What is a Mediterranean Style Diet?

The recently released 2018 Clinical Practice Guidelines (CPG) Guidelines of Diabetes Canada recommend that those with Diabetes continue to eat 45% to 65% of their daily calories as carbohydrate, 10% to 35% of their daily calories as protein and only 20% to 35% of their daily calories, yet affirm that there is “evidence to support a number of other macronutrient-, food- and dietary pattern-based approaches” and that “evidence is limited for the rigid adherence to any single dietary approach”[1] .

One of the dietary patterns they recommend is a “Mediterranean-style dietary pattern” in order to “reduce major cardiovascular events and improve glycemic (blood sugar) control.”

So what is a “Mediterranean-style dietary pattern”?

According to the Clinical Practice Guidelines,

A “Mediterranean diet” primarily refers to a plant-based diet first described in the 1960s. General features include a high consumption of fruits, vegetables, legumes, nuts, seeds, cereals and whole grains; moderate-to-high consumption of olive oil (as the principal source of fat); low to moderate consumption of dairy products, fish and poultry; and low consumption of red meat, as well as low to moderate consumption of wine, mainly during meals”

Countries with coastlines on the Mediterranean Sea include Albania, Algeria, Bosnia and Herzegovina, Croatia, Cyprus, Egypt, France, Greece, Israel, Italy, Lebanon, Libya, Malta, Morocco, Monaco, Montenegro, Slovenia, Spain, Syria, Tunisia and Turkey and the diets of these countries vary considerably, so there isn’t only ONE “Mediterranean Diet”.

What is the Mediterranean Diet that the Clinical Practice Guidelines are referring to?

It would seem that they are referring to dietary intake based of southern Italy from the 1960s from when rates of chronic disease were reported to be amongst the lowest in the world and adult life expectancy was reported to be amongst the highest. That is, the health benefits of “The Mediterranean Diet” came out of Ancel Keys’ Six Country Study (1953) and later his Seven Countries Study (1970).  More on that below.

One of the academic papers that the Guidelines cites as the basis for a “Mediterranean diet” makes the direct link to Ancel Keys clear;

“Ecologic evidence suggesting beneficial health effects of the Mediterranean diet has emerged from the classic studies of
Keys.” [2]

In 1953, Ancel Keys published the results of his “Six Countries Study“[3], where it is said he demonstrated that there was an association between dietary fat as a percentage of daily calories and death from degenerative heart disease.

Four years later, in 1957, Yerushalamy published a paper with data from 22 countries [4], which showed a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s six country data (see below).

from [3].Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y.20, 118–139 (1953).

from [4] Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343–54

Nevertheless, in 1970, Keys went on to publish his Seven Countries Study in which he maintained that there was an associative relationship between increased dietary saturated fat and Coronary Heart Disease – ignoring the data presented in Yerushalamy’s 1957 study and failing to study countries such as France, in which the relationship did not hold.

In Keys’ paper published in 1989 [5] which was based on food consumption patterns in the 1960s in the seven countries, he found that the average consumption of animal foods (with the exception of fish) was positively associated with 25 year Coronary Heart Disease deaths rates and the average intake of saturated fat was strongly related to 10 and 25 year CHD mortality rates. Keys published this study 32 years after Yerushalamy’s 1957 paper which showed a significantly weaker relationship, yet it seems that people only remember Key’s data.

Countries with coastlines on the Mediterranean Sea on which there was known dietary and disease data in 1957 and that Keys later ignored in 1970 included France (labelled #8 on Yerushalamy’s graph above) and Israel (labelled #11). France is known for the “French paradox” (a term which came about in the 1980s) because of their relatively low incidence of coronary heart disease (CHD) while having a diet relatively rich in saturated fats. According to a 2004 paper about the French Paradox, there was diet and disease data available from the French population that was carried out in 1986–87 and which demonstrated that the saturated fat intake of the French was 15% of the total energy intake, yet such a high consumption of saturated fatty acids was not associated with high Coronary Heart Disease incidence in France [6]. Nevertheless, Keys published his 1989 study [5] ignoring the French dietary and disease data that was available from 1986-1987 [6]. Was it because it didn’t fit his hypothesis?

The diet of the French in the 1960’s was every bit a “Mediterranean Diet” as that of southern Italy, but since Ancel Keys ignored (or did not study) the French data in the 1960s, that “Mediterranean Diet” remains ignored in the guidelines of today.

According to the French Paradox paper, high saturated fat intakes combined with low Coronary Heart Disease rates were also observed in other Mediterranean countries, including Spain and that rates in other non-Mediterranean Europeans countries such as Germany, Belgium are similar [6].

Perhaps then, a ‘true’ Mediterranean Diet which is protective of Coronary Heart Disease ought not to be defined as being largely “plant-based” and “low in consumption of red meat and dairy” – which the French diet clearly is not, but rather should focus on being a diet high in consumption of specific types of vegetables and fruit, nuts and seeds, abundant in the use of olive oil and that includes regular consumption of wine with meals.

As outlined in a recent article, eight recent meta-analysis and systemic reviews which reviewed evidence from randomized control trials that had been conducted between 2009-2017 did not find an association between saturated fat intake and the risk of heart disease. As well, recently published results from the Prospective Urban and Rural Epidemiological (PURE) Study, the largest and most global epidemiological study carried out to date and published in the Lancet in December 2017 found that those who ate the largest amount of saturated fats had significantly reduced rates of mortality (death) and that low consumption of saturated fat (6-7% of calories) was actually associated with increased risk of stroke.

Also as described in a recent article, a study published at the end of March 2017 in Nutrients and which examined health and nutrition data from 158 countries worldwide found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease, and that high carbohydrate consumption, particularly as cereals and wheat was most associated with the risk of cardiovascular disease – with both of these relationships holding up regardless of a nation’s average national income.

Final Thoughts…

The 2018 Clinical Practice Guidelines continue to recommend the health benefits of a “Mediterranean style diet” defined based on the 60-year-old-data of Ancel Keys’ Six Countries Study / 50 year old Seven Countries Study- when we now know that Keys excluded data that was available from countries including France, which did not fit his hypothesis.

Given that there seems to be increasing evidence that Keys’ Diet-Heart Hypothesis (the belief that dietary saturated fat causes heart disease) has been significantly challenged by newer data, is it not time to study the factors in the diet of this region that ARE protective against cardiovascular disease, and to redefine a Mediterranean diet in these terms?

Would you like to have a Meal Plan that emphasizes the foods of this region, including meat and cheese, fish and seafood, vegetables and fruit, nuts and seeds, olive oil and wine and which may play a protective role in heart heath?

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

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

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References

  1. Sievenpiper JL, Chan CB, Dwortatzek PD, Freeze C et al, Nutrition Therapy – 2018 Clinical Practice Guidelines, Canadian Journal of Diabetes 42 (2018) S64–S79 http://guidelines.diabetes.ca/docs/CPG-2018-full-EN.pdf
  2. Trichopoulou A, Costacou T, Bamia C et al, Adherence to a Mediterranean Diet and Survival in a Greek Population, N Engl J Med 2003;348:2599-608.
  3. Keys, A. Atherosclerosis: a problem in newer public health. J. Mt. Sinai Hosp. N. Y.20, 118–139 (1953).
  4. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343–54
  5. Kromhout D, Keys A, Aravanis C, Buzina R et al, Food consumption patterns in the 1960s in seven countries. Am J Clin Nutr. 1989 May; 49(5):889-94.
  6. Ferrières J. The French paradox: lessons for other countries. Heart. 2004;90(1):107-111.

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

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

Diabetes Canada 2018 Clinical Practice Guidelines – option of a low carb diet


Diabetes Canada has released their long-awaited 2018 Clinical Practice Guidelines [1] which affirms that nutrition therapy is an integral part of people’s self-management of their Diabetes, as well as part of the treatment for the disease.  One of the main goals of nutrition therapy is to maintain or improve the quality of life and nutritional and physical health of those with the disease, while preventing the need to treat both sudden (acute) and long term complications. Effective nutrition therapy can improve blood sugar control, including reducing three-month average blood glucose (i.e. HbA1C, glycated hemoglobin) by 1.0% to 2.0%.

Diabetes Canada 2018 Clinical Practice Guidelines

The new Guidelines mention that since Canada has wide ethnic and cultural diversity, with each group having their distinct foods, preparation methods, and dietary patterns and lifestyles. Effective nutritional therapy needs to take these cultural variations into account and needs to be individualized;  specific to the individual, their age, the duration they’ve had type 2 diabetes, their goals, personal values and preferences, along with their individual need, lifestyle and economic situation. They recognize that nutrition therapy for those with Diabetes is not “one-size-fits-all”.

“Nutrition therapy should be individualized, regularly evaluated, reinforced in an intensive manner and should incorporate self-management education. A registered dietitian (RD) should be involved in the delivery of care wherever possible.”

The Nutrition Therapy Guidelines recommend that those with Diabetes follow the recommendations of Eating Well with Canada’s Food Guide;

“The starting point of nutrition therapy is to follow the healthy
diet recommended for the general population based on Eating Well With Canada’s Food Guide.”

They recommend that those with Diabetes continue to eat 45% to 65% of their daily calories as carbohydrate, 10% to 35% of their daily calories as protein and only 20% to 35% of their daily calories as fat, yet at the same time say that “the ideal macronutrient distribution for the management of diabetes can be individualized”;

“The ideal macronutrient distribution for the management of diabetes can be individualized. Based on evidence for chronic disease prevention and adequacy of essential nutrients, the DRIs (Dietary Reference Intakes) recommend acceptable macronutrient distribution ranges (AMDRs) for macronutrients as a percentage of total energy. These include 45% to 65% energy for CHO, 10% to 35% energy for protein and 20% to 35% energy for fat.”

They recommend that those with Diabetes continue to follow the same macronutrient distribution (percent of carbs, protein and fat) as the general population because it

“may help a person attain and maintain a healthy body weight while ensuring an adequate intake of carbohydrate (CHO), fibre, fat, protein, vitamins and minerals.”

What is encouraging is that they also have said that there is evidence to support a number of other macronutrient-, food- and dietary pattern-based approaches and advise against any rigid adherence to any one approach;

“There is evidence to support a number of other macronutrient-, food- and dietary pattern-based approaches. As evidence is limited for the rigid adherence to any single dietary approach, nutrition therapy and meal planning should be individualized.”

These Guidelines leave it open to individuals to choose other dietary approaches and outline a number of those approaches in the body of the text and in a summary table (Table 1). Figure 1 and Figures 2 and Table 1 in the Clinical Practice Guidelines (below) present an algorithm that summarizes the approach to nutrition therapy for diabetes which includes;

“allowing for the individualization of therapy in an evidence-based framework”.

