind, this graph represents the average blood sugar response of these individuals. These folks had normal fasting blood glucose but after 2 hours blood glucose did not return to baseline but was not high enough to meet the criteria for impaired glucose tolerance. Unless someone was looking between 30 and 60 minutes, no one would know it not was not normal. Rather than blood glucose going up to a moderate peak and then falling gradually in a straight line, a two-stage rise in glucose can be clearly seen between 30 minutes and 60 minutes before beginning to drop.

Early Carbohydrate Intolerance (Early Abnormal Glucose Response) – graph by Joy Y. Kiddie, MSc, RD (based on [1] 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.)
A little more than 1200 people (1208) had the following abnormal glucose response which represents Advanced Carbohydrate Intolerance. These people had normal fasting blood glucose, but their blood glucose did not fall to baseline at 2 hours but was below the cut-offs for impaired glucose tolerance. Between 30 and 60 minutes their blood sugar went slightly higher at 60 minutes than at 30 minutes compared to the Early Carbohydrate Intolerance curve, before beginning to fall.

Advanced Carbohydrate Intolerance (Advanced Abnormal Glucose Response) – graph by  Joy Y. Kiddie, MSc, RD (based on [1] 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.)
Slightly more than 800 people (807) had an abnormal glucose response curve shaped as follows, indicating Severe Carbohydrate Intolerance.  They had normal fasting blood glucose and 2-hour postprandial blood glucose results that were higher than at baseline yet did not meet the criteria for impaired glucose tolerance. What was significant is that blood sugar was significantly higher at 60 minutes than at 30 minutes, compared to the Advanced Carbohydrate Intolerance curve.

Severe Carbohydrate Intolerance (Severe Abnormal Glucose Response) – graph by Joy Y. Kiddie, MSc, RD (based on [1] 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 Significance of These Curves

The results of this study show that even if fasting blood glucose is totally normal and 2-hour postprandial blood glucose does not meet the criteria for impaired glucose tolerance, it often does not return to baseline and the blood sugar response between fasting and 2 hours is very abnormal. What can’t be seen from these graphs is what happens to the hormone insulin at the same time. This will be covered in the next chapter but suffice to say that Normal Carbohydrate Tolerance, blood sugar response mirrors what is happening with insulin but in Early, Advanced and Severe Carbohydrate Intolerance, insulin secretion is both much higher and lasts much longer. This is called hyperinsulinemia (high blood insulin) and contributes to many of the health risks associated with Type 2 Diabetes, including cardiovascular risks (heart attack and stroke), abnormal cholesterol levels and hypertension (high blood pressure).  This is like having “silent Diabetes“.

A “Waste of Healthcare Dollars”

As a Dietitian, when a person’s clinical symptoms and risk factors warrant it, I’ll request a 2-hour Oral Glucose Tolerance Test (2-h OGTT) with an extra glucose assessor at 30 minutes (and sometimes at 60 minutes) to determine how their glucose response compares to the above curves. While these blood tests are done with 75 g of glucose and not 100 g, the shape of the curves and the endpoint as well as the size of the peak between 30- and 60-minutes reveals much about their carbohydrate intolerance. Since these people have normal fasting blood glucose test results, a request for an Oral Glucose Tolerance Test (with or without the extra glucose assessor) is often declined as a “waste of healthcare dollars”. Unfortunately, this is where being “penny wise” can be “pound foolish” as these people don’t know they are at risk and as a result, are not motivated to change their eating habits or lifestyle.

What About Glycated Hemoglobin (HbA1C)?

A glycated hemoglobin test (HbA1C, also called A1C) measures a form of hemoglobin that binds glucose (the sugar in the blood) and is used to identify the person’s three-month average glucose concentration because blood cells turnover (get replaced) on average every 3 months.

While having a glycated hemoglobin test and a fasting blood glucose test is better than only having fasting blood glucose, it will still miss a significant percentage of people who are able to control their sugars between meals and overnight but who have significant spikes between 30 minutes and 60 minutes, immediately after eating carbohydrate-based food, but that return to normal by 2 hours. Most physicians will not requisition a HbA1C test if a person’s fasting blood glucose is normal, and even if they do, that test may miss that glucose ever spikes at all between 30 minutes and 60 minutes.

In the absence of available lab testing, I sometimes resort to using a Glucose Response Simulation.

Glucose Response Simulation

A simple, if somewhat crude means of assessing glucose response under a load can be done at home using an ordinary glucometer (a meter for measuring blood sugar) such as would be used by people with Diabetes, and either a 100 g of dextrose (glucose) tablets available at most pharmacies or the equivalent. As part of the services I provide to my clients, I work with those that want to do this type of estimate so that they can understand whether they fall into the 75% of people that have normal fasting blood sugar and do not have impaired glucose tolerance at 2 hours postprandial but do have an abnormal glucose response. I explain how to prepare for the test, step by step instruction for conducting the test and then I graph and analyze the data then teach them what the results mean.

Basis for Individualizing Carbohydrate Intake

These results are very helpful as firstly they help people understand the reason for reducing their carbohydrate intake over an extended period of time, in order to restore insulin sensitivity and insulin secretion. These results also enable me in time to individualize their carbohydrate intake once they have reversed some of their metabolic response, based on their own blood sugar response to a specific carbohydrate load.  In time, some of these individuals may want to add some carbohydrate back into their diet in small quantities, so with this information, I can guide them to test a standard size serving of rice, pasta or potato compared to their own blood glucose response to 100 g of glucose.

Below are three curves that I’ve plotted from individuals that used the same type of glucometer (Contour Next One) and a standard 100 g glucose load as dextrose tablets or equivalent to 100 g of glucose [2]. I provided each one with identical instructions on how to run this simulation, how to collect the results and ensured each one understood.

Example 1: The person below had a single glucose peak (similar to the early carbohydrate intolerance of the first abnormal curve, above) but blood glucose did not come back down to the fasting level even after 3 hours.

Early Abnormal Glucose Response – graph by Joy Y. Kiddie MSc, RD

Example 2: The person below had a single glucose peak  that reached abnormally high levels and that didn’t fall continuously downward but slowed, then dipped below baseline at 2 hours (mild reactive hypoglycemia) and that gradually came back to baseline over the following couple of hours.

Advanced Abnormal Glucose Response – graph by Joy Y. Kiddie MSc, RD

Example 3: This person had a similar initial rise as the person above, but no hypoglycemic dip however, this person’s glucose didn’t fall to baseline until almost 5 hours.

Some Final Thoughts…

An abnormal fasting blood glucose test may warrant further testing; however, a normal result is frequently dismissed as being a sign that “everything’s fine”. Data from this study indicates that as many as 75% of people with normal fasting blood sugar may have abnormal glucose responses and associated hyperinsulinemia, meaning they could have the same risks to other chronic diseases as someone who has already been diagnosed with Type 2 Diabetes. They simply don’t know it.

With reliable and relatively inexpensive glucometers, as well as continuous glucose monitors (CGM) people don’t need to wonder whether they have an abnormal glucose response to eating carbohydrate (are carbohydrate intolerant). They can use simulation tests, such as the ones I did above, to find out.

Not knowing one is at risk does nothing to provide motivation to make dietary and lifestyle changes, but knowing one has an abnormal response to carbohydrates not only enables people to want to make these changes, it also helps them to find which carbohydrates they can eventually add back into their diet, once they’ve lowered their glucose and insulin levels, and in what quantities.

If you have questions as to how I can help you get started in knowing your own glucose response and to lower risk factors, please send me a note using the Contact Me form located on the tab, above.

To your good health!

Joy

Note: The second article in this series explains what hyperinsulinemia is and why it's a problem. It's titled Carbohydrate Intolerance & the Chronic Disease Risk of High Insulin Levels and can be read by clicking here.

You can follow me at:

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References

  1. 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.
  2. Lamar, ME et al, Jelly beans as an alternative to a fifty-gram glucose beverage for gestational diabetes screening, Am J Obstet Gynacol, 1999 Nov 18 (5 Pt 1): 1154-7

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.

 

 

 

Will This Knock Me Out of Ketosis?

Earlier this week I heard someone ask in a low-carb Facebook group if eating a particular food would ‘knock them out of ketosis‘ and I decided it was time to write an article about this, but first I ran a short poll on Twitter to find out what my readers thought.

The first answer in the poll was my tongue-in-cheek reaction to hearing the question asked for the umpteenth time and the other three options were reasonable answers that people could choose from.

Twitter poll: “Will this knock me out of ketosis?”

So what’s the answer?

According to Dr. Stephen Phinney, MD, PhD. Professor of Medicine Emeritus at the University of California, Davis who has over 25 years of clinical experience studying multi-disciplinary weight management programs, including the use of a ketogenic diet;

“Carbohydrate tolerance varies among individuals.  Some people may need to limit themselves to no more than 30 grams of total carbohydrates per day to remain in nutritional ketosis and maintain its benefits; while others may be able to consume more.  However, most people with underlying metabolic issues find that they need to maintain a carbohydrate intake below 50 grams per day, especially if they have Type 2 Diabetes.”

For the most part, men who are insulin sensitive and seeking to follow a ketogenic diet can do very well on 50-100 g of carbohydrate per day and women who are insulin sensitive who want to follow a ketogenic diet can do well on 50-75 g of carbohydrates per day. As Dr. Phinney points out, those with metabolic issues such as Type 2 Diabetes will usually need to keep their carbohydrate intake less than 50 g per day.

People with epilepsy or seizure disorder or who have been prescribed a ketogenic diet as an adjunct treatment to chemotherapy for specific types of cancer will need to follow a very strict high-fat ketogenic diet and the level of carbohydrate restriction is specific for those conditions.  For those who are insulin sensitive who are simply seeking weight loss, a low carbohydrate diet is often sufficient. I’ve found over the last several years of designing low carbohydrate diets for my clients that insulin-sensitive individuals often do very well simply cutting the total amount of carbohydrate down significantly and altering the types of carbohydrate they eat. For those with pre-Diabetes and Type 2 Diabetes, the types and amounts of carbohydrates they eat can be individually determined by testing glycemic responses to specific foods and I help my clients do this and understand the results.

What is the difference between someone who is insulin sensitive and someone who is insulin resistance?

People who have Type 2 Diabetes or pre-diabetes or Metabolic Syndrome are by definition insulin resistant but for those without these conditions, how would someone know?  There are two blood tests that can be done together (fasting blood sugar and fasting insulin) that can help estimate the degree of insulin resistance but there are visual cues that can also help.

insulin sensitive (from Klöting N, Fasshauer M, Dietrich A et al, Insulin-sensitive obesity, Am J Physiol Endocrinol Metab 299: E506–E515, 2010, pg. 5)

People who store most of their fat as subcutaneous fat, rather than visceral fat (fat in their abdomen) are often insulin-sensitive — even those that are very obese. These are people whose fat is mostly the type that hangs loosely over their belt and jiggles when they walk or laugh. Surprisingly, these are not the people that necessarily have metabolic issues, provided they also don’t have significant amounts of visceral fat (where it can’t be pinched and where it wraps the organs, resulting in metabolic disruption).

insulin resistant (from Klöting N, Fasshauer M, Dietrich A et al, Insulin-sensitive obesity, Am J Physiol Endocrinol Metab 299: E506–E515, 2010, pg. 5)

Those who store most of their fat inside their abdomen as visceral fat rather are often insulin resistant and as a result may have high blood pressure, abnormal cholesterol (lipids) or been diagnosed as having either pre-Diabetes or Type 2 Diabetes.

In order to reverse the symptoms of these chronic diseases, people with insulin resistance often need to maintain their intake of carbohydrate at a lower level than those who are insulin sensitive.

As far as the question as to whether eating a particular food will “knock someone out of ketosis“, if that food contains more grams of carbohydrate than their daily limit then yes, they will temporarily burn glucose instead of producing ketones from burning fat.

That said, for a low-carbohydrate lifestyle to be sustainable long term for the average individual without metabolic issues seeking weight loss, I don’t understand why some are focused on how many ketones they are producing.  This is not one of those cases that ‘more is better’. The body is very good at not wasting energy, be it as glucose or ketones so if people have been in ketosis for a considerable length of time, their body will often stabilize and produce a lower level of ketones, so as not to produce more than is needed. A lower level is just fine.

If you have been prescribed a low carb or ketogenic diet for a specific health condition or are taking one of the medications that puts you at risk of developing ketoacidosis (a potentially life-threatening condition which is very different than ketosis!) then yes, tracking ketones is important, but for the average person, eating the foods are on your Meal Plan will enable you to enjoy your meals while keeping to the amount of carbohydrate that your body tolerates, without counting anything!

That’s the beauty of this style of eating! There’s no need to weigh and measure food, so why become focused on carbohydrate counting or on ketone measuring?

If it’s a special occasion and you want to have a piece of something that is not normally part of what you eat then decide if eating a small serving fits your own health and nutrition goals.  If it does, have a small piece and enjoy it. If it doesn’t than choose not to.

Overall, if you focus on eating real, whole foods including plenty of healthy animal protein, low carbohydrate vegetables and leafy greens with just enough fat to make it tasty, then relax, eat and enjoy!

If you would like to know more about what’s involved in me designing a Meal Plan for you, then please send me a note using the “Contact Me” form above and for information on the various in-person or distance consultation services I provide, please click on the “Services” tab.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

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Reference

Virta Health Blog, Dr. Stephen Phinney, https://blog.virtahealth.com/how-many-carbs-ketogenic-diet/

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

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.


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.

 

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

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

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.

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

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:

 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

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:

 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

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:

 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.

Evidence that Low Carb Diets are Safe and Effective

Claims are sometimes made that “low carb diets are a fad” and “there needs to be scientific evidence to demonstrate they are both safe and effective“. What is the evidence?

In fact, a low carbohydrate diet is not new and was the standard recommendation for treating Diabetes prior to the discovery of insulin. More than 150 years ago, the first weight-loss diet book (ironically written by William Banting, a distant relative of Sir Frederick Banting, the co-discoverer of insulin) focused on the limiting the intake of carbohydrates, especially those of a starchy or sugary nature. The book was titled Letter on Corpulence – Addressed to the Public (1864) and summarized the advice of the author’s physician, Dr. William Harvey that had enabled Banting to shed his ‘portly stature’.

Recent 10 week results of a nonrandomized, parallel arm, outpatient intervention using a very low carb diet which induced nutritional ketosis  was so effective at improving blood sugar control in Type 2 Diabetes, that at the end of six months >75% of people had HbA1c that was no longer in the Diabetic range (6.5%). Details of the findings from this study titled A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes are available here.