Figure 1 – Clinical Assessment – Diabetes Canada 2018 Clinical Practice Guidelines

Figure 2 – Stage Targeted Nutrition Flowchart – Diabetes Canada 2018 Clinical Practice Guidelines

Table 1:

Table 1: Properties of Dietary Intervention – Diabetes Canada 2018 Clinical Practice Guidelines

The new Diabetes Canada guidelines recognize that the ideal macronutrient distribution (the ratio of carbs, protein and fat) may vary and depend on, amongst other things, the individual’s values and preferences;

“The ideal macronutrient distribution for the management of diabetes may vary, depending on the quality of the various macronutrients, the goals of the dietary treatment regimen and the individual’s values and preferences.”

That is, they recognize that a person’s individual preference for the amount and type of protein (animal-based, plant-based, both), fat (from animal or plant based sources), as well as the amount and type of carbohydrate in their diet factors into their personal decision for how they choose to manage their diabetes.

The Clinical Practice Guidelines for Nutrition Therapy mentions that based on the 3 systematic and meta-analysis of controlled trials of carbohydrate restricted diets that they looked at (mean carbohydrate intake from 4% to 45% of total daily energy) that consistent improvements in HbA1C, lipids and blood pressure weren’t shown.

“As for weight loss, low-carbohydrate diets for people with type 2 diabetes have not shown significant advantages for weight loss over the short term. There also do not appear to be any longer-term advantages.”

So while they do not believe based on the few studies that they examined that there is any advantage to someone following a low carbohydrate diet, there are no clear disadvantages. It comes down to individual preference.

The Guidelines also highlight that there may be a benefit of substituting monounsaturated fat (MUFAs) such as is found in olive oil for carbohydrate (something I regularly do when I design Meal Plans) and that systematic review and meta-analysis of randomized controlled trials found that monounsaturated fat substituted calorie for calorie for carbohydrate did not reduce HbA1C, but did improve fasting blood glucose, body weight, systolic BP, triglycerides and HDL (so-called “good cholesterol”) in people with type 2 diabetes over an average follow up of 19 weeks.

Another finding they reported is that replacement of refined high glycemic index carbohydrates with monounsaturated fat (up to 14.5% total energy) or nuts (up to 5% total energy) has been shown to improve HbA1C and lipids in people with type 2 diabetes over a 3 month period.

Together, these findings provide support to those who prefer to replace high glycemic carbs in their diet (such as white bread, pasta and rice) with monounsaturated fat sources such as olives, avocado as well as some nuts.

The new Clinical Practice Guidelines outline several popular weight-loss diets highlighting that there are a “range of macronutrient profiles are available to people with diabetes”;

“Numerous popular weight-loss diets providing a range of macronutrient profiles are available to people with diabetes. Several of these diets, including the Atkins™, Zone™, Ornish™, Weight Watchers™ and Protein Power Lifeplan™ diets, have been subjected to investigation in longer-term, randomized controlled trials in participants with overweight or obesity that included some people with diabetes, although no available trials have been conducted exclusively in people with diabetes.

They say that a systematic review and meta-analysis of four trials of the Atkins™ diet and 1 trial of the Protein Power Lifeplan™ diet showed that these diets were no more effective than conventional energy-restricted, low-fat diets in inducing weight loss, or with improvements in triglycerides and HDL for up to one year and have been reported to increase total cholesterol and LDL. As mentioned in an earlier article, without differentiating between particle size of LDL (small, dense versus large, fluffy), LDL and total cholesterol going up has not real meaning.

The Guidelines also mentioned that “The Dietary Intervention Randomized Controlled Trial (DIRECT) showed that the Atkins™ diet produced weight loss and improvements in the lipid profile compared with a calorie-restricted, low-fat conventional diet; however, its effects were not different from that of a calorie-restricted Mediterranean-style diet at two years.”

They add that “another trial comparing the Atkins™, Ornish™, Weight Watchers™ and Zone™ diets showed similar weight loss and improvements in the LDL:HDL ratio without effects on fasting blood sugar at one year in participants with overweight or obesity, of whom 28% had diabetes.

So again, it comes down to a matter of choice as to whether someone would prefer to do a calorie-restricted weight loss diet or a well-designed low carb one.

At the end of the paper, the authors make their final recommendations, some of which include that;

“People with diabetes should receive nutrition counselling by a registered dietitian to lower A1C levels and to reduce hospitalization rates”.

“Individuals with diabetes should be encouraged to follow Eating Well with Canada’s Food Guide in order to meet their nutritional needs.”

“In people with overweight or obesity with diabetes, a nutritionally balanced, calorie-reduced diet should be followed to achieve and maintain a lower, healthier body weight”.

“An intensive healthy behaviour intervention program, combining dietary modification and increased physical activity, may be used to achieve weight loss, improve glycemic control and reduce CV risk.”

“In adults with diabetes, the macronutrient distribution as a percentage of total energy can range from 45% to 60% carbohydrate, 15% to 20% protein and 20% to 35% fat to allow for individualization of nutrition therapy based on preferences and treatment goals.”

“People with type 2 diabetes should maintain regularity in timing and spacing of meals to optimize glycemic control.”

“To reduce the risk of cardiovascular disease, adults with diabetes should avoid trans fatty acids and consume less than 9% of total daily energy from saturated fatty acids, replacing these fatty acids with polyunsaturated fatty acids, particularly mixed n-3 / n-6 sources, monounsaturated fatty acids from plant sources, whole grains or low glycemic index carbohydrates”

“Adults with diabetes should select carbohydrate food sources with a low-GI to help optimize glycemic control to improve LDL and to decrease cardiovacular risk.”

“The following dietary patterns may be considered in people with type 2 diabetes, incorporating patient preferences, including:

(a) Mediterranean-style dietary pattern to reduce major cardiovascular events and improve glycemic control.

(b) Vegan or vegetarian dietary pattern to improve glycemic control and reduce myocardial infarction risk.

(c) DASH dietary pattern to improve glycemic control and reduce major cardiovascular events.

(d) Dietary patterns emphasizing dietary pulses (e.g. beans, peas, chickpeas, lentils) to improve glycemic control, systolic BP and body weight.

(e) Dietary patterns emphasizing fruit and vegetables to improve glycemic control and reduce CV mortality.

(f) Dietary patterns emphasizing nuts to improve glycemic control and LDL cholesterol.

Funding sources for the three authors of the Nutrition Therapy guidelines were as follows; Dr. John L. Sievenpiper, MD, PhD; Canadian Institutes of Health Research (CIHR), Calorie Control Council, INC International Nut and Dried Fruit Council Foundation, The Tate and Lyle Nutritional Research Fund at the University of Toronto, The Glycemic Control and Cardiovascular Disease in Type 2 Diabetes Fund at the University of Toronto (a fund established by the Alberta Pulse Growers), PSI Graham Farquharson Knowledge Translation Fellowship, Diabetes Canada Clinician Scientist Award, Banting & Best Diabetes Centre Sun Life Financial New Investigator Award, and CIHR INMD/CNS New Investigator Partnership Prize; grants and non-financial support from American Society for Nutrition (ASN), and Diabetes Canada; personal fees from mdBriefCase, Dairy Farmers of Canada, Canadian Society for Endocrinology and Metabolism (CSEM), GI Foundation, Pulse Canada, and Perkins Coie LLP; personal fees and non-financial support from Alberta Milk, PepsiCo, FoodMinds LLC, Memac Ogilvy & Mather LLC, Sprim Brasil, European Fruit Juice Association, The Ginger Network LLC, International Sweeteners Association, Nestlé Nutrition Institute, Mott’s LLP, Canadian Nutrition Society (CNS), Winston & Strawn LLP, Tate & Lyle, White Wave Foods, and Rippe Lifestyle, outside the submitted work; membership in the International Carbohydrate Quality Consortium (ICQC) and on the Clinical Practice Guidelines Expert Committees of Diabetes Canada, European Association for the study of Diabetes (EASD), Canadian S74 J.L. Sievenpiper et al. / Can J Diabetes 42 (2018) S64–S79 Cardiovascular Society (CCS), and Canadian Obesity Network; appointments as an Executive Board Member of the Diabetes and Nutrition Study Group (DNSG) of the EASD, Director of the Toronto 3D Knowledge Synthesis and Clinical Trials foundation; unpaid scientific advisor for the Food, Nutrition, and Safety Program (FNSP) and the Technical Committee on Carbohydrates of the International Life Science Institute (ILSI) North America; and spousal relationship with an employee of Unilever Canada. Dr. Chan reports grants from Danone Institute, Canadian Foundation for Dietetic Research, Alberta Livestock and Meat Agency, Dairy Farmers of Canada, Alberta Pulse Growers, and Western Canada Grain Growers. Dr. Catherine B Chan has a patent No. 14/833,355 pending to the United States. Dr. Catherine Freeze, MEd, RD reports personal fees from Dietitians of Canada and Government of Prince Edward Island.

Some Final Thoughts…

Much of the same wording  regarding supporting individual preference was previously embodied in the 2013 Clinical Practice Guidelines of the Canadian Diabetes Association. While not “recommended”, there was previously the same option for individuals to choose to follow a low carb lifestyle, based on personal preference.

As a Dietitian, I keep reading and reviewing the literature in order to provide the most current, evidence-based low carbohydrate diet to support those that choose to follow a low carb lifestyle — or who’s doctors recommend that they do, and in this way allow for the individualization of nutrition therapy in an evidence-based framework.

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

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

 

References

  1. Sievenpiper JL, Chan CB, Dwortatzek PD, Freeze C et al, Nutrition Therapy – 2018 Clinical Practice Guidelines, Canadian Journal of Diabetes 42 (2018) S64–S79 http://guidelines.diabetes.ca/docs/CPG-2018-full-EN.pdf

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.

Concerns with Polyunsaturated Vegetable Oils – Part 2

This article is Part 2 in a two-part series on concerns with Polyunsaturated Vegetable Oils.Part 1 can be read here.

There are a few key things about polyunsaturates vegetable oils that need to be understood to understand this article, so I’ll keep the science simple.

There are two class of polyunsaturated fats; (PUFAs); omega 3 (ω-3 also written n-3) and omega 6 (ω-6 / n-6) which compete with each other for enzymes, and which becomes significant at one branch point (marked with the red and green box).

At that junction point (where the red box is at Arachidonic acid and green box is at Eicosapentanoic acid) if there is more n-6 fats than n-3 fats, then the pathway will favour the n-6 pathway. If there are more n-3 fats than n-6 fats, then the pathway will favour the n-3 pathway. The issue, as I will elaborate on below, is that in the Western diet, the n-6 pathway is always favoured.

Of significance, the n-6 polyunsaturated fats are pro-inflammatory and the n-3 polyunsaturated fats are anti-inflammatory. This is important to understand why eating lots of foods high in n-6 fats can lead to health consequences.

When people take low-dose Aspirin® for example, to lower the risk of heart attack or stroke, it acts on Arachidonic acid in the n-6 polyunsaturated fat pathway, to keep it from making certain inflammatory products that can lead to heart attack or stroke.

In our evolutionary history it was thought that n-6 fats (from nuts and seeds that were gathered in the wild) and n-3 fats (from the fish and meat we hunted) were eaten in close to a 1:1 ratio – providing the two essential fatty acids from both classes. When man began domesticating grain and growing beans and lentils and nuts and seeds for food (all high in n-6 fats), the shift towards a diet higher in n-6 fats occurred. The modern Western diet is estimated to have an omega-6 to omega-3 fatty acids of 15–20:1 in favour of n-6 fats [6].