I recently reviewed 2 two-year studies that demonstrated that low carb diets are both safe and effective for weight loss and improving metabolic markers;

  1. This long-term study titled Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet clearly demonstrated that a low carb non–calorie-restricted diet was both safe and effective and produced the greatest weight loss, lower FBS and HbA1C, the most significantly lower TG and higher HDL and lower C-reactive protein (when compared with a  low-fat calorie-restricted diet and a Mediterranean calorie-restricted diet).
  2. This 2-year, randomized control study of more than 300 participants  titled Low Fat Calorie Restricted Diet versus Low Carbohydrate Diet – a two year study found that both diet groups achieved clinically significant and nearly identical weight loss (11% at 6 months and 7% at 24 months) and that people who ate the low-carbohydrate diet had greater 24-month increases in HDL-cholesterol concentrations than those who ate a low-fat calorie restricted diet. As well, a significant finding of this study was a very favourable lowering of LDL for the first 6 months and lowering of both TG and VLDL for the first year.

These long-term data provide evidence that a low-carbohydrate diet is both a safe and effective option for weight loss and that this style of eating has a prolonged, positive effect on metabolic markers.

But is this all the evidence we have?  By no means!

Below is a list of research studies and meta-analyses (complied by Dr. Sarah Hallberg) that used a low-carb intervention. These span 18 years, 76 publications, involve 6,786 subjects, and include 32 studies of 6 months or longer and 6 studies of 2 years or longer. At the bottom of this post is a downloadable pdf of this list. [Note: text in green represents meta-analyses.]

Hardly a passing fad!

Low carb diets have been well-studied and found to be both safe and effective.

Many thanks to Dr. Sarah Hallberg, a Physician and exercise physiologist from West Lafayette, Indiana (Twitter: @DrSarahHallberg) for compilation of this list.

A complete list of the Low Carb Diet studies to date (compiled by Dr. Sarah Hallberg) is available here.

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

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.

Understand High Blood Sugar & High Cholesterol

INTRODUCTION: All the science in the world isn’t helpful if people can’t understand it.  This is a simple, yet accurate explanation of how we get high blood sugar, fatty liver disease, high triglycerides and high cholesterol. Science made simple.


Most people know that Diabetes is having “high blood sugar” but just how much sugar is actually in the human body?

An adult has 5 liters of blood circulating in their body at any one time.

A healthy person’s body keeps the range of sugar in the blood (called ‘blood glucose’) tightly-controlled between 3.3-5.5 mmol/L (60-100 mg/dl) — that is, when they eat food with carbohydrate the body breaks it down to sugar,  and insulin takes the extra sugar out of the blood and moves it into cells.

Where does it put it?

First, the body makes sure that glycogen stores are sufficient, which is the body’s “emergency supply of energy”. There’s about a day’s worth of energy (2000 calories) in our muscle and liver glycogen. Once the liver and muscle glycogen is full, the rest of the blood sugar is moved to the liver where it is converted into LDL cholesterol and triglycerides and then the rest stored in fat cells. Fat is where the sugar that we make from the food we’ve eaten goes if it is not needed right away. Fat is storage for later.

So how much sugar is there in the blood of a healthy adult?

Doing the math (see illustration below), there are only 5 grams of sugar in the entire adult human body — which is just over one teaspoon of sugar.

That’s it!

One heaping teaspoon of sugar in the entire adult body!

understand sugar in body
The amount of sugar in the blood of a healthy adult

How Do We Understand Diabetes in Terms of Blood Sugar?

How much sugar does someone with Diabetes have in their blood compared to a healthy person?

Someone with a fasting plasma glucose level of 7 mmol/L (126 mg/dL) meets the diagnostic criteria for Diabetes — which is just 6.25 grams of sugar or 1 -1/4 teaspoons.  

That is, the difference between the amount of sugar in the blood of a healthy person and the amount of sugar in the blood of someone with  Diabetes is just a quarter of a teaspoon of sugar

That’s it!

A quarter teaspoon of sugar is such a small amount but it makes the difference between someone who is healthy and someone who has Diabetes

The difference between the amount of sugar in the blood of a healthy person and the amount of sugar in the blood of someone with Diabetes is just a quarter of a teaspoon of sugar.

In a person with Type 2 Diabetes, the once tightly-controlled system that is supposed to keep the range of sugar in the blood between 3.3-5.5 mmol/L  (60-100 mg/dl) is “broken”. When someone with Diabetes eats food with carbohydrate in it, their insulin is unable to take the sugar out of their blood fast enough, so the sugar stays in their blood longer than it should.

Just as with a healthy person, the body of someone with Diabetes takes the sugar that results from the food they’ve eaten and ‘tops up’ their liver and muscle glycogen stores, then the rest is sent to the liver where it is converted into LDL cholesterol and triglycerides, and then the rest is stored in fat cells.

Some people have the ability to store the sugar overload in the form of fat under the skin (called sub-cutaneous fat). In this way, obesity is a way of protecting the body from this sugar overflow.  Eventually though, if the constant flow of carbohydrate continues, the ability of the body to store the excess as sub-cutaneous fat is limited and then fat around the organs (called visceral fat) increases and this is what ends up causing Diabetes and fatty liver disease.

subcutaneous vs visceral fat
Sub-cutaneous fat (LEFT) versus visceral fat (RIGHT) – from Klöting N, Fasshauer M, Dietrich A et al, Insulin-sensitive obesity, Am J Physiol Endocrinol Metab 299: E506–E515, 2010, pg. 5

The problem with all of us (both those that are healthy and those with  Diabetes) is that we never get to access our fat stores because we keep eating significant amounts of carbohydrate every few hours, storing the excess sugar in our fat stores. According to recent statistics, three-quarters of us lead sedentary (inactive) lives and barely get to make a dent in the energy we take in each day.  As a result, we just keep getting fatter and  fatter.

We eat breakfast — maybe a bowl of cereal (30 gms of carbs) or two toast (30 gms of carbs) or if we’re in a rush we grab a croissant breakfast sandwich at our favourite drive-through (30 gms of carb). Each of these contains the equivalent of a bit more than 6 teaspoons of sugar

Mid-morning, maybe we eat a fruit – say, an apple (30 gm of carbs) to hold us together until lunch — and take in another 6+ teaspoons of sugar  in the process. If we didn’t bring a fruit, maybe we go out for coffee and pick up an oat bar at Starbucks® (43 gms of carbs) — the equivalent of almost 10 teaspoons of sugar.

At lunchtime, maybe we’ll have a sandwich (30 gm of carbs) or some leftover pasta from the night before (30 gm of carbs) or we’ll go to the food court and have a small stir-fry over rice (30 gm of carbs) — the equivalent of another 6+ teaspoons of sugar

Maybe we eat another piece of fruit mid-afternoon, this time an orange (30 gms of carb) — and we’ve provided our body with the equivalent of another  6+ teaspoons of sugar

In the scenario above, by mid afternoon (assuming we didn’t eat any fast-food or convenience foods, but only eating the food from home) we’ve eaten the equivalence of 24 teaspoons of sugar!

If we go to MacDonald®’s and eat a Big Mac® (20 g of carbs), large fries (66 g of carbs) and a large soft drink (86 g of carbs) – we’ve eaten a total of 172 g of carbs – which is equivalent to 43 teaspoons of sugar in just one meal!

In short, a healthy person will keeps moving the excess carbohydrate they eat off to their liver and will keep making triglyceride and LDL cholesterol out of it and storing the rest as fat and a person who is not insulin resistant or does not have Type 2 Diabetes will have normal blood sugar level, but their high carbohydrate intake can be reflected in their "cholesterol tests" (called a lipid panel) – where we may see high triglyceride results or high LDL cholesterol results or both.

The body takes the triglycerides into very-low-density lipoprotein (VLDL) cholesterol. Think of these as “taxis” that  move cholesterol, triglycerides and other lipids (fats) around the body.

When the VLDL reach fat cells (called “adipose tissue”), the triglyceride is stripped out and absorbed into fat cells. The VLDLs shrink and becomes a new, smaller, lipoprotein, which is called Low Density Lipoprotein, or LDL — the so-called ‘bad cholesterol’. This is a misnomer, because not all LDL is harmful.  LDL which is normally large and fluffy in texture is  a good cholesterol (pattern A) that can become bad cholesterol (pattern B) when it becomes small and dense.

In a healthy person, LDL is not a problem because they find their way back to the liver after having done their job of delivering the TG to cells needing energy. In a person with insulin resistance however ,the LDL linger a little longer than normal, and get smaller and denser, becoming what is known as “small, dense LDL” and these are the ones that put us at a risk for cardiovascular disease.

There are two important points here: (1) the only source of LDL is VLDL not the fat we take in though our diet and (2) only the “small dense LDL are “bad” cholesterol and these occur as a result of insulin resistance.

People often believe that because their blood sugar is ‘normal’ on a lab test, that there isn’t any problem, but as Dr. Joseph Kraft discovered in his 25+ years of research measuring blood glucose and insulin response in some 10,000 people, 75% of people with normal glucose levels are actually insulin resistant and are at different stages of pre-diabetes or “silent Diabetes” (what Dr. Kraft called “Diabetes in situ”).

These people (and maybe their doctors) think they are “fine” because their blood sugar seems normal. Perhaps however, their triglycerides and LDL blood tests come back high. The origin of the problem is not because they are eating too much fat, but too much carbohydrate. Remember above, it is the excess sugar that is shuttled off to the liver, turned into triglycerides (protein linked fat) packaged up into VLDL and delivered around the body.  Once the triglyceride is “off-loaded” to the cells for energy, the VLDL becomes LDL.  The only source of LDL is VLDL.

The body is trying to store the excess sugar somewhere.  First it stores it in glycogen, then the rest is made into triglyceride and LDL and shipped all over the body, with the rest stored as fat.  The fat cells in the body keep filling up — in the muscle, in and around our organs, and some get “fatty liver disease” and some even get fat cells in their bones if their body needs a place to put it.  Bone is not supposed to have fat cells it in, but the body has to store it somewhere, because the carbohydrates just keep arriving every few hours!

Think of it this way;

Imagine you are at home and you hear the doorbell ring. You go to the door and there’s a package and it’s for you.  You take the package, close the door and head to the kitchen table to open it.  Just as you’re about to open it, the door bell rings again.  You go to the door, and there’s another package — and it’s for you, again.  You take the package and head back to the kitchen and set it down beside the first, when (you guessed it) the doorbell rings again. You take that package and the ones that keep arriving, finding places to put them.  When the kitchen table is full, you put the packages on the floor underneath the table, but then you get a delivery of several packages.  You set those down wherever there’s a spot, just in time to answer the door yet again.  Package after package arrives and before you know it, you look like something out of the TV series Hoarders.  You can barely move for all the boxes, and all of them are unopened.

This is what eating meals and snacks with carbohydrates in them every few hours is like.

We overwhelm our body’s tightly-regulated system that is supposed to maintain our blood sugar level between 3.3 and 5.5 mmol/L (60-100 mg/dl) by continually requiring it to process the equivalent of anywhere from 6 teaspoons of sugar in a bowl of cereal or two toasts to the equivalent of 43 teaspoons of sugar in a fast-food meal. 

This is how the system gets “broken”.

In time, we may get Type 2 Diabetes or fatty liver disease or high triglycerides or high cholesterol or group of symptoms called Metabolic Syndrome. This is the result of the constant strain we put our bodies under by eating a steady diet of foods containing a large percentage of  carbohydrate.

It is easy to see where the high rates of obesity and Diabetes have come from. We have become a nation of “hoarders”.

What’s the solution?

We stop the constant delivery of packages of carbohydrate every few hours.

We feed our body the protein and the nutrients it needs with enough fat to use as fuel (in place of carbs) and allow it to take the extra energy it needs from our “stored fat”.  We finally take the fat out of storage and we do this by following a low carb high fat diet.

Science made simple.

Want to know more?

Please send me a note using the “Contact Me” form above and for a complete summary of my services (pdf format), click here.

To our good health!

Joy

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Reference

Michigan State University, How to convert grams of sugars into teaspoons,  http://msue.anr.msu.edu/news/how_to_convert_grams_of_sugars_into_teaspoons

Klöting N, Fasshauer M, Dietrich A et al, Insulin-sensitive obesity, Am J Physiol Endocrinol Metab 299: E506–E515, 2010 – http://www.physiology.org/doi/10.1152/ajpendo.00586.2009

 


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.

PART 1: The Role of Protein in the Diet

What all low carb diets have in common is that they are low in carbohydrates and high in healthy fats, but they vary with respect to the amount of protein and fat. This is part 1 in a new series titled The Role of Protein in the Diet, and outlines the problem with current carbohydrate intake in terms of the recommended dietary requirements.

This article is based largely on a lecture given by Dr. Donald Layman, PhD - Professor Emeritus from the University of Illinois (Nutrition Forum, June 23, 2013, Vancouver, British Columbia, Canada)

Sometimes, when people debate what is, or isn’t a “high protein diet” they define it in terms of the percentage of calories in the diet but this is really meaningless.

For example, someone may be eating only 56 gm of protein  which was 28% of the 800 calories per day they ate and someone else may be eating 160 gm of protein which is 34% of the 2000 calories they are eating per day.

Both are eating ~30% of calories as protein but there is a big difference between 56 gm of protein and 160 gm of protein.

According to Dr. Donald Layman PhD [1], when we speak of a “high protein diet“, we need to discuss the absolute amount of protein in grams, not as a percentage of calories,  because adequacy in determined on the basis of absolute intake.

The Recommended Daily Allowance (RDA) for Protein

The Recommended Daily Allowance (RDA) for any nutrient is the average  daily dietary intake level that is sufficient to meet the requirements of 97 – 98 % of healthy people. This is not the optimum requirement, but the  absolute minimum. The RDA for Protein, Carbohydrate and Fat are as follows;

Protein: 56 g (224 kcals)
Carbohydrate: 130 g* (520 kcals)
Fat: 30 g (270 kcals)

The RDAs for Carbohydrate[2] is set at 130 g / day, but as established in an earlier article, How Much Carbohydrate is Essential in the Diet, we know that even in the absence of dietary carbohydrate (not recommended!), the minimum amount of glucose needed by the brain of 130 g / day can be made from protein and fat,  provided they are eaten in adequate amounts.

The RDA for Protein is set at 56 gm per day, so whether a person is eating 800 calories a day or 2000 calories per day, their body has an absolute requirement for 56 gm of protein per day.

Recommended Daily Allowance (RDA) for Protein [slide from Dr. Donald Layman, PhD – The Evolving Role of Dietary Protein in Adult Health]
The minimum amount of protein (56 g / day) is calculated based on 0.8 g protein per kg of body weight and the maximum amount of protein (~200 g / day) is calculated based on >2.5 g protein per kg of body weight.

This range from 56 g to 200 g of protein per day is referred to as the range of safe intake[2].