Many people take omega-3 fish oil capsules in an effort to protect their body from inflammation, but because the amount of n-6 fats in the diet is so much higher than the amount of n-3 fats, the n-6 pathway is still favoured.

Unless we significantly lower the amount of n-6 fats in the diet, taking fish oil doesn’t really help as the n-6 pathway will always be favoured.

Changing the Makeup of Cell Components

Industrial seed oils have very high levels of linoleic acid which is at the top of the n-6 pathway.  These industrial seed oils are pro-inflammatory and will elongate to Arachidonic acid, resulting in many pro-inflammatory products being produced.

When we eat a lot of food made with soybean oil or fried in soybean oil we eat way more linoleic acid then our body has evolved to handle.

A major problem with polyunsaturated fatty acids such as linoleic acid are that they are very unstable fats that are easily oxidized (similar to a fat becoming ‘rancid’ or a metal ‘rusting’). Even if we never buy these industrial seed oils to cook with at home, when we buy French fries at restaurants they are fried in either soybean or canola oil. When we pick up a donuts, same thing.  Bottle salad dressing and mayonnaise (even the one that is called ‘olive oil mayonnaise’) are made with one of these industrial seed oils. These oils are found in products one would never expect to find them, including peanut butter! Start reading labels and you will be shocked how many products they are in – or rather, how few products they are NOT in.

Industrial seed oils are in most of the prepared food we buy and almost all of the food we eat out in fast-food restaurants.

According to a 2011 journal article published in the American Journal of Clinical Nutrition;

“The most striking modification of the US food supply during the 20th century was the >1000-fold increase in the estimated per capita consumption of soybean oil from 0.006% to 7.38% of energy.” [7]

When the linoleic acid content of the diet is high because we are eating foods made with industrial seed oils, important components of our cells membranes incorporate higher amount of linoleic acid into them.

For example, cardiolipin is a phospholipid component found in the inner mitochondrial membrane, which is where all energy metabolism in our body occurs. Cardiolipin plays an important role in the function of several enzymes involved in mitochondrial energy metabolism.

When we eat a lot of pre-made and processed foods and food made in fast-food restaurants, cardiolipin ‘s fatty acid content becomes 90% linoleic acid, making it easily oxidized, affecting its function. If the diet is high in coconut oil and olive oil, cardiolipin will be higher in stearic and oleic acids and these fats are more stable fats than linoleic acid.

Literally, we are what we eat!

Cooking with Industrial Seed Oils

When industrial seed oils are heated such as they are in the making of commercial foods using them, they undergo rapid oxidation which means that they react with oxygen in the air to form toxic substances, including aldehydes and lipid peroxides.  Aldehydes are known neurotoxins and carcinogens, and are documented to contribute to DNA mutations, inflammation and hypersensitivity [8].

Heating polyunsaturated vegetable oils for just 20 minutes produces 20 times the permitted levels of aldehydes recommended as a maximum limit by the World Health Organization [8].

Keep in mind that at fast-food restaurants and in the preparation of commercial donuts and other fried food products, these industrial seed oils are used for frying everything from French fries to donuts and are heated over and over for extended periods of time, creating alarming levels of aldehydes and lipid peroxidation products.

When heated, industrial seed oils produce oxidized metabolites known as oxidized linoleic acid metabolites (OXLAMs) which have been also been implicated in the development of non-alcoholic fatty liver disease (NAFLD)[9].

In the body cell components such as cardioleptin with high amounts of linoleic acid are easily oxidized producing an oxidation product known as 4-hydroxynonenal (4-HNE) which has been implicated in the development of cancer [10].

Increasing Appetite

The high linoleic acid content of industrial seed oils also act on two endo-cannibinoids in the body (2-AG and Anandamide) which results in us feeling hungry, even when we have recently eaten –  in much the same way as cannabis (marijuana) does [11-12].  As a result, these industrial seed oils are believed to contribute to obesity and the associated health risks such as Type 2 Diabetes and high blood pressure.

Final Thoughts…

For fifty years, the public ate industrially-created trans fats in place of natural saturated fats and we only found out later that they were a major contributor to heart disease.

For the last forty years we have been eating industrial seed oils in greater and greater quantities place of natural saturated fat, but (a) given how these industrial seed oils are produced (solvents, high heats for extended period of time, bleach, etc.) and (b) given what is known about the very toxic products they produce when heated in production and how they are oxidized in the body and oxidized through heating when cooking, it is warranted to be very cautious about eating prepared foods made with them.

To avoid these industrial seed oils will take a concerted effort as they are in virtually everything we buy ready-made and many of the foods we eat out, but one solution is to cook real food using healthy sources of fat and to avoid these industrial seed oils that were created and marketed to us as supposedly healthy substitutes for natural fats.

The butter, lard and tallow of years gone by were made from animals that were pasture raised, not fed soybeans and corn as commercial animals are now, but in light of the mounting number of studies that indicate that saturated fat is not associated with increased risk of cardiovascular disease, perhaps it might be preferable to buy grass fed butter or render tallow or lard from the fat of pasture-raised animals for some cooking applications – rather than use these industrial seed oils that were created as substitutes.  Butter, lard and coconut oil (a vegetarian saturated fat) are all very low in linoleic acid and thus are very stable.  They are not easily oxidized in the body or by heating and produce very low levels of aldehyde and lipid peroxidation products when heated, compared with many of the industrial seed oils.

These are all factors we need to consider when deciding which fats our food should be made with.

The chart below shows the linoleic content of some common fats in blue.  Keep in mind that fats with the smallest amount of linoleic acid are the most stable and the least prone to oxidation (either in the body or when heated).

Comparison of Dietary Fats – linoleic acid content

A personal note: For non-heating uses, I use natural sources of monounsaturated fat such as cold pressed macadamia nut oil, hazelnut oil, avocado oil, and extra virgin olive oil and for cooking and heating uses I use a mixture of olive oil and coconut oil (to raise the smoke point), clarified butter (ghee) at higher temperatures and butter at lower temperatures and for baking. I read labels of all products I buy and deliberately avoid purchasing any food products that contain soybean oil, canola oil or sunflower oil and when I eat out, I ask that my food be prepared with coconut oil, butter or ghee.

While the jury is still “out” when in comes to saturated fat, it is my opinion that with the mounting evidence that eating saturated fat does not contribute to heart disease, using moderate use of butter, ghee (clarified butter) and coconut oil seems to me to be a more acceptable risk than eating foods made with, or fried in industrial seed oils.

I trust having the information contained in this article will help you make an informed choice for yourself and for those you cook for.

If you have questions about how I might be able to help you follow a low carb lifestyle -including selecting appropriate fats for use in your own cooking, please feel free to send me a note using the “Contact Me” form located on the tab above.

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

(continued from Part 1)

6. A.P. Simopoulos, Evolutionary aspects of the dietary omega-6:omega-3 fatty acid ratio: medical implications,World Rev Nutr Diet, 100 (2009), pp. 1-21

7. Tanya L Blasbalg, Joseph R Hibbeln, Christopher E Ramsden, Sharon F Majchrzak, Robert R Rawlings; Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century, The American Journal of Clinical Nutrition, Volume 93, Issue 5, 1 May 2011, Pages 950–962.

8. Grootvelt M, Rodada VR, Silwood CJL, Detection, monitoring, and
deleterious health effects of lipid oxidation products generated in culinary oils during thermal stressing episodes, Lipid Oxidation, November/December 2014, Vol. 25 (10)

9. Maciejewska, Dominika & Ossowski, Piotr & Drozd, Arleta & Karina, Ryterska & Dominika, Jamioł & Banaszczak, Marcin & Małgorzata, Kaczorowska & Sabinicz, Anna & Wyszomirska, Joanna & Stachowska, Ewa. (2015). Metabolites of arachidonic acid and linoleic acid in early stages of non-alcoholic fatty liver disease-A pilot study. Prostaglandins & other lipid mediators.

10. Zhong H, Yin H. Role of lipid peroxidation derived 4-hydroxynonenal (4-HNE) in cancer: Focusing on mitochondria. Redox Biology. 2015;4:193-199. doi:10.1016/j.redox.2014.12.011.

11. Alvheim AR, Malde MK, Hyiaman DO et al; Dietary Linoleic Acid Elevates Endogenous 2-AG and Anandamide and Induces Obesity, Obesity (2012) 20;1984-1994

12. Alveim AR, Torstensen BE, Lin YH et al, Dietary Linoleic Acid Elevates the Endocannabinoids 2-AG and Anandamide and Promotes Weight Gain in Mice Fed a Low Fat Diet, Lipids (2014) 49:59–69


Copyright ©2018 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.

Concerns with Polyunsaturated Vegetable Oils – Part 1

INTRODUCTION: Both the US and Canadian Dietary Guidelines encourage us to limit saturated fat in order to reduce the risk of heart disease and to eat unsaturated fat, including polyunsaturated fats and oils instead but what are these fats, where do they come from and what role might these play in development of obesity, Type 2 Diabetes, non-alcoholic fatty liver disease and even cancer?  This article is part 3 in the series titled Bad Fats and Enduring Beliefs.

Part 1 titled the Vilification of Saturated Fat can be read here and Part 2 titled Saturated Fat and Heart Disease can be read here.

“Polyunsaturated vegetable oils” is really a misnomer, as neither soybeans nor rapeseed / Canola are “vegetables”.  More accurately these should be called “industrial seed oils”, as they are seed crops that have been deliberately engineered for food use.  These are created oil products which are quite unlike natural oils that can be easily expressed from nuts, seeds and fruit using a millstone, as has been done since the Bronze Age [1].

Image result for ancient olive press
Ancient olive oil press

If you simply press olives, almonds, sesame or poppy seeds between your fingers you will be able to express a little bit of their oil on your fingers.

Not so with soybeans!

You can squeeze a soybean as hard as you like and for as long as you like and you are not going to get any oil out of it!

The first attempt at trying to express oil from soybeans occurred in the United States, a few years after the creation of Crisco® shortening in 1911.  For 3 long years (1922 – 1925) scientists tried over and over again to extract oil from soybeans  imported from Manchuria using hydraulic presses,  and time and time again they failed. Finally, in 1925 scientists turned to the use of chemical solvents  to get oil from soybeans and solvent extraction of soybean oil has been used ever since.

Trans Fats and Industrially Produced Shortening

In days gone by, deep-fat frying in restaurants (e.g. for French fries) was done in beef tallow, sometimes in lard. Pastry crusts were made with lard or butter, and baked goods such as cakes and brioches were usually made with butter – that is until 1911 when Crisco® shortening was invented. When it was noticed that hardened cottonseed oil used in the soap-making industry had an appearance like lard, scientists decided to further process it to remove the strong odor inherent with cottonseed oil, and market it to housewives as the ‘modern’ way to bake. You can read more about that here.

Beginning in the 1950s, trans fats (which occurs naturally in very small quantities) were industrially produced from other industrial seed oils such as soybean oil for use in other natural fat substitutes, including  margarine, fat for commercial baked goods and fat for deep-fat frying in the fast food industry [2]. Unfortunately, it was only in the late 1990s and early 2000s that it became widely-accepted by the scientific community that eating foods made with trans fats or fried in trans fats raised LDL-cholesterol while lowering protective HDL cholesterol, and also raised triglycerides; promoting systemic inflammation and contributing to the development of heart disease.

How ironic that the fats that were created to replace naturally-occurring saturated fats ended up being so detrimental to health!

After trans fats were discontinued due to their adverse health effects, industrial seed oils such as soybean oil and canola oil became the number one and number two oils of the food industry. These unsaturated (liquid) industrial seed oils have replaced saturated (solid) trans fat industrial oils in our food supply, however there is considerable evidence emerging which should cause us to question whether these fats are any safer (more on that below).

The Created Market for Industrial Seed Oils

The market for industrial trans fats and liquid industrial seed oils was itself created based a belief that ‘dietary saturated fat led to heart disease’.  Much  of what we have come to believe about this originated with a pathologist named Ancel Keys who proposed his ‘diet-heart hypothesis’ in the 1950s.

In 1970, Keys published his “Seven Country  Study” that reported that populations that consumed large amounts of saturated fats in meat and dairy had high levels of heart disease but when data from 22 countries that was available since 1957 was plotted, it was a great deal more scattered, indicating a much weaker association than Keys’ Seven Country  Study data indicated.

In August of 1967, Stare, Hegsted and McGandy, 3 Harvard researchers paid by the sugar industry published their reviews in the New England Journal of Medicine which vindicated sugar as a contributor of heart disease and laid the blame on dietary fat and in particular, saturated fat and dietary cholesterol (previous article on that topic here). Sponsorship of this research by the sugar industry certainly casts a dark shadow over their findings.

These 3 researchers insisted in their conclusion that there was a link between dietary cholesterol and heart disease and that there was “major evidence” which suggested that there was “only one avenue for diet to contribute to hardening of the arteries and the development of heart disease”,  but as covered in the previous article, it is known that a year after their publications (1968), the report of the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease because such a study had not yet been done.

Just 10 years after the sugar industry paid Stare, Hegsted and McGandy to write their reviewsHegsted was directly involved with developing and editing the 1977 US Dietary Guidelines which recommended that Americans decrease intake of saturated fat and cholesterol and increase dietary carbohydrate – entrenching the belief that saturated fat caused heart disease into American public health policy. That same year (1977), based on the same body of literature, Canada adopted very similar dietary guidelines around saturated fat…and the rest is history.

Public Health Policy Based Rooted in a Belief

For the last forty years Americans and Canadians have shunned natural fats such as butter, cream and lard in place of man-made margarine, non-dairy creamer and Crisco® – all in the enduring belief that ‘saturated fat is “bad” and leads to heart disease’.  Given that published reports vilifying saturated fat were funded by the sugar industry and that Ancel Keys study left out 2/3 of the nutrition and health data available at the time, it has become evident that public health policy was founded on what is now questionable data.

In addition, more and more current peer-reviewed published studies are concluding that saturated fat is not associated with an increased risk of developing cardiovascular disease. In the recent article titled Saturated Fat and Heart Disease, I outlined the findings of 8 recent meta-studies and systematic reviews and one worldwide epidemiological study which call into question the enduring belief that dietary saturated fat increases the risk of developing heart disease.

In a follow up to the above article, titled More Animal Fat Consumption Less Cardiovascular Disease, I also summarize the findings of a newly published worldwide study which found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease.

If saturated fat is not associated with increased risk of heart disease then should we be eating industrial seed oils that were created and marketed as a replacement for them?

Creation of Industrial Seed Oils

Inexpensive soybean oil has been the leading oil used in food production in the United States since 1945 [3]. It was previously made into a hard fat through hydrogenation and sold to consumers as trans-fat based shortening and margarine and came into wide-spread use as both synthetic hard fat and as a food-based oil product in the late-1960s.

In Canada, soybean oil is just behind canola oil in terms of the most used, and canola is another industrial seed oil that was created by science. In 1978 rapeseed, a prairie weed was specially bred in Canada to produce a novel plant that was lower in erucic acid (a toxin found in rapeseed) and this new plant was named “canola” (‘Canadian Oil’).

A 2015 study on Canadian vegetable oil purchased and eaten in Canada found that in 2013, 42% was canola oil (a Canadian bio-engineered industrial seed oil) and 20% was soybean oil, an industrially-engineered seed oil developed in the US [4]. Keep in mind this figure excludes food products available in Canada that are manufactured in the US, which uses predominantly soybean oil.

Soybean Oil is a Modern, Industrial Product

According to an article titled “Soybeans Are Ancient; Oil Is Not” published in the Wall Street Journal in 2011 [5], soybeans as the basis for tofu and soy sauce is an ancient food in China, but soybean oil was virtually unknown until global food oil shortages during World War I created an interest to extract the fatty part of the soybean for oil. Soybean oil is a modern creation.

How is oil made from seeds such as soybean and canola?

“Soybeans are first crushed into crude oil and then refined to remove impurities like free fatty acids. Over days, the crude is “neutralized” of acidity with phosphoric acid, “winterized” through filters that remove wax, bleached at high heat to lighten the color and finally vacuum “deodorized” to eliminate impurities.” [5]

The extraction of soybean oil involves the industrial processing of soybeans with solvents at very high heats over an extended length of time in order to have the soybean give up its small amount of oil.

Solvent extraction of canola oil occurs in a similar method, beginning with an hour or more ‘wash’ of the rapeseed with a hexane solvent, then a sodium hydroxide wash. Bleach is then used to lighten the cloudy color of the processed oil and then it is steamed injected at high temperatures to
remove the bitter smell.

Yummy! Now this oil is ready to sell to the public to cook with and eat!

Should we even be eating these industrial seed oils?

Are they any safer than trans fats that were approved for consumption for 50 years and later found to contribute to heart disease?

Part 2 of this article will continue in Concerns with Polyunsaturated Vegetable Oils – Part 2.

If you have questions about how I might be able to help you follow a low carb lifestyle -including selecting appropriate fats for use in your own cooking, please feel free to send me a note using the “Contact Me” form located on the tab above.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Alfred Thomas (2002). “Fats and Fatty Oils”. Ullmann’s Encyclopedia of Industrial Chemistry. Weinheim: Wiley-VCH.
  2. “Tentative Determination Regarding Partially Hydrogenated Oils”. Federal Register. 8 November 2013. 2013-26854, Vol. 78, No. 217.
  3. Dutton, HJ. Journal of the American Oil Chemists Society, Vol. 58, No.3 Pages: 234-236 (1981),  https://pubag.nal.usda.gov/pubag/downloadPDF.xhtml?id=26520&content=PDF
  4. Schaer, L., Grainews, Canola gets competition from soybeans, Feb 01, 2016, https://www.grainews.ca/2016/02/01/canola-gets-competition-from-soy/
  5. Wall Street Journal, “Soybeans Are Ancient; Oil Is Not”, 2011, https://blogs.wsj.com/chinarealtime/2011/01/03/soybeans-are-ancient-oil-is-not/

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.

Special thanks to Tucker Goodrich for getting me thinking in this regard.

 

New Study – More Animal Fat Consumption less cardiovascular disease

INTRODUCTION: A brand new study published last week in Nutrients looked at health and nutrition data from 158 countries worldwide and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease. As well, the study found that high carbohydrate consumption, particularly as cereals and wheat was most associated with the risk of cardiovascular disease. Significantly, both of these relationships held up regardless of a nation’s average national income.

Data from this study adds to the mounting evidence from 8 recent meta-analyses and systemic reviews of randomized control trials (RCT) summarized in this article that did not find an association between  saturated fat intake and the risk of heart disease[1-8]. It also supports evidence from the recent global PURE (Prospective Urban and Rural Epidemiological) study published in The Lancet this past December which found that those who ate the largest amounts of saturated fats had significantly reduced death rates, and that those that ate the lowest amounts of saturated fat (6-7% of calories) had increased risk of stroke [9].

Global Correlates of Cardiovascular Risk: a comparison of 158 Countries

This new study compared the average intake of 60 food items with obesity rates and life expectancy in 158 countries and found that a relationship existed between eating specific foods and raised blood pressure, death from cardiovascular disease and raised blood glucose (high blood sugar) — all of which are associated with cardiovascular disease.  The study examined nutritional data from  1993-2011 and found that total fat consumption and animal fat consumption were the dietary factors least associated with the risk of cardiovascular disease and that high carbohydrate consumption, especially as cereals and wheat was the dietary factor most associated with the risk of cardiovascular disease [10].

These findings add to the mounting evidence which calls into question whether dietary saturated fat is related to heart disease.

Total Cholesterol and Cardiovascular Risk

The present study found that eating animal fat and animal protein raised total cholesterol, however total fat and animal protein consumption were found to have a very impressive negative relationship with cardiovascular death in the European data, and a moderately negative relationship to cardiovascular death, worldwide. That is, the more total fat and animal protein eaten, the lower cardiovascular death rates were.

Often in studies,  the assumption is that high LDL is linked to risk of cardiovascular disease – not that there is a direct relationship between animal / saturated fat and cardiovascular disease.  That is, high LDL is a surrogate marker of cardiovascular disease. But does that assumption hold weight?

Perhaps a better question is “which LDL”? Small, dense LDL cholesterol  which easily penetrates the artery wall is associated with heart disease [11,12,13,14], but the large, fluffy LDL cholesterol is not [15,16], so studies seeking to impute LDL as the cause of cardiovascular diseasee need to differentiate between these LDL particles.

As well, total cholesterol is made up of the different sub-particles of LDL cholesterol, HDL cholesterol, VLDL cholesterol and triglycerides (TG), so lumping them all in together as ‘total cholesterol’ doesn’t tell us anything about risk of cardiovascular disease. We know that dietary saturated fat consistently raises the “good” HDL-cholesterol — which moves cholesterol away from the arteries and back to the liver where it can either be re-used or eliminated [17,18], so higher saturated fat intake will raise “good” HDL cholesterol, which in turn will raise total cholesterol. Total cholesterol going up is not a ‘bad’ thing.

What is important is not that total cholesterol went up but that along with increased total cholesterol, cardiovascular disease went down.

Higher Blood Sugar Associated with Higher Consumption of Cereals and Wheat

One finding of this study was that higher blood sugar (a known risk factor for cardiovascular disease) was most strongly associated with indicators of obesity such as high body mass index (BMI). What was new however is that higher consumption of cereals, especially cereals and wheat was associated with higher cardiovascular disease.

Researchers remarked that such results were not surprising “because the links between raised blood glucose, obesity, type 2 diabetes and cardiovascular disease are well established [19]”.