According to Dr. Layman, a high protein diet doesn’t start “until well above 170 g / day“.

There are low carb diets that are higher in protein than others, and to distinguish between the two, the one that is higher in fat than protein (in grams) is referred to as a low carb high fat (LCHF) diet and the one that is higher in protein (in grams) is referred to as a low carb high protein (LCHP) diet - but it really isn't "high protein", but higher protein.

Current Dietary Intakes – the problem with carbs

Protein Intake in the US and in Canada is ~70 g of protein per day in women and in men about 90 g of protein per day (~15-16% of calories). Given the range of safe intake of protein from 56 g to 200 g of protein per day, dietary intake of protein in the US and Canada is very low.

The RDAs of macronutrients, which is the minimum amount required per day is just over 1000 calories per day, as follows;

Protein: 56 g (224 kcals)
Carbohydrate: 130 g (520 kcals)
Fat: 30 g (270 kcals)*
         1017 calories*

RDA minimum diet definition [slide from Dr. Donald Layman, PhD – The Evolving Role of Dietary Protein in Adult Health] — *typo corrected above
But what about current intake?

Current Intake of macronutrients is as follows;

Protein: 70 g (280 kcals)
Carbohydrate: 300 g (1200 kcals)
Fat: 90 g (820 kcals)
         2300 calories

***That means there are between 1000 calories and 1300 calories per day of ‘discretionary calories’ – calories above and beyond the minimum requirements of 97-98% of healthy individuals.***

How should we eat to make the most of these calories?

What is going to give us the best health?

Currently, we are eating 3 times the RDA for carbohydrate (300 g carbohydrate per day!) and very close to the minimum for protein. Is this the right balance?

What evidence is there for this being the ‘right balance’?

Eating Well with Canada’s Food Guide, as with the US Dietary Recommendations emphasizes lots of whole grains and high carb intakes and very low protein intake. For a long time in both countries, we’ve highlighted that the issue is fat. But is this correct?

It was thought that since fat has a high caloric density, reducing fat intake would reduce calorie intake and that’s where the US Food Pyramid and Eating Well with Canada’s Food Guide comes from.

Eating Well with Canada’s Food Guide
USDA Food Guide Pyramid

In both cases, the message is ‘stay away from fats‘, ‘stay away from proteins‘, ‘eat lots of cereal grains‘.

So how did that work out for us?

The Food Guide Pyramid first appeared in the US in 1988– exactly when obesity rates exploded.  It tracks back almost to the date…obesity, Diabetes.

This occurred as we started consuming more and more cereal grains and this, according to Dr. Layman “is the origin of the problem”.

Obesity Trends Among US Adults [slide from Dr. Donald Layman, PhD – The Evolving Role of Dietary Protein in Adult Health]
 What about Canada?

Let’s first look at children;

  • In 1978, only 15% of children and adolescents were overweight or obese.
  • By 2007, that rate had doubled to 29% of children and adolescents being overweight or obese.
  • By 2011, obesity prevalence alone for boys was 15.1% and for girls was at 8.0% in 5 to 17 year olds.

What about adults?

  • The prevalence of obesity [body mass index (BMI) ≥30 kg/m2] in Canadian adults increased from 10% in 1970-72 to 26% in 2009-11
  • Based on waist circumference 37% of adults and 13% of youth are abdominally obese.
  • Looking at these numbers slightly differently, as of 2013, there were approximately 7 million obese adults and 600 000 obese school-aged children in Canada.

What exactly changed in the Dietary Guidelines that caused us to  get fat?

For one, Dr. Layman points out, caloric intake was increased by 300 calories per day and according to the Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010 these extra 300 calories per day came from these 6 categories:

  1. grain based desserts and snacks
  2. yeast bread
  3. pasta
  4. pizza
  5. chicken and chicken products
  6. soda and sports drinks

These are all grain-derived products in excess of our caloric needs. See the pattern? The fifth category includes breaded chicken products, such as chicken fingers and chicken nuggets and even soda and sports drinks, sweetened with high fructose corn syrup are grain derived.

All of these grain-derived products are in excess of our caloric needs. This is only part of the problem with current dietary intake of carbohydrates.

In the next article in this series, I’m going to take a look at our current high intake of dietary carbohydrates in terms of the history of man’s diet and the length of time that we’ve had to adapt to eating them.


If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


References

1 – Layman, Donald, The Evolving Role of Dietary Protein in Adult Health, Nutrition Forum, British Columbia, Canada, June 23, 2013 https://youtu.be/4KlLmxPDTuQ

2 – Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005), pg 275

3 – Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010

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 Ideal Protein®?

Recently, there has been a lot of buzz about a weight-loss program called Ideal Protein® which is often talked about as being a “low carb diet” so I decided to look into what this system is, and how it works. A local pharmacy is participating in this program, so I was able to obtain information directly from the pharmacist.

Ideal Protein®, in it’s weight-loss phase (called “Phase 1”) is both low carb and low fat diet – and is most significantly a calorie-restricted diet promoted for weight loss.

Pharmacy-based

“Lifestyle Clinics”,  many of which are located at participating pharmacies are supervised by a pharmacist (or a nurse) who oversees the promotion of the Ideal Protein® line of products required for the diet, as well as the Natura® vitamin and mineral supplements and “Ideal Salt®“, which clients are instructed to use daily.

The designated pharmacist (or nurse) reviews the sign up, but “Ideal Protein® weight loss “coaches” are the ones who review weekly “food journals” that clients are required to keep, as well as records client’s weight, body measurements and fat % readings at their weekly “check-ins”.

Restricted Foods

In addition to limiting both carbs and fats, many foods are not permitted to be eaten by those on the Ideal Protein® diet until clients achieve 100% of their weight-loss goals.

For example, no cheese or dairy is permitted during the weight loss phase, except for 30 ml (1 oz) of regular milk in coffee or tea at breakfast. Natura® supplements are prescribed to clients to ensure adequate intake of calcium and magnesium.

The only vegetables permitted during the weight-loss phase of the Ideal Protein® diet during lunch and dinner are what are called “selected vegetables”  – which exclude green and wax beans, Brussels sprouts, eggplant, heart of palm, rutabaga, snow peas, tomatillo, and tomatoes. These are considered “occasional vegetables” and are allowed to a maximum of 4 cups per week.

*NOTE: I have been advised from a pharmacist that sells these products that these vegetables have “extra carbohydrates” and “slightly higher GI (glycemic index) for the most part“,  which is the reason they are limited.

Glycemic Index (GI) is a measure of the effect of carbohydrates on a person's blood sugar. I am more interested in a food's Insulin Index (II) which is a measure of the effect of a carbohydrate on a person's insulin levels.

Permitted “selected vegetables” are alfalfa, asparagus, bamboo shoots, bean sprouts, bell peppers, broccoli, cabbage, cauliflower, celeriac, celery,  chayote, chicory, collards, cucumbers, dill pickles, fennel, Chinese broccoli, green onions, jicama, kale, kohlrabi, mushrooms, okra, onions (raw only), hot peppers, radish, rhubarb, sauerkraut, spinach, Swiss chard, turnip, and zucchini / yellow summer squash.

Only unlimited “raw vegetables and lettuce” in the list below are permitted during the weight-loss phase (and only during lunch and dinner). These are arugula, bibb lettuce, Boston lettuce, celery, chicory lettuce, cucumber, endives, escarole lettuce, frisée lettuce, green and red leaf lettuce, iceberg lettuce, mushroom, radicchio, radish, romaine lettuce, spinach and watercress lettuce. All others raw vegetables and lettuce are prohibited.

Even in Phase 2, clients are instructed to only “eat the vegetables permitted” and to “continue to omit cheese and other dairy with the exception of 30 ml (1 oz.) of milk in coffee or tea only“.

Ideal Protein® “Meals”

During the weight loss phase (Phase 1), clients are instructed to have meals as follows;

BREAKFAST: 1 Ideal Protein® diet food product, with the option of having coffee or tea with 1 oz. (30 ml) milk, plus Natura® vitamin and mineral supplements.

LUNCH:Ideal Protein® diet food product, with 2 cups of “selected vegetables” and unlimited “raw vegetables and lettuce” from the above list.

DINNER: clients can eat 8 oz (225g) of lean fish / seafood, lean beef, skinless poultry, lean cuts of pork, veal or wild game meat and 2 cups of “selected vegetables” and unlimited “raw vegetables and lettuce” from the above list plus Natura® vitamin and mineral supplements and omega 3 plus.

SNACK: For a snack, clients eat another Ideal Protein® diet food product and more Natura® vitamin and mineral supplements.

In “Phase 2”, which occurs after 100% of weight loss goals have been achieved, the number of Ideal Protein® diet food products required to be consumed is reduced to 2 and clients can eat the protein choice they wish from the approved list at both lunch and dinner, for 2 weeks. The “selected vegetables” and unlimited “raw vegetables and lettuce” remains the same.

In “Phase 3”,  the number of Ideal Protein® diet food products required to be consumed is reduced to 1 and clients can continue to eat the protein choice they wish from the approved list at both lunch and dinner, for 2 weeks. The “selected vegetables” and unlimited “raw vegetables and lettuce” remains the same.

It is only in “Phase 4”, the maintenance phase” of the Ideal Protein® weight loss system where clients are allowed to eat “all whole foods, including protein and fats, and do not need to eat the Ideal Protein®  products”.

Additional Instructions

Clients are instructed to follow the strict carbohydrate and fat restriction until they achieved “100% of their weight loss goals” and to “eat no more / no less” than the amount of food listed for each meal and snack. That is, “Phase 1” last as long as necessary until a person loses all the weight they planned.

They are cautioned that during Phase 1 and possibly beyond that, six symptoms may occur – especially if they “don’t follow the weight loss method as prescribed”. These symptoms are hunger, headache, nausea, fatigue, constipation and bad breath.

Restricted Calories

Ideal Protein® provides only 850-1000 calories per day, which makes it a calorie-restricted diet.

Low Carb

The Ideal Protein meal replacement packets provide ~20 gm net carbs per day and the “selected vegetables” and “raw vegetables and lettuce“provide ~ 20 gm net carbs per day. Total net carbs are ~40 gm / day.

High Protein

In the Ideal Protein® system,   the meal supplements contain ~15-20 gm protein each and 3 of those are to be eaten each day, along with 8 oz of lean animal protein per day. From the ‘meal packets’, there are 60-80 gms of protein and anywhere from 56 gm of protein (lean ground beef) to 72 gms of protein  (chicken breast).  In total, the Ideal Protein system has people eating between 120 gm – 152 gm of protein per day.

According to Statistics Canada (www.statcan.gc.ca/daily-quotidien/170620/dq170620b-eng.htm), the average protein intake for an adult is 16.5% to 17.0%. Based on Ideal Protein® system having a caloric intake of 850-1000 kcals/day, and the 3 meal supplement packets providing 15-20 gm of protein each, plus the 8 oz of lean protein (another 56-72 gms of protein), the Ideal Protein® system supplies 53 – 67.5% of calories as protein. 

Costs

In terms of cost, it is ~ $500 to sign up to begin the Ideal Protein® diet, which includes a ‘coaching fee’, first round of supplements and 2 weeks worth of meal replacement and meal supplement sample products.

After sign up, the cost works out to ~$100 a week to purchase the Ideal Protein® products, plus supplements  i.e. each box of 7 Ideal Protein® “meal replacements” or diet food product (required to be eaten for meals and snacks) costs ~$30 and for weight loss, 3 boxes a week are required.

Each additional month is another ~$400.

Ideal Protein® – the company 

The Ideal Protein® company is headed by Dr. Randall Wilkenson MD, who has 20 years experience specializing in allergy and environmental medicine and who now works with his son Denver Wilkenson, whose experience is in managing a weight-loss clinic in Idaho for 3 years.

Ami-Higbee, RN serves  as Clinic Director and Mike Ciell, RPh, a registered pharmacist certified in geriatric pharmacy, is VP of Clinic Operations.

At the time of writing, no Registered Dietitians are listed on the team, but they do have a ‘chef’ from Quebec who designs their recipes, almost all of which include ingredients from their Ideal Protein® product list.

According to a local pharmacist that I spoke with, Ideal Protein® has over 4000 of these “Lifestyle Clinics” worldwide.


A few thoughts…

This diet is very popular, but it is not a “low carb diet” but is a “low carb, low fat, calorie restricted diet”.

It’s easy because people don’t need to think what to to eat and can buy meal replacement products to satisfy breakfast and the protein component of lunch.  For supper, clients are provided with recipes that use the special branded products that they already purchase to make cooking easy. A snack (deemed necessary, I presume) is another food replacement product. There is limited food preparation required.

The diet system promotes fast weight loss — where both carbohydrates and fats are limited.

Since it is overseen by a pharmacist or a nurse, it has the image of being healthy. But is it “ideal”?

As discussed in an earlier article, our bodies have an absolute requirement for specific essential nutrients; nutrients that we must take in our diet because we can’t synthesize them. These are listed in several volumes called the Dietary Reference Intakes (DRIs), published by National Academies Press. There are essential amino acids, fatty acids, vitamins and minerals – and it is necessary to take in adequate protein and fat, when carbohydrate is restricted.

In the Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005) it reads;

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

… however, Ideal Protein® diet restricts both carbs and fats.

It restricts calories.

It restricts cheese and all dairy except for one ounce of milk per day.

It restricts which non-starchy vegetables can be consumed.

It allows no fruit.

It allows no nuts or seeds.

It offers vitamin and mineral supplements and food replacements in place of those real foods.

In the Ideal Protein® system, people are required to eat 4 times a day with carbs contained in the branded meal supplements on each occasion. Research supports that to begin to lower insulin release in insulin-resistant people requires periods of at least a 12 hour where no food is eaten, which naturally occurs after dinner before the first meal of the day breakfast). Having people eat a ‘snack’ would appear to be self-defeating.

Eating a low carb high healthy fat with 3 meals per day, with nothing between supper and breakfast supports the lowering of insulin release, improving the cells insulin sensitivity, in time.  Adding to this periods of intermittent fasting (which is not a total fast, but has no carbohydrates or significant amounts of protein) allows insulin levels to fall even further, which is often the goal of eating a low carb diet.

In the Ideal Protein® system, the meal supplements contain ~15-20 gm protein each and there are 3 of those per day and there is also 8 oz of lean animal protein per day. From the ‘meal packets’, there are 45-60 gms of protein and anywhere from 56 gm of protein (lean ground beef) to 72 gms of protein (chicken breast). In total, the Ideal Protein®  system supplies between 100 gm – 132 gm of protein per day. While carb intake in the Ideal Protein®  system is low, the body would synthesize glucose from the excess protein (called gluconeogenesis) resulting in insulin release. From my understanding, this appears to be self-defeating if the goal is to lower insulin release.

It would seem that the increased gluconeogenesis from the high protein intake in the Ideal Protein® system would not support increased insulin sensitivity as much as a low-carb-high-fat moderate protein diet, even without intermittent fasting.

Another factor is the $500 start-up cost for the first month, plus another  $400+ for each additional month to eat ‘meals’ comprised of largely of meal replacements and supplements, along with some real food.

Ideal Protein® makes it easy and promotes rapid weight loss, but is it really “ideal” for people who have made poor eating choices in the past — when they don’t learn how to make healthy meal choices while achieving weight loss? Weight loss may be quick, but weight loss also has to be sustainable.

Also, is it really “ideal” for people who are insulin resistant when it has them eating food with carbohydrate and protein 4 times per day?

I encourage my clients to eat a wide variety of real foods – foods such as dairy products including cheese,  domesticated and wild meat, poultry and fish, especially fatty fish that are rich in omega 3 fats, low-carb fruit and a vast array of low-carb vegetables. There are fats from all sources, including some healthy saturated fat, with most fat coming from healthy monounsaturated sources such as olives avocadosnuts and seeds. There are no food diaries to keep and no mandatory “weigh-ins” or “check-ins”.  My clients eat real food when they are hungry and don’t eat if they are not hungry.  Most significantly, they learn to make healthy food choices with whole, real food as they lose weight.

Each person needs to evaluate for themselves whether use of the Ideal Protein® system makes sense for them.

As I always do, I recommend that people consult with their own doctor before beginning any weight-loss program.

To your good health!

Joy

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

 

Note: Everyone's results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.

Copyright ©2017 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.

 

Four Diets over Two Years – long term findings

INTRODUCTION: To date, there have been 3 long-term clinical trials (2 years) published over the past 10 years involving “low carb diets”.

The first long-term study that was presented in the previous article (which can be read here) clearly demonstrated that a low carb non–calorie-restricted diet was both safe and effective and produced the greatest weight loss, lower FBS and HbA1C, the most significantly lower TG and higher HDL and lower C-reactive protein (when compared with a low-fat calorie-restricted diet and a Mediterranean calorie-restricted diet).

In this, the second of the three long term studies, researchers looked at the effectiveness of four dietary interventions with different composition of fat, protein and carbohydrate – including one “low carb” diet..

Did this study demonstrate that a “low carb” diet was safe and effective to result in weight loss?

Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates

Participants

This study involved over 800 overweight and obese subjects, of which 40% were men. Subjects were between the ages of 30 and 70 years and had a Body Mass Index (BMI) of 25-40, where BMI is the weight in kilograms divided by the square of the height in meters.

BMI =25.0-29.9 is considered overweight
BMI = 30.0-34.9 is Class I obesity
BMI = 35.0-39.9 is Class II obesity
BMI ≥ 40.0 is Class III obesity

Major criteria for exclusion from this study were the presence of Diabetes or unstable cardiovascular disease, the use of medications that affect body    weight and insufficient motivation as assessed by interview and questionnaire.

Of the 811 subjects that began the study, at the end of two years, 645 subjects remained enrolled. Approximately 80% of the participants were white, 15% black, 4% Hispanic and the remaining 1% Asian.

The Four Diets – high/low fat, high/low protein

The 811 overweight adults were randomly assigned to one of four diets:

  1. Low Fat, Average Protein: fat: 20%, protein: 15%, carbohydrate: 65% (202 subjects)
  2. Low Fat, High Protein: fat: 20%, protein: 25%, carbohydrate: 55% (202 subjects)
  3. High Fat, Average Protein: fat: 40%, protein: 15%, carbohydrate: 45% (204 subjects)
  4. High Fat, High Protein: fat: 40%, protein: 25%, carbohydrate: 35% (201 subjects)
Two Diets were Low Fat but Two were not High-Fat Diets

The researchers stated that “two diets were low-fat and two were high-fat”, but it is important to note that none of the diets were “low carb high fat”/ ketogenic diets, which are ≥ 65% fat (not 40% fat). Two of the diets were higher in fat than the recommended dietary intake (in both the US and Canada).

Two Diets were Average Protein but not High Protein

The researchers said that “two diets were average protein and two were high protein” and while the ‘average protein intake’ in the US in 2008 was ~15%  (16.1% for men and 15.6% for women), diets such as two of the ones in this study that have only 25% protein are really at the very lowest range of what are considered high-protein diets – which normally contain between  27 – 68 % protein. Also important to note, a “low carb high fat”/ ketogenic diet usually has ~20% protein (considered ‘moderate protein’) and are not high protein diets.

Two Diets were High Carb and One Diet was Moderate Carb

The first and second dietary interventions would both be considered high carb, as they fall within the range of the dietary recommendations in both  Canada and the USA, 45-65% carbohydrate, with one being higher protein and one being average protein.

The third diet would be consider “moderate carb” according to Diabetes Canada’s standards, at 45 % carbohydrate, and higher fat and higher protein.

One Diet was Low Carb but not Ketogenic – and not Low Carb High Fat

The fourth diet could be considered ‘low-carb’ at 35% carbohydrate, but it is not a ketogenic diet, as the percent of carbohydrate is too high. A ketogenic diet has between 5-10% carbohydrate.  It was not a “high fat diet”, as the fat is only 40%, not ≥ 65% fat.

None of the dietary interventions in this study was 'low-carb high fat' or ketogenic, however one diet was "low carb".
Other Study Goals and Information

Other goals for all the dietary interventions were that the diets had;
– 8% or less of saturated fat
20 g or more of dietary fiber
150 mg or less of cholesterol per 1000 kcal

Each participant’s calories represented a deficit of 750 kcal per day
from baseline, as calculated from the person’s resting energy expenditure and activity level (which should have promoted a weight loss of ~ 1.5 pounds per week).

Blinding between the groups was maintained by the use of similar foods in each of the dietary interventions.

Staff as well as participants were taught that each diet adhered to principles of a “healthful diet” and that each had been recommended for “long-term weight loss”.

Group dietary counselling sessions were held once a week, 3 of every 4 weeks during the first 6 months and 2 of every 4 weeks from 6 months to 2 years; individual sessions were held every 8 weeks for the entire 2 years. Behavioral counseling was integrated into the group and individual sessions to promote adherence to the assigned dietary intervention.

Participants were instructed to record their food and beverage intake in a daily food diary and in a web-based self-monitoring tool that provided information on how closely their daily food intake met their dietary intervention’s goals for macronutrients and calories.

The goal for physical activity was 90 minutes of moderate exercise per week. Participation in exercise was monitored by questionnaire and by
the online self-monitoring tool.

Measurements

Body weight and waist circumference were measured in the morning before breakfast on 2 days at baseline, 6 months, and 2 years, and on a single
day at 12 and 18 months.

Levels of serum lipids, glucose, insulin, and glycated hemoglobin (HbA1C) were measured via fasting blood samples, and 24-hour urine samples, and measurement of resting metabolic rate were obtained on 1 day, and blood-pressure measurement on 2 days, at baseline, 6 months and 2 years.

Results

Weight loss and Waist Circumference

The amount of weight loss after 2 years was similar in participants assigned to a diet with 25% protein and those assigned to a diet with 15% protein.

Weight loss was the same in those assigned to a diet with 40% fat and those assigned to a diet with 20% fat.

There was no effect on weight loss of carbohydrate level through the target range of 35 to 65%.

Most of the weight loss occurred in the first 6 months, however 23% of the participants continued to lose weight from 6 months to 2 years.

The change in waist circumference did not differ significantly among the diet groups.

At 2 years, 31 to 37% of the participants had lost at least 5% of their initial body weight, 14 to 15% of the participants in each diet group had lost at least 10% of their initial weight, and 2 to 4% had lost 20 kg or more.

Risk Factors for Cardiovascular Disease and Diabetes

All the diets reduced risk factors for cardiovascular disease and Diabetes at 6 months and 2 years.

At 2 years, the two low-fat diets and the highest-carbohydrate diet decreased low-density lipoprotein (LDL) cholesterol levels more than did the high-fat diets or the lowest-carbohydrate diet, 5% vs 1%. And at 2 years, the highest carbohydrate decreased LDL more (6%) versus the lowest carbohydrate diet (1%).

The lowest-carbohydrate diet increased HDL cholesterol levels more (9%) compared with the highest-carbohydrate diet (6%).

All the diets decreased triglyceride (TG) levels similarly, by 12 to 17%.

All the diets except the one with the highest carbohydrate content decreased fasting serum insulin levels by 6 to 12% – and the decrease was larger with
the high-protein diet than with the average-protein diet (10% vs. 4%).

Blood pressure decreased from baseline by 1 to 2 mm Hg, with no significant differences among the groups.

The metabolic syndrome (defined as elevated fasting blood glucose, elevated blood pressure and abnormal triglycerides or cholesterol levels) was present in 32% of the participants at baseline, and the percentage at 2 years ranged from 19 to 22% in the four diet groups.

Diet Adherence

Mean reported intakes at 6 months and at 2 years were not at the target levels for macronutrients (fat, protein and carbohydrate). This limits the applicability of the data.

In the Low Fat, Average Protein group (fat: 20%, protein: 15%, carbohydrate: 65%), carbohydrate intake decreased from baseline by 12.8% and by 9.3% from baseline at 2 years and fat intake decreased from baseline by 11.8% at 6 months and 12.0% at two years. As it should have, protein intake hardly changed at 6 months (0.2%) but by 2 years it had increased by 2.1% to 19.6%.

In the Low Fat, High Protein group (fat: 20%, protein: 25%, carbohydrate: 55%) at 6 months carbohydrate intake decreased from baseline by 7.4% and at 2 years, it decreased from baseline by 6.8%. Protein intake increased from baseline by 3.9% at 2 years it had increased by 2.5% – but it is important to note that such a modest increase meant that this group did not consume a diet of 25% protein (but slightly less than 19% at 6 months and 17.5% at 2 years). Fat intake decreased from baseline by 11.8% at 6 months and 12.0% at two years.

In the High Fat, Average Protein group (fat: 40%, protein: 15% carbohydrate: 45%), at 6 months carbohydrate intake  decreased from baseline by 5.0% and at 2 years, it decreased from baseline by 2.4%. Protein intake hardly increased from baseline at 6 months (0.5%), but at 2 years it had increased from baseline by 2.1%. Fat intake in this group was supposed to have increased, but actually decreased from baseline by 3.8% at 6 months and decreased from baseline by 2.1% at two years.

In the High Fat, High Protein group (fat: 40%, protein: 25%, carbohydrate: 35%) – which was the only intervention that was “low carb”, at 6 months carbohydrate intake only decreased from baseline by 0.2% and at 2 years, it decreased from baseline by 0.4%. In fact, carbohydrate remained at ~ 43% the entire time. Protein intake was supposed to increase substantially, but only increased from baseline by 4.3%, and at 2 years it had had only increased from baseline by 3.4%. It is important to note that such a modest increase in protein meant that this group did not consume a diet of 25% protein but ~19.3 % at 6 months and ~18.4% at 2 years. Fat intake in this group was supposed to have increased, but actually decreased from baseline by 3.7% at 6 months and decreased from baseline by 3.4% at two years.

Neither of the "high protein" groups achieved anywhere near 25% of daily calories as protein.

Despite the intensive behavioral counseling in this study, participants did not achieve the goals for macronutrient intake of their assigned group and while some data in this study is helpful, the one group that was supposed to be “low carb” (high fat, high protein) was none of those!

Researcher’s Conclusion

The researchers concluded;

“we did not confirm previous findings that low-carbohydrate or high protein diets caused increased weight loss at 6 months”

High Protein Diet “Fail”

The reason that this study failed to confirm whether a high protein diet causes increased weight loss at 6 months is because neither of the two “high protein” diet groups in this study ate anywhere near the target protein level of 25%, but rather ate between 17.5%-19% protein,  which is remarkably close to the average protein intake of 15%  (16.1% for men and 15.6% for women). Subjects also ate no where near the lower limits of a “high protein” diet, which is 27-68% of daily calories as protein.

Low Carbohydrate Diet “Fail”

The reason that this study failed to confirm that a low carbohydrate diet causes increased weight loss is because the one group of the four diet interventions that was supposed to eat what the researchers defined as “low carb” (35% of calories as carbohydrate) ate ~43% of calories as carbohydrate the entire duration of the study. This as a moderate carb diet, not a low carb diet.

Final Thoughts

In this long term study, researchers set out to look at the effectiveness of four dietary interventions including a “low carb” diet group, however poor study design failed to produce even one of the four groups that ate low carb.


If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

Sacks FM, Bray GA, Carey VJ et al, Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates, N Engl J Med. 2009 Feb 26;360(9):859-73

Why I am the Low Carb High Fat Dietitian

This article provides the references for the text which appears on the front of my webpage.A low carb diet isn't new. In fact this was the standard recommendation prior to the discovery of insulin.

Several years ago, I began to ask myself how it is that 2/3 of men and ~1/2 of women in Canada are either overweight or obese. In the early 1970s, only ~8% of men and ~12% of women were obese and now almost 22% of men and 19% of women are obese- even though statistics show we are eating much less fat, drinking way less pop and eating more fish than ever before. I wondered if the increase in overweight and obesity might be related to the changes in the Dietary Recommendations that began in 1977 and which encourage us to eat 45-65% of daily calories as carbohydrate and to limit all kinds of fat to 20-35%.

In early 2015, after scouring the scientific literature and reading about the clinical use of a Low Carb High Fat (LCHF) diet, I came to the understanding that those who are insulin resistant or have Type 2 Diabetes or have other indicators that they are not tolerating large amounts of carbohydrate well could improve their symptoms significantly by following a lower carb style of eating, with the oversight of their doctors.  Such an adjustment in lifestyle seemed like a small price to pay for the potential of significantly improving – and in some cases reversing symptoms of these conditions, especially when compared with the reality that at best these symptoms will stay the same and very likely will get worse over time.

Many scientific studies as well as physician’s clinical experience indicate that a lower carb style of eating combined with extending the time between meals lowers insulin resistance (which is the underlying cause of high blood sugar). When insulin levels are lowered, blood pressure comes down and triglycerides and some other lipid ratios normalize.

Physicians across Canada, the US, the UK and Australia that prescribe a LCHF Diet to their patients have found that they experience a significant improvement in the symptoms of insulin resistance, Type 2 Diabetes, high blood pressure, high triglycerides and that a natural reversal of many symptoms is possible. Such improvements often enable these doctors to reduce- and sometimes discontinue medications that were previously prescribed to their patients for these conditions. While the American Diabetes Association enables Type 2 Diabetics to choose to follow either  moderate low carb diet (130g carbohydrate) or a low fat calorie restricted diet for up to a year for weight loss, as of yet this approach is not approved by Diabetes Canada.