“…regardless of the statistical method used, the results always show very similar trends and identify high carbohydrate consumption (mainly in the form of cereals and wheat, in particular) as the dietary factor most consistently associated with the risk of CVDs.

High carbohydrate consumption, particularly as cereals and wheat was the dietary factor most consistently associated with the risk of cardiovascular disease.

Researchers looked at a maximum number of potentially significant variables and compared them to results across different regions and time periods and while they acknowledged that the accuracy of the data from developing countries may be lower, the global results that they found confirmed their earlier 2016 study data from European data only which found a significant link between cardiovascular disease and high carbohydrate consumption [20].

Of significance, the above associations held up regardless of a nation’s average national income.

Given these finding support those of the PURE epidemiological study [9] would lend support the notion that one can compare data between countries of substantially different level of income (as the PURE study did) and that high-carbohydrate and low-fat diets are not necessarily associated with poverty, as claimed [21].

The PURE study findings and those of this present study challenge the very basis of the long-standing ‘diet-heart hypothesis’ and it certainly results in some uncertainty as to what constitutes a healthy diet.

In my view, what is needed are some well-designed randomized controlled trials to determine if saturated fat intake is directly associated with cardiovascular disease – and not associated with a surrogate marker, such as LDL cholesterol.

Purported Weakness of the Data

Self-reported food-frequency questionnaires on which this study is based have long been criticized as being unreliable, however it is important to note that in the United States the NHANES Dietary Data and the Continuing Survey of Food Intakes by Individuals (USA) has also collected data using food-frequency questionnaires and such data is used as the “cornerstone to inform nutrition and health policy” [22].

In Canada, the Canadian Community Health Survey (CCHS) relies on a 24-hour recall data which is known to researchers to result in under-reporting of food intake, especially among those with a high BMI and with adolescents [23].  Given that the 2017 Obesity Update found Canada among its most overweight countries — with 25.8% of the population aged 15 and over considered obese [24], the CCHS data becomes less and less reliable, as obesity rates continue to climb.

Enduring Belief – despite recent evidence

The results of this most recently published study embody the same findings as the recent global PURE (Prospective Urban and Rural Epidemiological) study [9] publish this past December in The Lancet which found a link between raised cholesterol and lower cardiovascular risk.

This study also confirms the findings of the eight recent meta-analysis and systemic reviews of randomized control trials (RCT) summarized in the previous article which did not find an association between saturated fat intake and the risk of heart disease [1-8].

Yet, in spite of recent robust evidence there is an enduring belief that ‘saturated fat causes heart disease’ — a belief which has influenced nutrition guidelines in both the US and Canada for 40 years (since 1977).

As elaborated on in a recent article, it is now known that the ‘diet-heart hypothesis’ originated by Ancel Keys and supposedly confirmed in his ‘Seven Countries Study’ omitted known data from 22 available countries  and that when all countries were factored in there was a great deal more scatter showing a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s data.

Also as covered previously, it has been known since December 2016 that the three Harvard researchers who vindicated sugar as the cause of heart disease and blamed dietary fat — were funded by the sugar industry and that one one of those 3 researchers, Dr. DM Hegsted contributed to and edited the 1977 US Dietary Guidelines which embodied his findings of 10 years earlier, advising Americans to reduce their intake of saturated fat and cholesterol in order to reduce their risk of heart disease.

Also covered in a previous article, Canadian Dietary Recommendations regarding dietary intake of saturated fat were based on ‘health claim assessments’ conducted by Health Canada in 2000 (18 years ago) titled Dietary Fat, Saturated Fat, Cholesterol, Trans Fats and Coronary Heart Disease which was based on the US literature available from 1993-2000 and which concluded that a health risk exists between saturated fat and heart disease.

Given all of the factors mentioned above, it is my conviction that before the American and Canadian governments revise their respective national Dietary Guidelines what is needed is for them to conduct a long-overdue external, independent scientific review of the current evidence for the enduring belief that saturated fat contributes to heart disease.

If you have questions as to how I can help you live a low carb lifestyle, please send me a note using the “Contact Me” form located on the tab above.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
  2. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
  3. Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406
  4. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
  5. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
  6. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
  7. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
  8. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
  9. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  10. Grasgruber P, Cacek J, Hrazdira E, et al, Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries, Nutrients 201810(4), 411.
  11. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189–99
  12. Gardner CD, Fortmann SP, Krauss RM, Association of Small Low-Density Lipoprotein Particles With the Incidence of Coronary Artery Disease in Men and Women, JAMA. 1996;276(11):875-881
  13. Lamarche B, Tchernof A, Moorjani S, et al, Small, Dense Low-Density Lipoprotein Particles as a Predictor of the Risk of Ischemic Heart Disease in Men, 
  14. Packard C, Caslake M, Shepherd J. The role of small, dense low density lipoprotein (LDL): a new look, Int J of Cardiology,  Volume 74, Supplement 1, 30 June 2000, Pages S17-S22
  15. Genest JJ, Blijlevens E, McNamara JR, Low density lipoprotein particle size and coronary artery disease, Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:187-195
  16. Siri-Tarino PW, Sun Q, Hu FB, Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, The American Journal of Clinical Nutrition, Volume 91, Issue 3, 1 March 2010, Pages 502–509
  17. Mensink RP, Zock PL, Kester A, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, The American Journal of Clinical Nutrition, Volume 77, Issue 5, 1 May 2003, Pages 1146–1155
  18. Toth PP, The “Good Cholesterol” – High Density Lipoprotein, Circulation 2005;111:e89-e91
  19. Després, J.P.; Lemieux, I.; Alméras, N. Abdominal obesity and the metabolic syndrome. In Overweight and the Metabolic Syndrome; Springer: New York, NY, USA, 2006; pp. 137–152
  20. Grasgruber, P.; Sebera, M.; Hrazdira, E.; Hrebickova, S.; Cacek, J. Food consumption and the actual statistics of cardiovascular diseases: An epidemiological comparison of 42 European countries. Food Nutr. Res. 201660, 31694.
  21. Sigurdsson, AF, The Fate of the PURE Study – Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/
  22. Ahluwalia N, Dwyer J, Terry A, et al; Update on NHANES Dietary Data: Focus on Collection, Release, Analytical Considerations and Uses to Inform Public Policy, Advances in Nutrition, Volume 7, Issue 1, 1 January 2016, Pages 121–134
  23. Health Canada, Reference Guide to Understanding and Using the Data – 2015 Canadian Community Health Survey – Nutrition, June 2017
  24. OECD Health Statistics 2017, June 2017, http://www.oecd.org/els/health-systems/Obesity-Update-2017.pdf

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

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

Saturated Fat and Heart Disease – Bad Fat Enduring Beliefs Part 2

This is Part 2 in the series which examines the enduring belief that dietary saturated fat causes heart disease.

INTRODUCTION: The “diet-heart hypothesis” is the belief that saturated fat and dietary cholesterol cause heart disease was first proposed by Ancel Keys in the 1950s. He encouraged Americans to reduce their fat intake by a third, while at the same time openly admitted as late as 1967 that there was little direct evidence that a change in diet would reduce the risks of arteriosclerosis [1]. As covered in the first part of this article, three Harvard researchers, Stare, Hegsted and McGrady were paid generously by the sugar industry to publish their review in the New England Journal of Medicine vindicating sugar as a cause of heart disease and laying the blame squarely on dietary fat; and in particular on saturated fatThese researchers concluded that there was “only one avenue” by which diet contributed to the development and progression of “hardening of the arteries” (atherosclerosis), resulting heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids [2].  This sounds like a very certain claim, however it is known that they lacked evidence because a year later (1968) a report from the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease – because such a study had not yet been done (see Part 1) [3].

Fast forward ten years and in 1977, one of the three researchers who was paid by the sugar industry, Dr. DM Hegsted contributed to and edited the 1977 US Dietary Guidelines [4], which embodied his findings 10 years earlier. Americans were told they should reduce their intake of saturated fat and cholesterol to reduce their risk of heart disease.

The rest, they say, is history.

The same year (1977), Canada’s Food Guide recommended that Canadians  limit fat to <30% of daily calories with no more than 1/3 from saturated fat, but did not specify an upper limit for dietary cholesterol. This was based on the belief that total dietary fat and saturated fat were responsible blood levels of LDL cholesterol levels and total serum cholesterol, not dietary cholesterol [5].

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

The question is does it?

NOTE TO CANADIANS: Canadian Dietary Recommendations regarding dietary intake of saturated fat are based on ‘health claim assessments’ conducted by Health Canada which are directly tied to American research and recommendations.  Eighteen years ago, Health Canada reviewed the ‘health claim’ regarding Dietary Fat, Saturated Fat, Cholesterol, Trans Fats and Coronary Heart Disease and based on the US literature available from 1993-2000 and concluded that a health risk exists between saturated fat and heart disease, as stated here; “The effectiveness of lowering dietary saturated fat in reducing plasma cholesterol, especially low-density lipoprotein (LDL)- cholesterol, the major risk factor for CHD, is well established.” Since Health Canada’s review in 2000 (18 years ago), the link between dietary saturated fat and heart disease remains public health policy.

While it has been shown that saturated fats can raise LDL-cholesterol such a finding is meaningless unless it is specified which type of LDL-cholesterol  goes up. There is more than one type of LDL-cholesterol, small, dense LDL cholesterol which easily penetrates the artery wall is associated with heart disease [6,7,8,9], whereas the large, fluffy LDL cholesterol is not [10, 11].

Another factor that needs to be considered is that dietary saturated fat also consistently raises the “good” HDL-cholesterol which moves cholesterol away from the arteries and back to the liver, where it can either be re-used or eliminated [12,13].

What are the findings of current scientific literature?

Eight recent meta-analysis and systemic reviews which reviewed evidence from randomized control trials (RCT) that had been conducted between 2009-2017 did not find an association between saturated fat intake and the risk of heart disease [14-21].

Furthermore, recently published results of the largest and most global epidemiological study published in December 2017 in The Lancet [23] found that those who ate the largest amount of saturated fats had significantly reduced rates of mortality and that low consumption (6-7% of calories) of saturated fat was associated with increased risk of stroke.

Here is a synopsis of the findings of the eight meta-analysis and systemic reviews;

“Intake of saturated fatty acids was not significantly associated with coronary heart disease mortality” and “saturated fatty acid intake was not significantly associated coronary heart disease events”

Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled

“There were no clear effects of dietary fat changes on total mortality or cardiovascular mortality”.

Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)

“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406

“The present systematic review provides no moderate quality evidence for the beneficial effects of reduced/modified fat diets in the secondary prevention of coronary heart disease. Recommending higher intakes of polyunsaturated fatty acids in replacement of saturated fatty acids was not associated with risk reduction.”

Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4

“The study found no statistically significant effects of reducing saturated fat on the following outcomes: all-cause mortality, cardiovascular mortality, fatal MIs (myocardial infarctions), non-fatal MIs, stroke, coronary heart disease mortality, coronary heart disease events.”

Note: The one significant finding was an effect for saturated fats on cardiovascular events however this finding lost significance when subjected to a sensitivity analysis (Table 8, page 137).

Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)

“Epidemiological evidence to date found no significant difference in CHD mortality and total fat or saturated fat intake and thus does not support the present dietary fat guidelines. The evidence per se lacks generalizability for population-wide guidelines.”

Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749

“Available evidence from randomized controlled trials (1968-1973) provides no indication of benefit on coronary heart disease or all-cause mortality from replacing saturated fat with linoleic acid rich vegetable oils (such as corn oil, sunflower oil, safflower oil, cottonseed oil, or soybean oil).”

Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353

“Available evidence from adequately controlled randomised controlled trials suggest replacing saturated fatty acids with mostly n-6 PUFA is unlikely to reduce coronary heart disease events, coronary heart disease  mortality or total mortality. These findings have implications for current dietary recommendations.”

Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30

Only one recent meta analysis conducted by the American Heart Association (by the authors of the Diet-Heart Policy for Americans, mentioned above) found a relationship between saturated fat intake and coronary heart disease, yet failed to examine cardiovascular mortality (death) or total mortality [22].

NOTE: In 1961, the American Heart Association was the author of the original policy paper recommending to limit saturated fats to protect against heart disease and therefore has a significant interest in defending its longtime institutional position.

With the exception of the American Heart Association review, the conclusion of 9 different meta-analysis and review papers of randomized control trials conducted by independent teams of scientists worldwide do not support the belief that dietary intake of saturated fat causes heart disease.


The PURE (Prospective Urban Rural Epidemiology) was the largest-ever epidemiological study and was published in The Lancet in December 2017 [23]. It recorded dietary intake in 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations.  It found;

“High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.”

Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062

Those critical of the study say that it has methodological problems, including problems related to the authors dividing consumption of macronutrients (protein, fat and carbohydrate) into 4 groups (quintiles).  Some say that this is reason the data showed an inverse relationship between saturated fat and cardiovascular disease [24]. Criticisms also include that one cannot compare data between countries of substantially different level of income because “low fat consumption is very uncommon in high income countries” and that ‘the ability to afford certain foods may change the dietary pattern (e.g. high-carbohydrate and low-fat diets may be associated with poverty) [24].

Final thoughts…

Both the American and Canadian governments are currently in the process of revising their Dietary Guidelines and I feel that what is needed now is an external, independent scientific review of the current evidence-base for the belief that saturated fat contributes to heart disease.

Have questions or need support following a low carb lifestyle in a way that makes sense for you?

Please send me a note using the “Contact Me” tab above and I will reply shortly.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

 

References

  1. Keys A, Aravanis C, Blackburn HW et al. Epidemiological studies related to coronary heart disease: characteristics of men aged 40–59 in seven countries Acta Med Scand 1967 460: 1–392.
  2. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242–47
  3. The National Diet-Heart Study Final Report.” Circulation, 1968; 37(3 suppl): I1-I26. Report of the Diet-Heart Review Panel of the National Heart Institute. Mass Field Trials and the Diet-Heart Question: Their Significance, Timeliness, Feasibility and Applicability. Dallas, Tex: American Heart Association; 1969, AHA Monograph no. 28.
  4. Introduction to the Dietary Goals for the United States – by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF
  5. McDonald BE, The Canadian experience: why Canada decided against an upper limit for cholesterol, J Am Coll Nutr. 2004 Dec;23(6 Suppl):616S-620S.
  6. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189–99
  7. Gardner CD, Fortmann SP, Krauss RM, Association of Small Low-Density Lipoprotein Particles With the Incidence of Coronary Artery Disease in Men and Women, JAMA. 1996;276(11):875-881
  8. Lamarche B, Tchernof A, Moorjani S, et al, Small, Dense Low-Density Lipoprotein Particles as a Predictor of the Risk of Ischemic Heart Disease in Men, 
  9. Packard C, Caslake M, Shepherd J. The role of small, dense low density lipoprotein (LDL): a new look, Int J of Cardiology,  Volume 74, Supplement 1, 30 June 2000, Pages S17-S22
  10. Genest JJ, Blijlevens E, McNamara JR, Low density lipoprotein particle size and coronary artery disease, Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:187-195
  11. Siri-Tarino PW, Sun Q, Hu FB, Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, The American Journal of Clinical Nutrition, Volume 91, Issue 3, 1 March 2010, Pages 502–509
  12. Mensink RP, Zock PL, Kester A, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, The American Journal of Clinical Nutrition, Volume 77, Issue 5, 1 May 2003, Pages 1146–1155
  13. Toth PP, The “Good Cholesterol” – High Density Lipoprotein, Circulation 2005;111:e89-e91
  14. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
  15. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
  16. Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406
  17. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
  18. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
  19. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
  20. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
  21. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
  22. Sachs FM, Lichtenstein AH, Wu JHW et al, Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association,  Circulation. 2017 Jul 18;136(3)
  23. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  24. Sigurdsson, AF, The Fate of the PURE Study – Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/

Note: References 11-23 were from a document prepared by the Nutrition Coalition

Special thanks to Dr. Carol Loffelmann and Dr. Barbra Allen Bradshaw of The Canadian Clinicians for Therapeutic Nutrition for their tireless research.


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.

 

Low Carb Diets are not one size fits all

Some people imagine that a low carb lifestyle involves plates laden with bacon and eggs, huge steaks and meals devoid of vegetables, dairy foods, and nuts or seeds, but this is a misconception.

While there are individuals that choose to eat “zero-carb” for a variety of personal reasons, it is not something I promote outside of being prescribed by a physician for therapeutic management of a specific medical condition.

I encourage people to eat a wide variety of low carb vegetables, some fruit and dairy products, as well as nuts and seeds – all of which have some carbohydrate in them. There is no one-size-fits-all low carb diet, but there are a few low carbohydrate approaches which can be chosen from depending on a person’s medical and metabolic conditions, any medications they may be taking, as well as stage of life and lifestyle factors.

Another fallacy is that low carb diets involve “lots of meat for dinner” and “eggs every morning for breakfast” but people eating low carb can eat a wide variety of food for breakfast and meals can be vegetarian or pescatarian (include fish and seafood) and involve no meat whatsoever. This makes a low carb suitable for those that don’t eat meat or eggs for religious or ethical reasons.

Three main low carb approaches are;

(1) low carb higher protein

(2) low carb higher healthy fat

(3) higher protein / lower fat intake during weight loss, then a moderate protein / high healthy fat intake during weight maintenance.

What makes a low carb diet ketogenic is the low amount of carbohydrate that is eaten relative to the overall caloric intake, so not all low carb diets are ketogenic.

Low carbohydrate and therapeutic ketogenic diets have a variety of clinical applications. For example, a ketogenic diet may be prescribed by a person’s physician for management of epilepsy or seizure disorder, for treatment of some kinds of cancer, or for weight loss before and after bariatric surgery. Different types of low carb diets may be used for improving insulin sensitivity in Type 2 Diabetics or those with pre-diabetes, improving fatty liver disease, for reducing symptoms of Polycystic Ovarian Syndrome (PCOS) or for gradual weight loss.

[Another misconception is that low carb diets are used for “rapid weight loss”, which is not the case.]

For each type of low carb diet the ratio of protein to fat is specific to the clinical condition and person’s requirements. Everybody’s macronutrient  needs (the amount of protein, carbs and fat they require) as well as overall energy needs are different and are dependent on several factors including their gender, age, height, weight, clinical conditions and any medications they’re taking.

Our body requires essential amino acids found in the protein foods we eat, as well as essential fatty acids found in the different types of fat we eat, along with essential vitamins and minerals however there is no essential requirement for dietary carbohydrate – provided that “adequate amounts of protein and fat are consumed” (Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids, 2005). This article will elaborate, but explaining it in simple terms, it means is that our body does not need to have carbohydrate in food if we eat sufficient protein with all the essential amino acids and sufficient fat with the essential fatty acids.

That doesn’t mean that I recommend that people without a clinical reason eat food with no carbohydrate in it (I don’t), as they wouldn’t be able to eat any vegetables, fruit, dairy, nuts or seeds – as these all of these have some carbohydrate in them.

I encourage people to eat a wide range of food from a variety of categories to ensure they have adequate dietary intake. I recommend whole, unprocessed foods that are naturally low in carbohydrate, including non-starchy vegetables, plant fats (such as olive oil, avocado oil, macadamia or walnut oil, coconut oil), low sugar fruit (such as tomato, lemon, lime, cucumber), meat, fish, poultry and seafood of all varieties, and small amounts of animal fat such as butter and cream.

If people working toward losing weight then the fat that is naturally found in meat is okay, but I would encourage them to trim excess visible fat. Unless there is a compelling reason not to, folks can add a bit of cream to their coffee or some butter on top of their cooked vegetables if they like it (especially if they’ll eat more veggies that way) but I don’t encourage people to ‘add fat’ to foods for the sake of adding fat (e.g. ‘bulletproof’ coffee or ‘fat bombs’).  That said, there is nothing intrinsically ‘dangerous’ about eating fat, even saturated fat but what needs to be considered is “how much” and “how often”.

High blood cholesterol and high triglycerides is the result of eating too much carbohydrate, not eating too much saturated fat, or dietary cholesterol.

A healthy person that eats more carbohydrate than their body can use will move the excess carbohydrate they eat off to their liver and will make triglyceride and LDL cholesterol and store the rest as fat.  A person who is insulin resistant or has Type 2 Diabetes may have high blood sugar levels but even if a person has normal blood sugar levels, their high carbohydrate intake may be reflected in their “cholesterol tests”.  Often what we see in such cases is high triglyceride results or high LDL cholesterol results or both. This easy-to-understand article titled Understand High Blood Sugar & High Cholesterol will explain the process in more detail. If eating excess carbohydrates continues for an extended period of time, it ‘s possible that non-alcoholic fatty liver disease (NAFL) may develop.

Each person’s ability to tolerate carbohydrate is different – depending whether they are insulin sensitive, insulin resistant or Type 2 Diabetic. Someone who is insulin sensitive for example can eat considerably more carbohydrate without causing a spike in their blood glucose level than someone who is insulin resistant. For those who are Type 2 Diabetic, both the degree of insulin resistance and the length of time they’ve been Type 2 Diabetic will affect the amount of carbohydrates they can tolerate. To explain this, I like to use the analogy of ‘lactose intolerance’.  Some people who are lactose intolerant can manage to drink and eat milk products, provided the quantities are small and the person doesn’t have it too often. Others who are lactose intolerant can’t even tolerate a small amount of lactose without symptoms. Ability to tolerate carbohydrate is similar.  People who are insulin sensitive or only mildly insulin resistance will be able to tolerate more carbohydrate than those who are very insulin resistant or have had Type 2 Diabetes a long time.

The average intake of carbohydrate in the Canadian diet is ~ 300 g per day, which is a lot. People who are insulin sensitive or mildly insulin resistance may do well lowering their carbohydrate amount to a moderate level whereas those who are insulin resistant or Type 2 Diabetic will likely need to eat considerably less carbohydrate in order to begin to see their blood sugar levels or cholesterol / triglyceride levels come down.