A low carb diet isn’t new. In fact this was the standard recommendation prior to the discovery of insulin.

It seems to me that a lower carbohydrate intake resulting in improved symptoms and lab results as overseen by one’s own doctor is preferable to living with chronic disease symptoms and taking increasing numbers of medications in an effort to manage symptoms, but each person needs to evaluate the alternative and make their own choice.

For those who want to aim to improve or reverse the symptoms of these chronic diseases, I offer services as the LCHF-Dietitian. 


If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.


you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

1942-2015 Canada Food Guides: https://www.canada.ca/en/health-canada/services/food-nutrition/canada-food-guide/background-food-guide/canada-food-guides-1942-1992.html

Canadian Medical Association Journal, Early Releases (May 11, 2015), Food Guide Under Fire at Obesity Summit:  www.cmaj.ca/site/earlyreleases/11may15_food-guide-under-fire-at-obesity-summit.xhtml

2015 Acceptable Macronutrient Distribution Ranges:  https://www.canada.ca/en/health-canada/services/food-nutrition/reports-publications/eating-well-canada-food-guide-resource-educators-communicators-2007.html#a9

1970-1972 Obesity Rates:  https://lop.parl.ca/content/lop/ResearchPublications/prb0511-e.htm

2014 Obesity Rates, Statistic Canada – Overweight and obese adults (self-reported), 2014 http://www.statcan.gc.ca/pub/82-625-x/2015001/article/14185-eng.htm

Janssen I, The Public Health Burden of Obesity in Canada, Canadian Journal of Diabetes, 37 (2013), pg. 90-96

from the Public Health Collaborative, Summary Table of Randomized-Controlled Trials Comparing Low Carb to Low-Fat Diets – https://phcuk.org/:

[1] A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on
Body Weight and Cardiovascular Risk Factors in Healthy Women. Brehm et al.
http://press.endocrine.org/doi/full/10.1210/jc.2002-021480

[2] A Randomized Trial of a Low-Carbohydrate Diet for Obesity. Foster et al.
http://www.nejm.org/doi/full/10.1056/NEJMoa022207

[3] A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. Samaha et al.
http://www.nejm.org/doi/full/10.1056/NEJMoa022637

[4] Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.
Sondike et al. http://www.sciencedirect.com/science/article/pii/S0022347602402065

[5] The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein
and Monounsaturated Fat A Randomized Trial. Aude et al. http://archinte.jamanetwork.com/article.aspx?
articleid=217514

[6] A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia: A
Randomized, Controlled Trial. Yancy et al. http://annals.org/article.aspx?articleid=717451

[7] Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body
composition in overweight men and women. Volek et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC538279/

[8] Comparison of a Low-Fat Diet to a Low-Carbohydrate Diet on Weight Loss, Body Composition, and Risk
Factors for Diabetes and Cardiovascular Disease in Free-Living, Overweight Men and Women. Meckling et
al. http://press.endocrine.org/doi/full/10.1210/jc.2003-031606

[9] Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a highfat,
low-carbohydrate diet. Hernandez et al. http://ajcn.nutrition.org/content/91/3/578.long

[10] Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women
Consuming a Low-Carbohydrate/High-Protein vs High-Carbohydrate/Low-Fat Diet. Nickols-Richardson et al.
http://www.sciencedirect.com/science/article/pii/S000282230501151X/

[11] Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes—a randomized
controlled trial. Daly et al. http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract

[12] Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Krauss et
al. http://ajcn.nutrition.org/content/83/5/1025.full

[13] Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk
Factors Among Overweight Premenopausal Women The A TO Z Weight Loss Study: A Randomized Trial.
Gardner et al. http://jama.jamanetwork.com/article.aspx?articleid=205916

[14] Low- and high-carbohydrate weight-loss diets have similar effects on mood but not cognitive
performance. Halyburton et al. http://ajcn.nutrition.org/content/86/3/580.long

[15] A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic
and non-diabetic subjects. Dyson et al. http://onlinelibrary.wiley.com/doi/10.1111/j.1464-
5491.2007.02290.x/full

[16] The effect of a low-carbohydrate, ketogenic diet versus a low-glycemic index diet on glycemic control in
type 2 diabetes mellitus. Westman et al. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2633336/

[17] Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet. Shai et al.
http://www.nejm.org/doi/full/10.1056/NEJMoa0708681

[18] Effects of weight loss from a very-low-carbohydrate diet on endothelial function and markers of
cardiovascular disease risk in subjects with abdominal obesity. Keogh et al.
http://ajcn.nutrition.org/content/87/3/567.long
www.PublicHealthCollaboration.org

[19] Metabolic Effects of Weight Loss on a Very-Low-Carbohydrate Diet Compared With an Isocaloric HighCarbohydrate
Diet in Abdominally Obese Subjects. Tay et al.
http://www.sciencedirect.com/science/article/pii/S0735109707032597

[20] Carbohydrate Restriction has a More Favorable Impact on the Metabolic Syndrome than a Low Fat Diet.
Volek et al. http://link.springer.com/article/10.1007/s11745-008-3274-2

[21] Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet
after 12 mo. Brinkworth et al. http://ajcn.nutrition.org/content/90/1/23.long

[22] Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese
Adolescents. Krebs et al. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892194/

[23] In type 2 diabetes, randomisation to advice to follow a low-carbohydrate diet transiently improves
glycaemic control compared with advice to follow a low-fat diet producing a similar weight loss. Guldbrand et
al. http://link.springer.com/article/10.1007/s00125-012-2567-4/fulltext.html

[24] A Randomized Pilot Trial of a Moderate Carbohydrate Diet Compared to a Very Low Carbohydrate Diet
in Overweight or Obese Individuals with Type 2 Diabetes Mellitus or Prediabetes. Saslow et al.
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0091027

[25] Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial. Bazzano et al.
http://annals.org/article.aspx?articleid=1900694

[26] The Role of Energy Expenditure in the Differential Weight Loss in Obese Women on Low-Fat and Low Carbohydrate
Diets. Brehm et al. http://press.endocrine.org/doi/full/10.1210/jc.2004-1540

[27] Effects of a Low Carbohydrate Weight Loss Diet on Exercise Capacity and Tolerance in Obese Subjects.
Brinkworth et al. http://onlinelibrary.wiley.com/doi/10.1038/oby.2009.134/full

[28] Comparative Study of the Effects of a 1-Year Dietary Intervention of a Low-Carbohydrate Diet Versus a
Low-Fat Diet on Weight and Glycemic Control in Type 2 Diabetes. Davis et al.
http://care.diabetesjournals.org/content/32/7/1147

[29] Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet: A
Randomized Trial. Foster et al. http://annals.org/article.aspx?articleid=745937

[30] Effects of a Low-intensity Intervention That Prescribed a Low-carbohydrate vs. a Low-fat Diet in Obese,
Diabetic Participants. Iqbal et al. http://onlinelibrary.wiley.com/doi/10.1038/oby.2009.460/full

[31] Consuming a hypocaloric high fat low carbohydrate diet for 12 weeks lowers C-reactive protein, and
raises serum adiponectin and high density lipoprotein-cholesterol in obese subjects. Ruth et al.
http://www.metabolismjournal.com/article/S0026-0495(13)00223-0/abstract

[32] Comparison of isocaloric very low carbohydrate/high saturated fat and high carbohydrate/low saturated
fat diets on body composition and cardiovascular risk. Noakes et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1368980/

[33] Long-term Effects of a Very Low-Carbohydrate Diet and a Low-Fat Diet on Mood and Cognitive
Function. Brinkworth et al. http://archinte.jamanetwork.com/article.aspx?articleid=1108558

[34] The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year
follow-up of a randomized trial. Stern et al. http://www.ncbi.nlm.nih.gov/pubmed/15148064

[35] A Randomized Trial of a Low-Carbohydrate Diet vs Orlistat Plus a Low-Fat Diet for Weight Loss. Yancy
et al. 2010. http://www.ncbi.nlm.nih.gov/pubmed/20101008

[36] A randomized controlled trial of low carbohydrate and low fat/high fiber diets for weight loss. Baron et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1646726/

[37] A very low-carbohydrate, low-saturated fat diet for type 2 diabetes management: a randomized trial. Tay
et al. http://www.ncbi.nlm.nih.gov/pubmed/25071075

[38] Randomised controlled trial of four commercial weight loss programmes in the UK: initial findings from
the BBC “diet trials”. Truby et al. http://www.bmj.com/content/332/7553/1309
www.PublicHealthCollaboration.org

[39] Comparison of the Atkins, Ornish, Weight Watchers, and Zone Diets for Weight Loss and Heart Disease
Risk Reduction:A Randomized Trial. Dansinger et al. http://jama.jamanetwork.com/article.aspx?
articleid=200094

[40] Very Low-Carbohydrate and Low-Fat Diets Affect Fasting Lipids and Postprandial Lipemia Differently in
Overweight Men. Sharman et al. http://jn.nutrition.org/content/134/4/880.long

[41] Comparison of high-fat and high-protein diets with a high-carbohydrate diet in insulin-resistant obese
women. McAuley et al. http://link.springer.com/article/10.1007/s00125-004-1603-4/fulltext.html

[42] Diet-Induced Weight Loss Is Associated with Decreases in Plasma Serum Amyloid A and C-Reactive
Protein Independent of Dietary Macronutrient Composition in Obese Subjects. O’Brien et al.
http://press.endocrine.org/doi/10.1210/jc.2004-1011

[43] Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2
diabetes compared with advice to follow a low-fat diet. Jonasson et al.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4025600/

[44] A non-calorie-restricted low-carbohydrate diet is effective as an alternative therapy for patients with type
2 diabetes. Yamada et al. http://www.ncbi.nlm.nih.gov/pubmed/24390522

[45] Low-Fat Versus Low-Carbohydrate Weight Reduction Diets Effects on Weight Loss, Insulin Resistance,
and Cardiovascular Risk: A Randomized Control Trial. Bradley et al.
http://diabetes.diabetesjournals.org/content/58/12/2741.long

[46] Weight loss with high and low carbohydrate 1200 kcal diets in free living women. Lean et al.
http://www.nature.com/ejcn/journal/v51/n4/abs/1600391a.html

[47] Evaluation of weight loss and adipocytokines levels after two hypocaloric diets with different
macronutrient distribution in obese subjects with rs9939609 gene variant. De Luis et al.
http://onlinelibrary.wiley.com/doi/10.1002/dmrr.2323/abstract

[48] Enhanced weight loss with protein-enriched meal replacements in subjects with the metabolic syndrome.
Flechtner-Mors et al. http://onlinelibrary.wiley.com/doi/10.1002/dmrr.1097/abstract

[49] Long-term effects of a low carbohydrate, low fat or high unsaturated fat diet compared to a nointervention
control. Lim et al. http://www.nmcd-journal.com/article/S0939-4753(09)00124-0/abstract

[50] A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on
lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. Seshadri et al.
http://www.amjmed.com/article/S0002-9343(04)00344-4/abstract

[51] Comparison of low- and high-carbohydrate diets for type 2 diabetes management: a randomized trial.
Tay et al. http://ajcn.nutrition.org/content/early/2015/07/29/ajcn.115.112581.abstract

[52] Weight loss on low-fat vs. low-carbohydrate diets by insulin resistance status among overweight adults
and adults with obesity: A randomized pilot trial. Gardner et al.
http://onlinelibrary.wiley.com/doi/10.1002/oby.21331/abstract

[53] Metabolic impact of a ketogenic diet compared to a hypocaloric diet in obese children and adolescents.
Partsalaki et al. http://www.ncbi.nlm.nih.gov/pubmed/23155696

[54] A randomized controlled trial of 130 g/day low-carbohydrate diet in type 2 diabetes with poor glycemic
control. Sato et al. http://www.clinicalnutritionjournal.com/article/S0261-5614(16)30169-8/pdf

[55] Short-term safety, tolerability and efficacy of a very low-calorie-ketogenic diet interventional weight loss
program versus hypocaloric diet in patients with type 2 diabetes mellitus. Goday et al.
http://www.nature.com/nutd/journal/v6/n9/full/nutd201636a.html

[56] Visceral adiposity and metabolic syndrome after very high–fat and low-fat isocaloric diets: a randomized
controlled trial. Veum et al. http://ajcn.nutrition.org/content/early/2016/11/30/ajcn.115.123463.abstract

[57] An Online Intervention Comparing a Very Low-Carbohydrate Ketogenic Diet and Lifestyle
Recommendations Versus a Plate Method Diet in Overweight Individuals With Type 2 Diabetes: A
Randomized Controlled Trial. Saslow et al. https://www.ncbi.nlm.nih.gov/pubmed/28193599

Caffeine Substantially Increases Plasma Ketones in Healthy Adults

INTRODUCTION: This recent Canadian study reports that the caffeine contained in 1  1/2 to 3 cups of unsweetened coffee is sufficient to increase plasma levels of ketones, including β-hydroxybuterate, for several hours.


A pilot Canadian study conducted at the Université de Sherbrooke in Sherbrooke, Quebec and published in the Canadian Journal of Physiology and Pharmacology on November 25, 2016 evaluated the effect of caffeine on the production of ketones in healthy adults. Researchers were interested in caffeine as a ketogenic agent based on its ability to increase lypolysis (the breaking down of fat for fuel).

Method of the Study

Two different doses of caffeine were administered to 10 healthy adults who had fasted for 12 hours and who then ate a breakfast that containing 85 gm carbohydrate, 9.5 gm fat and 14 gm of protein.

Subjects were either given;

(1) no caffeine

(2) a cup and a half of regular drip coffee

(3) three cups of regular drip coffee 

The subjects plasma caffeine levels were measured over the next 4 hours and it was found that those that drank 1  1/2 cups of coffee had~ 2.5 mg caffeine per kilogram of body weight and those that drank 3 cups of coffee had ~ 5.0 mg caffeine per kilogram of body weight. 

Plasma caffeine over time

Results – the effect of caffeine on ketone production

Subjects that had 1  1/2 cups of coffee (2.5 mg of caffeine per kilogram)  had 88% higher ketone production than subjects that had no caffeine.

Subjects that drank 3 cups of coffee (5.0 mg caffeine per kilogram of body weight) had 116% higher ketone production over subjects that had no caffeine. 

β-hydroxybuterate per hour

Expressed as the amount of βhydroxybuterate in μmol/L, it is evident that this ketone rises significantly in response to caffeine, and rises in a dose-dependent manner. That is, the more caffeine consumed the more βhydroxybuterate was produced.

Amount of β-hydroxybuterate produced in response to caffeine dose

Researchers reported that the level of ketones found in the blood after 3 cups of coffee was approximately twice that produced after an overnight fast.