Factors that can affect how much carbohydrate a person can tolerate include gender, whether or not they are insulin sensitive or insulin resistant (and to what degree) and whether they have Type 2 Diabetes and if so, for how long.

What some people find challenging about deciding to follow a low carb lifestyle is knowing how much protein they need to eat, the amount and types of fat they can use, as well as the total amount of carbohydrate they can tolerate, as well as how those carbohydrates should best be distributed throughout the day.

Where it becomes particularly challenging is when people have Type 2 Diabetes or high blood pressure and are prescribed medications for these conditions.  In such cases, it’s not as simple as them just “cutting carbs” because by not doing so gradually it could result in a sudden drop in blood sugar or blood pressure which could be dangerous. People taking medications for these conditions (or for some other conditions) need to be monitored by their doctors and the reality is that not all doctors have more than a few minutes to see patients and may not feel equipped to counsel them on diet. This is where working with a Dietitian that’s knowledgeable and familiar with the use low carb diet is very helpful as they can coordinate dietary and lifestyle changes with your doctor while they monitor your health and adjusts the levels of prescribed medications, as needed.

Another situation where it can be very helpful to have a Dietitian’s support is when youth or teenagers need to lose weight, or bring down their blood sugar, cholesterol or blood pressure levels, because a there’s a need to ensure that they have adequate intake to support healthy growth.

Have questions?

Please send me an note using the “Contact Me” form on the tab above and I will reply as I am able.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


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

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

 

 

Time Frame of an Epidemic

It occurred to me that the time frame for an epidemic to occur is absolutely critical in determining public response. If rates of a disease went from 1 in 10 people to 1 in 3 people in only 10 years, there would be public outcry for scientists to determine the cause and to find a cure quickly. If the disease caused debilitating metabolic effects such as very high blood pressure that resulted in heart attacks or strokes and people of all ages were getting this disease, with many dying – the outcry would be even more urgent.

But what if rates of the same disease went from 1 in 10 people to 1 in 3 people over a period of 40 or 50 years? The current generation would have no recollection of what it was like ‘before’ because things had always been this way since they were kids.  The older generation would remember what it was like ‘before’ and concluding that for whatever reason, that is the way it is now. Doctors and scientists of the older generation that might be able to apply their knowledge and skill to find the cause and a cure would be at the end of their working lives.

The disease is obesity.

Debilitating metabolic side effects of obesity include very high blood pressure that can lead to heart attacks and strokes and Type 2 Diabetes which can result in blindness, amputations and organ failure.

Once a rare disease, obesity has now reached epidemic proportions and the metabolic side effects are not just for the old, but are rampant among youth and young adults.

This disease epidemic has taken place over 50 years but few are noticing because it has fallen between the cracks of time.

Obesity Rates Then and Now

Photographs and videos of what people looked like fifty years ago are widely available, and a simple Google search will provide an abundance of them. Movies, documentaries and TV shows from the mid-1960s also provide a glimpse of what the average American and average Canadian looked like then.

In the 1960s only 10.7% of the US population and 10.2% of the Canadian population were obese; that’s approximately 1 in 10 people.

Below is a US sorority photo of a Sigma Iota Chi chapter from West Virginia from 1967. Look how slim most of the women are compared to today’s young adults.

SIX 1967.png
Sigma Iota Chi Sorority – West Virginia – 1967 (https://sororityhistories.wordpress.com/tag/sigma-iota-chi/)

West Virginia now has one of the highest adult obesity rate in the US.

Related image
1967 Kappa Alpha Fraternity Party Photograph – Cornell University

To the left is another photo from a 1967 Fraternity party at Cornell University. For the most part, the young men and their girlfriends are slim and lean – certainly much slimmer than university students today.

Below is what the average city-dwelling Canadian looked like in 1967, riding the subway in Toronto. Young adults, middle aged adults and older people were very slim compared to today’s standards – especially when compared to what the average public transit rider looks like today.

toronto subway rush hour

Most recent international data from 2015 found that 38.2% of the US population and 25.8% of the Canadian population are obese; that’s more than 1 in 3 people in the US and more than 1 in 4 people in Canada [1].

People in both countries are now some of the most obese in the world;

OECD Health Statistics 2017, June 2017

When one compares what university students looked above to what they look like now in a current photo of Fraternities and Sororities below, the difference in average body weight of the students from 50 years ago to today is quite apparent – despite the fact that university students come from families where the average family income is significantly higher than the national average.

Given this, their higher body weights cannot be dismissed due to low income, socioeconomic status or lack of education. So what is going on?

University of Nevada’s Fraternity and Sorority Community

What changed in the last 50 years that contributed to this obesity epidemic?

As written about in a previous article, in 1967 (fifty years ago) the sugar industry paid three Harvard researchers (Stare, Hegsted and McGandy) very handsomely to critique studies that vindicated sugar as contributing to abnormal fat metabolism and heart disease, and who instead laid the blame on dietary fat, and in particular  saturated fat and dietary cholesterol [2,3].

They concluded;

“Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol…the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.” [4]

These researchers who were sponsored by the sugar industry concluded that there was “major evidence” which  suggested that there was only ONE avenue for diet to contribute to hardening of the arteries and the development of heart disease – and that was dietary fat and cholesterol…yet only a year later in 1968, the Diet-Heart Review Panel of the National Heart Institute recommended that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease – because such a study had not yet been done [5].

No major study had yet been done to find out whether changing the types of fat we ate prevented heart disease, yet these researchers were SO certain that there was “only one avenue” for diet to contribute to hardening of the arteries and the development of heart disease. How much was their certainly impacted by their sponsors?

Their influence didn’t end there.

Only ten years later, one of the three Harvard researchers (Hegsted) was directly involved with developing and editing the 1977 US Dietary Guidelines [6] which recommended a decrease in saturated fat and cholesterol  consumption, and an increase in dietary carbohydrate. While Canadian Dietary Guidelines are distinct from the US ones, much of the research on which they are based is the same.

Comparing the US to Canadian dietary recommendations with respect to the consumption of fat in general, as well as the consumption of saturated fat in particular, one finds the recommendations mirror each other.

We are told to limit saturated fat ostensibly because of its negative impact on blood cholesterol and heart disease. We are told to increase consumption of vegetable oils, and to substitute polyunsaturated fats for saturated fat in cooking and baking and to eat 45-65% of our daily calories as carbohydrate.

It is increasingly my conviction that the simultaneous (1) marketing of polyunsaturated vegetable oil – more accurately called industrially-created seed oils, such as soybean oil and canola oil, along with (2) changes in the Dietary Recommendations in both Canada and the US for people to (a) limit calories from fat and especially to (b) limit saturated fat, combined with the recommendations for people to (c) eat 45-65% of calories as carbohydrate created the “perfect storm” that when viewed together,  explains the obesity epidemic we now have and the associated increase in metabolic health problems that we now see 50 years later.

I will be writing more in the days ahead on what is thought to be the role of these industrially-created seed oils in the process of obesity and inflammation that underlies many metabolic conditions, including Type 2 Diabetes.

Why isn’t the public alarmed by this massive increase in obesity?

I believe it’s because it took place over such a long period of time that those old enough to remember what things were like before have either died or are approaching retirement age and have left its solution to the next generation, and those young enough to do something about it have never known it any other way.

I think that looking at the magnitude of the epidemic without the time frame is helpful.

What if only 10 years ago, only 1 in 10 people were obese and now 1 in 3 people were obese? Would there not be a public outcry for scientists to determine what caused this and to research to find a cure quickly?

Obesity underlies debilitating metabolic effects such as very high blood pressure that can lead to heart attacks and strokes and people of all ages are getting this disease – including children and teenagers. Obesity underlies the huge increase in Type 2 Diabetes and when poorly managed can result in blindness, limb amputation and organ failure. People of all ages are dying from these metabolic effects of these disease, which at present are mainly being managed through medication and advising people to “eat less and move more”.

Is that the best we can do to curb this epidemic?

As covered in previous articles, there are peer-reviewed published studies – some a year or two long, that demonstrate that these metabolic effects can be put into remission by eating a diet with less carbohydrates yet government-funded research into use of this is not a priority.

Why?

What role does the sugar industry and the corn-producers (that manufacturer high fructose corn syrup found in much of our packaged food) play?

What role do the grain boards (that market wheat and other grains for baked goods) play?

What about the soybean and canola growers – multi-billion dollar a year  industries in both countries that grows the soybeans and canola seed that are processed into fats sold to consumers for cooking and baking?

These industries and their respective lobby groups play an influential role in the economies of both Canada and the United States and in that way (and others) influence what types of research should be funded.

There is an epidemic going on and people are living with terrible metabolic consequences of them or dying from them.

Before the Dietary Guidelines are updated in both countries, the governments of Canada and the US must approve external, independent scientific review of the evidence-base for the existing dietary recommendation as well as examine the evidence-base for use of a well- designed low carbohydrate diet in reducing obesity and managing the debilitating metabolic effects.

The length of time since the obesity epidemic began does not make this any less urgent.

Do you have questions about how I can help you in tackling obesity and lowering or putting metabolic side effects into remission?

Please send me a note using the “Contact Me” form located on the tab above.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


References

  1. OECD Health Statistics 2017, June 2017, http://www.oecd.org/els/health-systems/Obesity-Update-2017.pdf
  2. Kearns C, Schmidt LA, Glantz SA, et al. Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016 Nov 01; 176(11):1680-1685.
  3. Husten, L, How Sweet: Sugar Industry Made Fat the Villain, Cardio|Brief, 2016 Sept 13.
  4. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242–47
  5. The National Diet-Heart Study Final Report.” Circulation, 1968; 37(3 suppl): I1-I26. Report of the Diet-Heart Review Panel of the National Heart Institute. Mass Field Trials and the Diet-Heart Question: Their Significance, Timeliness, Feasibility and Applicability. Dallas, Tex: American Heart Association; 1969, AHA Monograph no. 28.
  6. Introduction to the Dietary Goals for the United States – by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF

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

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

 

Vilification of Saturated Fat – Bad Fat Enduring Beliefs Part 1

This is Part 1 in a new series titled Bad Fat Enduring Beliefs and this article looks at how and when saturated fat was vilified and why sugar was          vindicated as the cause of heart disease.

The Diet-Heart Hypothesis

The diet-heart hypothesis is the belief that eating foods high in saturated fat contributed to heart disease was first proposed in the 1950s by a scientist named Ancel Keys who believed that by replacing saturated fat from meat, butter and eggs with newly-created industrial polyunsaturated vegetable oil (such as soybean oil) that heart disease and the deaths allegedly associated with it would be reduced by lowering blood cholesterol levels.

In 1952, Keys suggested that Americans should reduce their fat consumption by 1/3 and in 1953, Keys published a study where he said that he had demonstrated that there was an association between dietary fat as a percentage of daily calories and death from degenerative heart disease [1].