This increase in plasma ketones obtained with these doses of caffeine could, at least in the short term (a few hours) contribute to ~5-6% of brain energy needs.

Mechanism

The increase in free fatty acids as well as β-hydroxybuterate is explained by caffeine blocking phosphodiesterase (PDE), preventing the inactivation of cyclic adenosine monophosphate (cAMP) – with increased caffeine leading to higher levels of cAMP.

Cyclic adenosine monophosphate (cAMP) is a cellular messenger that is involved with transferring hormones such as glucogon, which is the main catabolic hormone of the body and which functions to raise both the concentration of glucose and fat in the bloodstream and has the opposite effect of insulin).

Glucagon needs cAMP in order to pass through the plasma membrane, so as a result cAMP serves to regulate glucose, fats and glycogen.

cAMP activates hormone sensitive lipase, an enzyme which breaks down fat (lypolysis). This increased breaking down of fat, increases free fatty acids (FFAs), which can then be converted in the liver to the ketones acetoacetate and β-hydroxybuterate.

Final Thoughts…

While this is a small study, the data supports that a few cups of regular, unsweetened coffee (without any butter or coconut oil added) increases the amount of ketones produced for several hours.

If you are following a low carb diet and are monitoring your blood or urine ketones, be aware that having coffee can increase the amount of ketones your body is producing.


If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

Vandenberghe C, St-Pierre V, Courchesne-Loye A, et al, Caffeine intake increases plasma ketones: an acute metabolic study in humans, Canadian Journal of Physiology and Pharmacology, 2017, Vol. 95, No. 4 : pp. 455-458 
Dr. David Perlmutter, MD (www.drperlmutter.com/caffeine-ketosis-friend-or-foe)

Note: Everyone's results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.

Copyright ©2017 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 the Anti-Inflammatory Protocol and what is it used for?

Changing how and what we eat, as well as managing stress and getting enough restful sleep has been shown in research studies to reduce pain and symptoms in people with chronic inflammatory diseases such as Rheumatoid Arthritis, Fibromyalgia, Hashimoto’s Hypothyroidism, Celiac disease, etc.. As well, there is increasing evidence that cardiovascular disease, including heart attack and stroke are inflammatory in nature and that lowering risk is best managed through dietary and lifestyle changes. For those with a strong family history of heart disease, the Anti-Inflammatory Protocol dove-tails perfectly with a low-carb high healthy fat diet.


Knowing which foods promote inflammation and why and which foods are evidence-based to have anti-inflammatory properties  and why is essential for those seeking to reduce pain and symptoms associated with a chronic inflammatory condition. Choosing foods that are nutrient densepromote gut healthaddress diet-related disruptions in hormone-regulation and that target immune system regulation are key in the Anti-Inflammatory Protocol.

Nutrient density – Every system in the body, including the immune system requires an array of vitamins, minerals, antioxidants, essential fatty acids, and amino acids to function normally. Micronutrient deficiencies and imbalances are considered key players in the development and progression of autoimmune disease, therefor attention is put on consuming the most nutrient-dense foods available. A nutrient-dense diet provides the ‘building blocks’ that the body needs to heal damaged tissues. The goal is to supply the body with a surplus of micronutrients to correct both deficiencies and imbalances, supporting regulation of the immune system, hormone and neurotransmitter production.

Gut health – It is thought that ‘gut dysbiosis’ (gut microbial imbalance) and ‘leaky gut’ may be key facilitators in the development of autoimmune disease. The foods recommended on the Anti-inflammatory Protocol support the growth of healthy levels and a healthy variety of gut microorganisms. Foods that irritate or damage the lining of the gut are avoided, while foods that help restore gut barrier function and promote healing are encouraged.

Diet-related Disruptions in hormone regulation – What we eat, when we eat, and how much we eat affects a variety of hormones that interact with the immune system. Eating foods with too much sugar or ‘grazing’ throughout the day, rather than eating food at set meals spaced apart deregulate these hormones. As a result, the immune system is typically stimulated. Promoting regulation of these hormones through diet, in turn has a modulating effect on the immune system. As well, dietary hormones that impact the immune system are also profoundly affected by how much sleep we get, how much and what kinds of activity we do, and how well we reduce and manage stress, so looking at diet and lifestyle together, is key.

Immune system regulation – Our intestines are home to millions of bacteria which live in symbiotic relationship with us.  We provide food for them and when in balance, they maintain the integrity of the gut wall, which serves as a protective barrier. When our gut ‘flora’ gets out of balance, having an excess of pathogenic bacteria, this protective barrier becomes compromised, resulting in small ‘holes’ that permit exchange between the inside of our gut and the blood stream.  This is what is called “leaky gut“. Endotoxins produced by the proliferation of “bad” bacteria can get into the blood stream, stimulating the immune system, and resulting in systemic inflammation. What becomes critical is to limit the factors that contribute to excess of the “bad bacteria” and restore a healthy amount and diversity of “good” gut microorganisms, so that the gut once again functions as a protective barrier, and immune system regulation is achieved.

What is the Anti-Inflammatory Protocol?

The Anti-Inflammatory Protocol identifies foods that promote inflammation from those that research indicates have anti-inflammatory properties. It isn’t simply a list of “eat this” and “don’t eat that”, but explains what about a particular food promotes inflammation or inhibits it. It explains the role of key inflammatory -producing compounds such as lectinssaponins and protease inhibitors, and which foods they are found in, and how eating those foods contribute to “leaky gut“. Which grains can one eat?  Which should be avoided? What about beans and lentils? Are there some better than others?

The Anti-Inflammatory Protocol explains which healthy cooking and eating fats won’t contribute to the production of Advanced Glycation End-Products (AGEs) – and how this compound causes oxidative damage to the cells in the body. Knowing this enables people to know whether oils such as grapeseed for example, are a good choice and if not, why – as well as which other oils would be preferable.

I want people to understand in simple terms how omega 6 (ω-6) fats compete for binding sites and elongation enzymes with omega 3 (ω-3) fats, as this enables them to determine whether foods such as nuts and seeds should be included in an anti-inflammatory diet. If they understand the role of hormones such as insulin and what causes it’s release, they can determine for themselves whether products like agave syrup or coconut sugar are preferable to table sugar when following an anti-inflammatory protocol. I find that once people understand the theory as to why they should eat less of certain foods (explained in ways that don’t require an educational background in science!) and they also understand which types of foods they should aim to eat more of, they are empowered to make dietary choices that contribute to reducing inflammation, as well as symptoms, along with risk factors for other inflammation-related conditions.

I consider my primary role is as an educator. I don’t want to tell someone they need to eat this food on this day and this other food on the next day.  It is far more rewarding and helpful to them, if I help them know how to make these decisions themselves.

Want to know more? Why not send me a note using the “Contact Us” form above.

To our good health,

Joy

 

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Note: Everyone's results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.

Copyright ©2017 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.

Insulin and Leptin – very different effects in lean versus overweight people

The hormone insulin (involved in storing fat) and leptin (involved in burning fat) work very differently in lean people than in overweight people. This is why excess fat such as is found in “bullet proof coffee” or “fat bombs” results in overweight (or obese) people that follow a Low Carb High Fat diet gaining weight—whereas lean people will simply burn it off. This article explains the role of these hormones and how they impact lean people and overweight people very differently.

When we eat, the hormone insulin is released which signals our body to do two things; (1) it tells our cells to uptake energy (in the form of glucose) and (2) to store excess energy as fat. Insulin is the major driver of weight gain. If we are lean, when we eat more than usual and increase our body fat stores, the body responds by increasing secretion of a hormone called leptin.  Leptin acts as a negative feedback loop on the hypothalamus area of our brain, reducing our hunger, causing us to eat less and preventing us from gaining too much fat.

The problem occurs when we become insulin resistant.

Insulin Resistance

When we eat a diet that is high in carbs and we eat every few hours (3 meals plus snacks), insulin is released each time we eat (in order to cause our cells to take in energy and store the excess as fat). If we continue to eat this way, over time our body is inundated with insulin, so it sends signals to down-regulate the insulin receptors, making our cells less sensitive to insulin signals. This is called insulin resistance. When we are insulin resistant, our body releases more and more insulin to deal with the same amount of glucose in the blood.

Leptin Resistance

Consistently having high levels of insulin, will also keep stimulating the release of leptin, which normally results in us becoming less hungry and eating less. However, when we are insulin resistantwe keep producing more and more insulin, which results in us producing more and more leptin. Over time, this consistently high leptin level will result in the same type of down-regulation of hormonal receptors that occurred with insulin, resulting in leptin resistance.

Leptin resistance interferes with the negative feed back loop on our hypothalamus which normally reduces our hunger, causing us to eat less. When we are leptin resistance, even when we’ve eaten a great deal of food, we don’t feel satiated — even when our abdomens are straining from feeling full. As a result, we just keep eating, as if there is no “off” switch.

It is this leptin resistance that results in obesity. 

Obese people aren’t obese because they lack will-power, but because their body is responding to signals from very powerful hormones produced in response to the types of foods they eat.

Difference between a High Carb Diet and a High Fat Diet

When people consume diets high in carbs it stimulates insulin to be released. In response to all the insulin, energy that is not immediately needed for activity is stored as glycogen in the liver and muscle cells, and the remainder is shipped off to our adipose cells (fat cells), to be stored as fat. When eating a high carb diet, getting excess calories into fat cells is easy, getting the fat out of fat cells, not so much.

When people eat a diet high in fat and low in carbs, the fat is absorbed in the intestines as chylomicrons and is shuttled through the lymphatic system to the thoracic duct, going directly into the blood circulation. From there, the fat is either burned for energy or goes into our fat cells, to be stored. It is important to note that the fat does NOT go to the portal circulation of the liver and as a result, fat needs no help from insulin to be absorbed

That’s good, but if excess fat gets stored in fat cells, doesn’t eating fat make one fat?

Not for lean people, because lean people are leptin sensitive and obese people are leptin resistant. When overweight or obese people eat excess fat, it is a different matter.

Lean People versus Obese People

If a lean person eats a diet high in fat and low in carbs, the excess fat will be stored in fat cells, but insulin does not go up. So a lean person does not become insulin resistant, as described above.  As their fat mass goes up, leptin also goes up. Since the lean person is sensitive to leptin, the negative feedback loop acts on the brain causing them to stop eating, allowing their body weight to go back down. Even if a lean person deliberately eats more and more fat when they aren’t hungry, what happens is their body’s metabolism goes up, and they burn off the extra calories.

If an overweight or obese person eats a diet high in fat and low in carbs with moderate amounts of protein, insulin levels don’t go up — which is good of course, however from years of eating high carb low fat diets and from eating a carb rich foods every few hours, overweight and obese people are insulin resistant. This means that their blood glucose levels remain high for long periods after they’ve eaten and as importantly, it also means that they are also leptin resistant. In this case, if they eat too much fat – such as drinking “bullet-proof coffee” or having “fat bombs”, they will respond (as the lean person does) by making more leptin, but the problem is, they are not sensitive to leptin! Their brain doesn’t respond to the signals from leptin, so when an obese or overweight person eats excess fat, beyond that which is naturally found in a low carb high fat foods, their appetite doesn’t drop – nor does their metabolism go up to burn off the excess fat being stored in fat cells. They simply get fatter.

Weight Loss

For those that are overweight or obese and insulin resistant, it is important to keep in mind that with insulin resistance comes leptin resistance. Leptin resistance by definition means that the signals to stop eating don’t work.  The “off switch” is defective.  As well, the body doesn’t respond to signals from leptin to up-regulate metabolism, so when an overweight or obese person on a low carb diet eats too much fat, they gain weight.

Since increasing carbs is not an option and increasing protein results in glucose being synthesized from the excess (gluconeogenesis), the way to lower insulin resistance (and thus leptin resistance) is by extending the amount of time between meals.  This is known as intermittent fasting – a topic that will be covered in a future article.

Have questions?  

Want to know how I can help you get started on a low carb high healthy fat diet?  Please drop me a note using the “Contact Us” form, located on the tab above.

To our good health!

Joy

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2017 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 regular monitoring by a Registered Dietitian and with the knowledge of 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 something you have read in our content. 


References

Ebbeling CB, Swain JF, Feldman HA, et al. Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study. JAMA : The journal of the American Medical Association. 2012;307(24):2627-2634. doi:10.1001/jama.2012.6607.

Feinman RD, Fine EJ (2003) Thermodynamics and metabolic advantage of weight loss diets. Metabolic Syndrome and Related Disorders, 1:209-219.

One in Two People Will Get Cancer – new report finds

A new report released by the Canadian Cancer Society predicts that almost one in two Canadians will be diagnosed with cancer in their lifetime.

One half” is a very sobering number!

Currently, cancer is the leading cause of death in Canada, accounting for almost 1/3 of all  of all deaths (30%).

Heart disease is the second leading cause of death, accounting for 1/5 of all deaths (20%).

In an interview with Peter Goffin of the Toronto Star, Dr. Robert Nuttall, Assistant Director of Health Policy at the Canadian Cancer Society attributed this alarming new statistic that 1/2 will get cancer in their lifetime to the “aging population” – notlifestyle factors“. 

Nutall said;

“The important thing to remember here is that the biggest driver behind this is the aging population. “Canadians continue to live longer, and cancer is primarily a disease that affects older Canadians.”

Japan has the oldest population in the world, with ~1/3 of people aged over 60.

What do their statistics show?

According to the Institute for Health Metrics and Evaluation, Japan’s leading causes of death (2015) were:

  1. cerebrovascular disease (stroke)
  2. cardiovascular disease (heart disease)
  3. lower respiratory infection
  4. Alzheimer’s disease

Lung cancer was 5th, followed by stomach cancer (6th) and colorectal cancer (7th). In Japan, a country with the oldest population in the world, cancer of any kind wasn’t even in the top four!

Are half of us really going to get cancer because of the “aging population” or is it because of “lifestyle factors“?

Looking at the top 4 Causes of Cancer in Canada:

Ten Most Common Cancers in Canada – projected for 2017
  1. Lung cancer is the number one form of cancer and the Canadian Cancer Society indicates that more than 85% of lung cancer cases in Canada are related to smoking tobacco.

  2. Colorectal cancer is the second leading cause of cancer and the Canadian Cancer Society indicates that risk factors for colorectal cancer include (a) diet , (b) being overweight, (c) physical inactivity and (d) smoking.

  3. Breast cancer (in both men and women) is the third leading cause of cancer. Apart for personal and family history of breast cancer and other genetic factors, the Canadian Cancer Society list the following known risk factors: (a) exposure to ionizing radiation, (b) use of oral contraceptives (c) alcohol and (d) being obese.

  4. Prostrate cancer which only affects men, is the fourth leading cause of cancer and the only known risk according to the Canadian Cancer Society is family history.

Major Risk Factors for the top 4 Causes of Cancer

Here are the major risk factors for the top four leading causes of cancer in Canada;

  1. smoking
  2. diet
  3. being overweight
  4. physical inactivity 
  5. exposure to ionizing radiation (x-rays)
  6. use of oral contraceptives
  7. alcohol

Except for use of x-rays, all of these are lifestyle factors!

Diet, being overweight and being inactive are three things that can be changed easily and sustainably!

A low carb approach can be particularly helpful, as it can not only address being overweight, but new studies have found that a number of cancer cells feed exclusively on glucose.  It is thought that a ketogenic lifestyle may play a role in reducing the glucose available for some types of cancer.

We being told that the biggest driver behind the projection that half of us will get cancer in our lifetime is the aging population– when it would seem that the underlying risk factors of these cancers are lifestyle factors.

In fact, the Canadian Cancer Society says themselves that half of the cases are preventable;

“We already know a lot about how to prevent cancer. If we, as a society, put everything we know into practice through healthy lifestyle choices and policies that protect the public, we could prevent about half of all cancers.”

We will all age and this is not preventable, but by addressing lifestyle factors including smoking, diet, overweight and physical inactivity and others, we should be able to prevent almost 1/2 of all cancers.

Have questions on how I can teach you how to eat healthier and work with you to help you tackle being overweight and inactive, then please send me a note using the “Contact Us” form on this web page.

To your good health!

Joy

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2017 The Low Carb High Fat 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 regular monitoring by a Registered Dietitian and with the knowledge of 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 something you have read in our content. 


References

Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/lung/risks/?region=on#ixzz4kZ5AnNz6

Canadian Cancer Society, http://www.cancer.ca/en/about-us/for-media/media-releases/ontario/2011/not-enough-canadians-being-screened-for-colorectal-cancer-leading-to-many-unnecessary-deaths/?region=on#ixzz4kZ5vSGSS

Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/breast/risks/?region=on#ixzz4kZ8RvXbm

Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-type/prostate/risks/?region=on#ixzz4kZ9J6o64

Canadian Cancer Society, http://www.cancer.ca/en/cancer-information/cancer-101/cancer-research/prevention/?region=on#ixzz4kZ9jQJwt

Institute for Health Metrics and Evaluation, http://www.healthdata.org/japan

The Toronto Star, Peter Goffin (Staff Reporter), Tue June 20 2017, https://www.thestar.com/news/gta/2017/06/20/half-of-all-canadians-will-get-cancer-in-their-lifetime.html

Obesity Pandemic – new study

In the last few years, we’ve heard the term “obesity epidemic“, but a new study published this past Monday, June 12, 2017 in the New England Journal of Medicine seems to indicate that it is now an “obesity pandemic“.

Researchers analyzed data from 68.5 million adults and children in 195 countries to assess (1) the prevalence of overweight and obesity in 2015 and (2) the trends in the prevalence of overweight and obesity between 1980 and 2015.

The “short story” is that a 1/3 of people worldwide are now overweight or obeseput another way, two billion people globally are overweight or obese and are at increased risk of morbidity (chronic diseases) and morbidity (death), as a result.

The Significance

Epidemiological studies (studies of different populations from around the world) have identified high BMI as a risk factor for cardiovascular disease, type 2 Diabetes, hypertension, chronic kidney disease and many types of cancer.

Furthermore, overweight children are at higher risk for the early onset of diseases such as type 2 Diabetes, hypertension and chronic kidney disease.

Body Mass Index (BMI) is the weight in kilograms divided by the square of the height in meters

Obesity is defined as having a Body Mass Index (BMI) > 30 kg/(m)2

Overweight is defined as having a BMI between 25 and 29.9 kg/(m)2

Obesity Findings

Data showed that in 2015, there were 603.7 million obese adults worldwide and 107.7 million obese children.

The prevalence of obesity has more than doubled in 70 countries since 1980, and there has been a tripling of obesity in youth and young adults in developing, middle class countries such as China, Brazil, and Indonesia.

Worldwide, the prevalence of obesity is now 5% in children and 12% in adults — findings that mirror global trends in type 2 Diabetes.

Most alarming was that in 2015;

  • high BMI accounted for four million deaths globally
  • almost 40% of deaths resulting from high BMI occurred in people who were overweight, but not obese
  • more than 2/3 of deaths related to high BMI were due to cardiovascular disease

Varying Risk

It is important to note that risk of outcomes related to obesity has not been found to be uniform across populations. For example, it has been reported that at any given level of BMI, Asians have been shown to have a higher absolute risk of Diabetes and hypertension, whereas African Americans have a lower risk of cardiovascular disease than other groups.

Addressing the Problem

To address the problem of overweight and obesity both here and around the world, requires correctly identifying its cause and for the last 40 years, excess dietary fat — especially saturated fat has been blamed as the villain and ostensibly responsible for the “obesity epidemic” and resulting “diabetes epidemic”.

But is it?

When one compares the Dietary Recommendations in both Canada and the United States since 1977 to rates of overweight and obesity in both of these countries, it seems apparent that it has been the promotion of diets high in carbohydrate that lies at the root.

In the next article, I’ll take a look at the Dietary Recommendations of the country with the highest rate of childhood obesity and adult obesity in 2015, as well as some of the highest rates of stroke and heart disease per capita, in the world.

How I can help

If you have eaten a ‘low fat diet’ and counted calories (or points) until you are blue in the face and are tired of doing the same thing over and over again, expecting a different outcome, why not drop me a note using the “Contact Us” form, above. I’d be glad to explain how I can help you achieve a healthy body weight, while normalizing your blood sugar, blood pressure and cholesterol levels.

To your health!

Joy

If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2017 The Low Carb High Fat 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 regular monitoring by a Registered Dietitian and with the knowledge of 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 something you have read in our content. 


you can follow me at:

 https://twitter.com/joykiddieRD

  https://www.facebook.com/lchfRD/


References

Global Burden of Disease (GBD) 2015 Obesity Collaborators, Health Effects of Overweight and Obesity in 195 Countries over 25 Years, N Engl J Med, DOI: 10.1056/NEJMoa1614362

Gregg EW, Shaw JE, Global Health Effects of Overweight and Obesity, N Engl J Med, doi: 10.1056/NEJMe1706095

Karter AJ, Schillinger D, Adams AS, et al. Elevated rates of diabetes in Pacific Islanders and Asian subgroups: the Diabetes Study of Northern California (DISTANCE). Diabetes Care 2013; 36:574-9

Weight Gain as a Hormone Imbalance not a Calorie Imbalance

scaleAs covered in an earlier article, weight gain is not caused simply by taking in more calories than you burn (the so-called “calorie-in / calorie-out” model).  Calories in and calories out are interdependent factors, so when calories are restricted the body actually slows its metabolism, lowering the energy it uses for vital bodily functions. Basal Energy Expenditure (BEE) can decrease by as much as 30-50% in order to spare calories!

On the opposite end, when too many calories are taken in by someone who is already overweight, the body will try to get rid of them by increasing its Basal Energy Expenditure, usually by speeding up respiration, increasing heart rate and breathing and generating more heat.

The body does this because its ‘set point’; the weight at which your body likes to be and will tend to stay with very little effort, is highly regulated. It really isn’t that easy to gain or lose weight if we haven’t already compromised this built-in homeostatic mechanism.

That is why trying to control calories doesn’t work for long term weight loss. When we restrict calories, and increase our exercise, our body responds by increasing hunger, initiating craving (especially for foods such as simple carbs that can be broken down quickly to glucose for your blood) and by decreasing the amount of energy it uses.

Have you ever skipped a meal or lowered your calories so much that you feel cold; even though the room is at an adequate temperature and you are dressed appropriately? You are shivering because your body is sparing calories it would normally use for heat generation.

Body Weight is Regulated by Hormones

Body weight is not really under our control as much as we’d like to believe.  It is a tightly regulated process that involves a variety hormones including leptin (a hormone that regulates fat stores by inhibiting hunger), ghrelin (a hormone that increase hunger when your stomach is empty) and insulin, which plays a very significant role in hunger, eating behavior and fat management.

To understand how significant a role insulin plays in weight regulation, let’s look at a situation where there is insufficient insulin. Type I diabetes results from the destruction of the insulin-producing pancreatic islet cells stemming from an autoimmune disorder. One of the hallmarks of this disease and it’s very low levels of insulin is severe weight loss. Type I diabetics need to take insulin injections to correct for the insulin deficiency but the more insulin that is taken, the more weight gain there is. As insulin levels go up, hunger is triggered and we feel the urge to eat.

Insulin is one of the major controllers of the body set point.

As mentioned, if we don’t take in sufficient calories, then our body decreases our Basal Energy Expenditure so that we end up maintaining our body weight in response to whatever the number of calories are that we take in.  The issue in weight gain is not how to reduce calories but how to reduce insulin.

Insulin as the Main Factor in Weight Gain

When we eat food, our body releases insulin in response to the rise in glucose in our blood, coming from the digested food. Insulin acts as a messenger to instruct the body’s cells to absorb glucose, in effect reducing blood glucose levels.

Insulin resistance is a condition in which the cells of the body become resistant to insulin and fail to respond normally to normal levels insulin, leading to higher blood sugar. The pancreas tries to compensate to this condition by producing more and more insulin.  As long as the pancreas is able to produce enough insulin to overcome this resistance, blood glucose levels remain normal but when the pancreas can no longer produce enough insulin, the blood glucose levels begin to rise.

Initially, this added rise in blood glucose happens after meals (when glucose levels are already at their highest) and more insulin is needed – but eventually these higher levels of glucose are seen first thing in the morning when the person hasn’t eaten for 8 or 10 hours. When blood sugar rises abnormally above specific clinical levels, the person is diagnosed as having Type 2 diabetes. Insulin resistance is often called “pre-diabetes” because it precedes the development of Type 2 Diabetes.

Consistently high blood glucose levels along with insulin resistance lead to cells that are starved of glucose even though there is plenty of glucose in the blood. Since the cells aren’t getting any of the glucose even though it is there, it is not available to the cells because insulin is not binding it and taking it in. As a result, hunger signals are sent to the brain, leading to eating, even though the person has recently eaten.

As more and more glucose accumulates (both from the food being eaten and as you will see in a minute, through the making of glucose due to the effect of cortisol, another hormone) the high levels of glucose trigger the body to store the excess glucose as body fat.

The Effect of Stress on Weight Gain

Cortisol, the so-called stress hormone also plays a role in weight gain. Let’s look at another medical conditions to illustrate the effects of cortisol. In Cushing Syndrome, cortisol is over-produced by the body and weight gain results.  When we give people a synthetic form of cortisol as a medication (e.g. prednisone) they get something called Cushinoid Syndrome.  That is, they look like they have Cushing ’s disease. Not only do they gain weight, but there is a particular distribution of this weight gain called truncal obesity which means that fat is gained around the belly, rather than on the arms and legs.

In adrenal insufficiency (also known as Addison’s disease) which produces the opposite effect, the adrenal gland becomes damaged due an autoimmune condition and is unable to produce cortisol.  The hallmark of Addison’s disease is weight loss.

So what role does cortisol play in healthy individuals? Cortisol is released as a result of ordinary events such as waking up in the morning or exercising, but also is released in response to physiological and psychological stress.  Physiological stress might be an illness or injury and the release of cortisol services a needed function to make sure we have enough glucose to heal.

Under stressful conditions, cortisol also plays the role of providing the body with glucose by tapping into protein stores via gluconeogenesis in the liver. This energy can be helpful in a “fight or flight” type of stressor, such as when one is being chased by something however under constant levels of psychological stress, elevated cortisol over leads to higher levels of glucose being made from protein in the body the long term.  So in addition to glucose coming from the food we eat (exogenous sources), we now have the body making its own glucose (endogenous sources).  The combined exogenous glucose from good and the endogenous glucose triggered by cortisol, now leads to even higher blood sugar levels that without the long term stress.

With continually high levels of cortisol, the body will take fat that is stored as triglycerides in our liver and relocate them to visceral fat cells — those under the muscle, deep in the abdomen. Just like in Cushing’s syndrome, we now see truncal obesity triggered by stress, mediated by cortisol.

Weight Gain is due to Hormonal Triggers and not a Lack of Will-Power

Cortisol also directly influences appetite and cravings by binding to hypothalamus receptors in the brain, triggering us to eat and crave foods that are easily broken down to glucose.  Cortisol also indirectly influences appetite by modulating other hormones that stimulate appetite. Simple carbohydrates like bread, pasta, candy and pop are common foods that people reach for in response to these craving because they are easily broken down to simple sugars. So, it is actually the higher levels of cortisol that lead to increased appetite and in particular cravings for high-calorie foods, not simply a lack of will-power.

As you can see, we don’t really control our body weight any more than we control our heart rates.  To a large degree, body weight is regulated automatically under the influence of hormones; hormones that indicate to eat and indicate when we are satiated.  Hormones signal our bodies to increase energy expenditure and when calories are restricted, hormones will slow energy expenditure.

Why All Diets Work and often All Diets Fail

It doesn’t really matter which diet people follow, whether it is Atkins, South Beach, or the good old fashioned low fat, low calorie diet, all diets in the short term produce weight loss. Yes, some are healthier than others, but they all “work”.

One would hope that by continuing to eat according to what ever diet we’ve chosen and by exercising, that our body’s set point would reset at a lower level, but this doesn’t happen.

Insulin levels stay high, continuing to drive hunger and eating.

How does this affect weight loss?

A few months into our diet, regardless what diet we follow, weight loss begins to plateau.  As the plateau continues, people get discouraged, and think to themselves ‘if I’m not losing weight, then I may as well eat – fill in the blank’. This is either followed by an abandoning of the diet completely and a regaining of the weight previously lost (or more) or by a stubborn insistence to restrict calories and fat even further — leading to a downshifting of basal energy expenditure. It’s a vicious cycle.

But why does Body Weight Plateau in the First Place?

In response to weight loss, the body tries to return to its original set point.  First it slows metabolism to try and slow down weight loss – resulting in slowed weight loss and eventual plateauing.

The reason is because we’ve done nothing to lower insulin levels.

Think of set point like a ‘body weight thermostat’. With a thermostat, when the air is hot enough, the furnace turns off and when it is too cool, the thermostat turns the furnace on.  Regardless what kind of diet a person follows, there will be weight loss effects in the short term, but eventually, even with continued compliance, body weight plateaus and in time, the person begins to regain the weight.

What about exercise?

Surely exercise will help us lose weight, right?

Basal energy expenditure which is the amount of energy we use at rest is estimated to be approximately 12-15 calories per pound.  For someone confined to complete bed-rest, caloric needs are calculated as 1.2 times Basal energy expenditure (BEE).

To visualize the effect exercise has on calorie loss, let’s take a 140 pound person as an example, whose basal caloric needs are 2200 – 2500 calories per day. Say they start exercising.  They start walking at a moderate pace (2 miles/hour) for 45 minutes every day, and burn roughly 104 calories.  Let’s look at that in terms of basal energy expenditurethat is only 4% of the BEE.  Okay, so say the person starts working out at a more vigorous pace, calorie burning will go up, right?  But how much?  6% of BEE?  8% of BEE? That’s about it.

The bottom line is, the vast majority of calories you take it; about 95% of caloric intake is used to heat the body and other metabolic processes, including keeping your heart beating, breathing, digestion, brain function, liver and kidney function, etc.

Set point is a tightly regulated mechanism, like a thermostat.  When we burn more calories through exercise two things happen.  Studies show that people actually end up decreasing their activity outside of the period of exercise and the other is they increase their caloric intake in response to exercise. That’s where the phrase “working up an appetite” comes from.

The reason exercise is not that effective for weight loss is because of metabolic compensation.  We understand this intuitively though, don’t we? When know when we cut calories, restrict certain foods and increase our exercise that our body responds by being more hungry and increasing cravings. We try to take extreme measures only to find that we don’t really have a chance at making the weight loss last long term.

Don’t misunderstand; exercise is good for you.  There are many benefits to regular exercise such as improved cardiovascular function, increased strength and flexibility, and lowering stress which will lower cortisol but weight loss is not one of the significant benefits of exercise.

So if restricting calories causes are energy usage to slow and results in us being more sedentary outside of the times we exercise or eating more in response to exercise, how do we lose weight and keep it off?

To keep weight off long term, we need to address the underlying hormonal trigger to hunger and appetite; mainly insulin. To lower weight and keep it off, we need to lower our insulin level.

There are two aspects to lowering insulin levels (1) the foods we eat and (2) when we eat and this will be the topic of our next blog.

scale

 

 

 

 

 

Note: Everyone's results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.

Copyright ©2015 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.

Role of Green Tea Powder (Matcha) in Weight and Abdominal Fat Loss

Based on a meta-analysis of studies, it has been found that people can lose ~ 3 pounds in a 12 week period (making no other dietary or exercise changes) by consuming 1 – 4 tsp of green tea (matcha) powder per day. The effect of green tea catechins contained in matcha powder on body fat composition is great even when weight loss is small (i.e. ~5 lbs in 12 weeks), Total amount of abdominal fat decreases 25x more with green tea catechin consumption & the fat just below the skin of the abdomen decreases 8x more than when green tea catechins are not consumed !


matcha – green tea powder

UPDATE: 

(April 25, 2017) Be sure get the recipe for a Low Carb High Healthy Fat Matcha Smoothie here: https://www.lchf-rd.com/2017/04/24/low-carb-green-tea-matcha-smoothie-role-in-weight-and-abdominal-fat-loss/.

Less than 3 gm of carbohydrate at all the health benefits of Matcha!

 

 


Introduction

Recent estimates indicate that about 1/3 of the adult population in the US is obese [Centers for Disease Control and Prevention, 2009] and while 2011 estimates in Canada indicate that approximately 1/5 of Canadians adults are classified as obese based on self-reported height and weight [Statistics Canada], studies have found that obesity rates in self-reported weight is ~7.4% higher when based on measured height and weight [Shields et al].  Adjusting for this under self-reporting of weight, > 1/4 (25.6%) of the adult population in Canada would be considered obese.  Recent literature suggests that obesity and the related diseases of “metabolic syndrome” associated with obesity are not just a North American problem either, but a global health problem [Popkin].Although there are many genetic and environmental factors that may predispose people to weight gain, the main cause of overweight and obesity is believed to be an imbalance between dietary intake and energy expenditure (i.e. calories in > calories out).  Excess fat mass develops over time from a very small positive energy imbalance i.e. just taking in slightly more calories than needed.  In general, average weight gain per year is small; approximately 1 pound per year across all race, economic, and sex groups [Brown].There are many strategies used to address weight gain, including;-         

Dietary approaches; which usually focus on decreasing caloric intake through a variety of means and while some people go on self-chosen “diets” that are bizarre and even dangerous, weight loss will occur as long as energy intake is less than energy expenditure (i.e. calories in < calories out).

–          Lifestyle strategies that help individuals identify and modify their eating behaviour and patterns of eating.  When people understand why they eat and when they eat, it is easier for them to make long-term lifestyle changes.

–          Exercise and increased physical activity to help people attain and maintain a healthy body weight.

–          Food intake is sometimes addressed pharmacologically by doctors by using drugs such as Orlistat (which blocks lipase, an enzyme involved in fat absorption).

–          Surgical approaches provide the most dramatic weight loss and outside of the cosmetic value, may have a role in reducing long-term mortality and the incidence of diabetes [Bray].

 

Role of Green Tea Catechins in Weight Loss

Green tea is the unfermented leaves of the Camellia sinensis plant and contains a number of biologically active compounds called catechins and epigallocatechin gallate (EGCG) makes up almost 30% of the solids in green tea [Kim et al].  Recent studies have found that green tea catechins, especially EGCG play a significant role in both weight loss and body fat composition.

Green Tea Catechins and “Metabolic Syndrome”

Several large-scale population studies have linked increased green tea consumption with significant reductions in “metabolic syndrome” which is a cluster of diseases that include;

–          insulin resistance or diabetes

–          hyperinsulinemia (high levels of insulin in the blood)

–          cardiovascular diseases; high blood pressure & coronary heart disease

–          obesity

It is thought that epigallocatechin gallate (EGCG), the most abundant catechin in green tea, mimics the actions of insulin.  This has positive health implications for people with insulin resistance or diabetes [Kao et al] and EGCG also lowers blood pressure almost as effectively as the ACE-inhibitor drug, Enalapril, having significant implications for people with cardiovascular disease [Kim et al].

 

Green Tea in Population Studies

Population studies and several randomized controlled studies (where one group is “treated” and the other group is not) have shown that waist circumference is smaller and levels of body fat is less the more green tea consumed  [Phung et al] .  The anti-obesity effects of green tea are usually attributed to the presence of catechins [Naigle].

 

Green Tea Catechins

While catechins make up ~ 30% of green tea’s dry weight (of which 60–80% are catechins) oolong and black tea, which are produced from partially fermented or completely fermented tea leaves contains approximately half the catechin content of green tea.

Drinking 8-10 cups of green tea per day is enough to increase blood levels of EGCG into a measurably significant range [Kim et al]. Matcha, a powdered green tea used in the Japanese tea ceremony and popular in cold green tea beverages such as bubble tea, contains 137 times greater concentration of EGCG than China Green Tips (Mao Jian) tea [Weiss et al].

 

Green Tea Catechin Content of Brewed Green Tea vs Matcha Powder

A typical cup (250 ml) of brewed green tea contains 50–100 mg catechins and 30–40 mg caffeine, with the amount of tea leaves, water temperature and brewing time all affecting the green tea catechin content in each cup.

A gram (~1/3 tsp) of matcha powder contains 105 mg of catechins (of which 61 mg are EGCs) and contains 35 mg of caffeine. Most matcha drinks made at local tea and coffee houses are made and served cold and contain ~1 tsp of matcha powder which contains ~315 mg of catechins (of which ~183 mg are EGCs).  Since there is no brewing time involved in the preparation of cold matcha beverages, the amount of catechins remains relatively constant in each cup. Variation in catechin content in matcha powder is largely due to where the plant is grown and how it is processed.

 

Weight Loss Effect of Green Tea Catechins

A 2009 meta-analysis (combining the data from all studies) of 11 green tea catechin studies found that subjects consuming between 270 to 1200 mg green tea catechins / day (i.e. 1 – 4 tsp of matcha powder per day) lost an average of 1.31 kg (~ 3 lbs) over 12 weeks [Hursel].

 

Decreased Body Fat & Abdominal Fat even without Significant Weight Loss

The effect of green tea catechins on body composition is significant even when the weight loss between “treated” and “untreated” groups is small (~5 lbs in 12 weeks).

Even with such small amounts of weight loss;

– the total amount of abdominal fat decreases 25 times more with green tea catechin consumption than without it (−7.7 vs. −0.3%)

and

 total amount of subcutaneous abdominal fat (the fat just below the skin of the abdomen) decreases almost 8 times more with green tea catechin consumption thank without it (−6.2 vs. 0.8%).

 

How do Green Tea Catechins Work?

The mechanisms by which green tea catechins reduce body weight and reduce the amount of total body fat and in particular reduce the amount of abdominal fat are still being investigated.  It is currently thought that green tea catechins;

–          increased thermogenesis; i.e. increased heat production which would result in increased energy expenditure (or calorie burning)

–          increase fat oxidation (or using body fat as energy)

–          decrease appetite

–          down-regulation of enzymes involved in liver fat metabolism

–          decrease nutrient absorption

 

Green Tea Absorption

Green tea catechins are absorbed in the intestine.  Since the presence of food significantly decreases their absorption, green tea catechins are best taken 1/2 an hour before meals or 2 hours after meals.

The timing of green tea catechin intake may also affect the absorption and metabolism of glucose.  A study by Park et al found that when green tea catechins were given one hour before to a glucose (sugar) load, glucose uptake was inhibited and was also accompanied by an increase in insulin levels. Taking green tea catechins an hour before consuming highly sweet foods may be beneficial for those with insulin resistance or diabetes.

Green Tea Catechins and Milk

There seems to be some dispute in the literature as to whether the casein (a protein) in milk binds green tea catechins, making them unavailable for absorption in the body, which is why matcha drinks are often made with non-milk beverages such as soy milk, almond milk or rice milk (that don’t have casein).

Conclusion

Consuming between 1 – 4 tsp of matcha powder per day (270 to 1200 mg green tea catechins / day) is sufficient to result in weight loss of approximately 3 lbs in 12 weeks (with no other dietary or activity changes) and to significantly decrease body fat composition and reduce the quantity of abdominal fat.
 

***Warning to pregnant women***

While EGCG has also been found to be similar in its effect to etoposide anddoxorubicin, a potent anti-cancer drug used in chemotherapy [Bandele et al], high intake of polyphenolic compounds during pregnancy is suspected to increase risk of neonatal leukemia. Bioflavonoid supplements (including green tea catechins) should not be used by pregnant women [Paolini et al].

BetterByDesign’s Recipe for Iced Matcha 

For those of you that have been asking what I am always drinking in that thermos…this is it!

 

Ingredients

–          1 tsp matcha (green tea) powder (contains ~315 mg catechins)

–          500 ml soy milk

–          crushed ice

 

Method

  1. Place 1 tsp matcha powder in a small stainless steel sieve and gently press through the sieve into a small bowl with the back of a small spoon
  2. Put the sieved matcha powder into a ceramic or glass bowl (not metal, as the tannins in the tea will react and give the beverage and “off” metalic taste)
  3. With a bamboo whisk (available at Japanese and Korean grocery stores), whisk 3 Tbsp boiled and cooled water into the matcha powder, until all the lumps are gone and the mixture is smooth
  4. Place 1/4 cup of crushed ice in the bottom of a tall (16 oz / 500 ml) glass
  5. Pour matcha and water mixture over ice in the glass
  6. Fill glass with soy milk (or almond milk or rice milk) *

* I use 2/3 unsweetened soy milk and 1/3 sweetened soy milk

Note: once the matcha is blended with the soy milk, the tannins in the green tea are neutralized and no longer react with metal, so the beverage can then be put in an insulated stainless steel cup.

 

References

Bandele, OJ, Osheroff, N. Epigallocatechin gallate, a major constituent of green tea, poisons human type II topoisomerases”.Chem Res Toxicol 21 (4): 936–43, April 2008.

Bray GA. Lifestyle and pharmacological approaches to weight loss: efficacy and safety. J Clin Endocrinol Metab 2008;93:S81–88.

Brown WJ, Williams L, Ford JH, Ball K, Dobson AJ. Identifying the energy gap: magnitude and determinants of 5-year weight gain in midage women. Obes Res 2005;13:1431–41.

Centers for Disease Control and Prevention (CDC). Overweight and obesity. http://www.cdc.gov/obesity/index.html accessed Nov 20. 2009

Hursel R, Viechtbauer W, Westerterp-Plantenga MS. The effects of green tea on weight loss and weight maintenance: a meta-analysis. Int J Obes (Lond) 2009;33:956–61.

Kao YH, Chang MJ, Chen CL, Tea, Obesity, and Diabetes, Molecular Nutrition & Food Research, 50 (2): 188–210, February 2006

Kim JA, Formoso G, Li Y, Potenza MA, Marasciulo FL, Montagnani M, Quon MJ., Epigallocatechin gallate, a green tea polyphenol, mediates NO-dependent vasodilation using signaling pathways in vascular endothelium requiring reactive oxygen species and Fyn, J Biol Chem. 2007 May 4;282(18):13736-45. Epub 2007 Mar 15.

Nagle DG, Ferreira D, Zhou YD. Epigallocatechin-3-gallate (EGCG): chemical and biomedical perspective. Phytochemistry 2006;67:1849–55.

Park JH, Jin JY, Baek WK, Park SH, Sung HY, Kim YK, et al. Ambivalent role of gallated catechins in glucose tolerance in humans: a novel insight into nonabsorbable gallated catechin-derived inhibitors of glucose absorption. J Phyisiol Pharmacol 2009;60:101–9.

Popkin BM. Recent dynamics suggest selected countries catching up to US obesity. Am J Clin Nutr 2010;91:284S–8S.

Phung OJ, Baker WL, Matthews LJ, Lanosa M, Thorne A, Coleman CI. Effect of green tea catechins with or without caffeine on anthropometric measures: a systematic review and meta-analysis. Am J Clin Nutr 2010;91:73–81.

Paolini, M, Sapone, A, Valgimigli, L, “Avoidance of bioflavonoid supplements during pregnancy: a pathway to infant leukemia?”. Mutat Res 527 (1–2): 99–101. (Jun 2003)

Rains, TM, Agarwal S, Maki KC, “Antiobesity effects of green tea catechins; a mechanistic review” J or Nutr Biochem 22(2011):1-7

Shields M, Connor Gorber S, Trembaly MS, Estimates of obesity based on self-report versus direct measures, Statistics Canada (StatsCan), http://www.statcan.gc.ca/pub/82-003-x/2008002/article/10569-eng.htm

Statistics Canada(StatsCan) – Overweight and Obese Adults (self-reported), 2011 http://www.statcan.gc.ca/pub/82-625-x/2012001/article/11664-eng.htm

Weiss, DJ, Anderton CR, Determination of catechins in matcha green tea by micellar electrokinetic chromatography, Journal of Chromatography A, Vol 1011(1–2):173-180, September 2003