Four years later, in 1957, Yerushalamy et al published a paper with data from 22 countries[2] which showed a weak relationship between dietary fat and death by coronary heart disease – a much weaker relationship than was suggested by Keys’s in 1953. Nevertheless, in 1989 Keys and colleagues published their Seven Countries Study[3] which maintained there was an associative relationship between increased dietary saturated fat and Coronary Heart Disease – basically ignoring the data presented in Yerushalamy’s 1957 study, and which failed to study countries where Yerushalamy found no relationship between dietary fat and heart disease, such as in France. The paper maintained that the average consumption of animal foods (with the exception of fish) was positively associated with 25-year Coronary Heart Disease death rates and the average intake of saturated fat was strongly related to 10 and 25-year Coronary Heart Disease death rates. Keys and colleagues knew of the Yerushalamy’s data from 1957 and seemingly dismissed it.

Keys et al – Epidemiological studies related to coronary heart disease: characteristics of men aged 40–59 in seven countries [1]


Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note [2]
The paper has been widely criticized for selecting data only from the 7 countries that best fit their Diet Heart Hypothesis.

The Sugar Industry Funding of Research Vilifying Fat

In August of 1967, Stare, Hegsted and McGandy – the 3 Harvard researchers paid by the sugar industry published their review in the New England Journal of Medicine, titled “Dietary fats, carbohydrates and atherosclerotic vascular disease”[3] which vindicated sugar as a contributor of heart disease and laid the blame on dietary fat and in particular, saturated fat and dietary cholesterol (previous article on that topic here).

Stare, Hegsted and McGandy concluded that there was “only one avenue” by which diet contributed to the development and progression of “hardening of the arteries” (atherosclerosis) and resulting heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids;

“Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol…the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.” [4]

These researchers concluded that there was major evidence available at the time which suggested that there was only ONE avenue for diet to contribute to hardening of the arteries and the development of heart disease – yet a year later in 1968 the report of the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease because such a study had not yet been done [5];

“the committee strongly recommended to the National Heart Institute that a major definitive study of the effect of diet on the primary prevention of myocardial infarction be planned and put into operation as soon as possible. ”

This is an important point; prior to a major study having ever been conducted to determine whether changes in dietary cholesterol impacts heart disease, 3 Harvard researchers paid by the sugar industry concluded that there was “only one avenue” by which diet contributed to the development and progression of atherosclerosis (i.e. “hardening of the arteries”) and heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids.

Researcher Paid by the Sugar Industry Helps Develop the 1977 US Dietary Guidelines

Only ten years after the sugar industry paid Stare, Hegsted and McGandy to write their reviews, the same Dr. Hegsted was directly involved with  developing and editing the 1977 US Dietary Guidelines [6] which recommended an increase in dietary  carbohydrate and a decrease in saturated fat and cholesterol in the diet.

Historic changes in the Dietary Recommendation in Canada have largely been based on changes to the Dietary Recommendations in the US, and as a result both stemmed from a belief that eating saturated fat increases total cholesterol and therefore increases the risk of heart disease.

The problem is this belief is just that, a belief.

There have been many studies that have disproved this including a  randomized, controlled dietary intervention trial from 2008 which compared a low calorie, low in fat with a low carbohydrate, high fat diet of the same number of calories. This study found that overall heart health is significantly improved when carbohydrate is restricted, rather than fat [7,8].

Not all LDL cholesterol is “bad” cholesterol.

Small, dense LDL (“Pattern B”)  causes more “hardening of the arteries” than the large, fluffy LDL particles (“Pattern A”)[9].

It has been reported that when dietary fat is replaced by carbohydrate, the percentage of the small, dense LDL particles  (the ones that cause hardening of the arteries) is increased, increasing risk for heart disease.  Furthermore,  the low carb diet increased HDL (so-called “good” cholesterol), which are protective against heart disease and HDL and small, dense LDL were made worse on the low fat diet. Quite opposite to the “Diet-Heart Hypothesis, this study demonstrated improvements in the risk of heart disease for those eating a low carbohydrate, high fat diet compared to those eating a low fat, low calorie diet – which is not all that surprising given that it had been reported previously that a diet high in saturated fat actually lowers small, dense LDL (the type of LDL that causes hardening of the arteries) and raises the large fluffy LDL; actually improving risk factors for heart disease [15].

There are also other randomized controlled trials from 2004-2008 which demonstrate that a low carb diet improves blood cholesterol test results more than a low fat diet [10,11,12,13,14] – yet despite this, the belief that eating saturated fat increases blood cholesterol, persists.

Both the American and Canadian governments are in the process of revising their Dietary Guidelines and what is clear is that what is needed is an external, independent scientific review of the current evidence-base for the enduring false belief that dietary fat, especially saturated fat contributes to heart disease.

Have questions about how I can help you follow a low carb lifestyle?

Please send me a note using the “Contact Me” tab above and I will reply shortly.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. KEYS, A., Prediction and possible prevention of coronary disease. Am J Public Health Nations Health, 1953. 43(11): p. 1399-1407.
  2. Yerushalmy J, Hilleboe HE. Fat in the diet and mortality from heart disease. A methodologic note. NY State J Med 1957;57:2343–54
  3. Kromhout D, Keys A, Aravanis C, Buzina R et al, Food consumption patterns in the 1960s in seven countries. Am J Clin Nutr. 1989 May; 49(5):889-94.
  4. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242–47
  5. The National Diet-Heart Study Final Report.” Circulation, 1968; 37(3 suppl): I1-I26. Report of the Diet-Heart Review Panel of the National Heart Institute. Mass Field Trials and the Diet-Heart Question: Their Significance, Timeliness, Feasibility and Applicability. Dallas, Tex: American Heart Association; 1969, AHA Monograph no. 28.
  6. Introduction to the Dietary Goals for the United States – by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF
  7. Volek JS, Fernandez ML, Feinman RD, et al. Dietary carbohydrate restriction induces a unique metabolic state positively affecting atherogenic dyslipidemia, fatty acid partitioning, and metabolic syndrome. Prog Lipid Res 2008;47:307–18
  8. Forsythe CE, Phinney SD, Fernandez ML, et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids 2008;43:65–77
  9. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189–99
  10. Foster GD, Wyatt HR, Hill JO, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med 2003;348:2082–90.
  11. Stern L, Iqbal N, Seshadri P, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med 2004;140:778–85
  12. Gardner C, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women. JAMA 2007;297:969–77
  13. Yancy WS Jr., Olsen MK, Guyton JR, et al. A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med 2004;140:769–77
  14. Shai I, Schwarzfuchs D, Henkin Y, et al. Dietary Intervention Randomized Controlled Trial (DIRECT) Group. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med 2008;359:229–41
  15. Dreon DM, Fernstrom HA, Campos H, et al. Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. Am J Clin Nutr 1998;67:828–36

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

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

 

The Marketing of Vegetable Fats to an Unsuspecting Public

Yesterday, in preparing to begin a new series of articles on the relationship between polyunsaturated vegetable fats to obesity, I came across an old, yellowed sheet titled “Comparison of Dietary Fats” that I was given as an undergrad Dietetic student at McGill, in 1989.

(reverse side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989 – full size photo, below

It was designed to help us teach consumers how to choose the “healthiest” dietary fats.

As indicated at the bottom of both sides of the handout (see full size photos, below), it was “provided as a Professional Service by Proctor and Gamble“.

Why would Proctor and Gamble, a soap company provide future Dietitians with a teaching handout on choosing healthy oils for cooking? A bit of understanding about how soap is made, will help.

At the time, the making of soap required a mixture of animal fats and lye, however William Procter and James Gamble (brothers-in-law living in Cincinnati in the late 1800s and who formed Proctor and Gamble) needed to find an inexpensive replacement for animal fat for the creation of individually wrapped bars of soap.

The source of soap fat they turned to was a waste-product of the cotton industry – cottonseed oil. It was literally the garbage leftover when cotton was produced and is cloudy, red and bitter to the taste, and toxic to most animals.

They needed to make cottonseed oil solid in order to make bar soap and utilized a newly patented technology to produce a creamy, pearly white substance out of cottonseed oil. This fat resembled lard (the most popular natural animal fat baking and frying fat at the time), so with a little more tweaking, this hydrogenated cottonseed oil was then sold in 1911 by Procter & Gamble to home cooks as Crisco® shortening.

All that was needed now was for Proctor and Gamble to market this industrially-produced seed oil fat, and market it they did. They hired America’s first full-service advertising agency, the J. Walter Thompson Agency that employed graphic artists and professional writers.

“Samples of Crisco were mailed to grocers, restaurants, nutritionists, and home economists. Eight alternative marketing strategies were tested in different cities and their impacts calculated and compared.

Doughnuts were fried in Crisco and handed out in the streets.

Women who purchased the new industrial fat got a free cookbook of Crisco recipes. It opened with the line, “The culinary world is revising its entire cookbook on account of the advent of Crisco, a new and altogether different cooking fat.” [1]

From the very beginning, Proctor and Gamble marketed their industrially-created solid fat (Crisco®) to “nutritionists” and “home economists” – the forerunners to Dietitians.

When Procter & Gamble introduced Puritan Oil® in 1976, a liquid cooking oil made of sunflower oil which became 100% canola oil by 1988, it was natural for them to market their newly created oil to Dietitians.

Proctor & Gamble now had a lucrative business manufacturing industrial seed oils as dietary fats and they wanted to make sure that we, as Dietitians encouraged people to use their “healthy” fats.

I’ve scanned in both sides of the handout (it’s old and yellowed, having been kept in the back of my “new” 1988 Canada’s Food Guide book for almost 30 years). As can be seen, in first place on the front side of the handout is canola oil identified by the trade name “Puritan Oil®”, a registered trademark of Proctor and Gamble.

(front side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989

On the reverse side, is what consumers should know about these oils, including that canola oil is “better than all other types of vegetable oil“.

(reverse side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989

I’ve highlighted some of the wording that makes Proctor & Gamble’s bias apparent;

(reverse side) Comparison of Dietary Fats – “Provided as a Professional Service by Proctor & Gamble”, 1989 – red text mine

Some Final Thoughts…

From the very beginning, industrially-produced seed  fats and oils have been marketed to nutritionists, home economists and Dietitians by the companies that created them, in some cases as a “Professional Service”.

As will become clear in the next article we, as Dietitians were tasked by the Dietary Guidelines in both Canada and the US with promoting “polyunsaturated vegetable oils” to the public as ‘healthful alternatives’ to presumably unhealthy saturated animal fats. The manufacturers were there to ‘assist’ as a ‘Professional Service’.

Looking back on the role of fat manufacturers and the sugar industry (outlined in the preceding article) on which foods were recommended and promoted, it makes me question what I was taught and who affected what I was taught. Given that it was known at the time the sugar industry funded the researchers that implicated saturated fat as the alleged cause of heart disease, I wonder what we don’t know about which industry funded which research.  After all, the knowledge about the sugar industry having funded the researchers that implicated saturated fat only ‘came out’ in November 2016 when it had occurred decades earlier.

NOTE: It is increasingly my conviction that the simultaneous (1) marketing of polyunsaturated vegetable oil (soybean oil, canola oil) along with (2) changes in the Dietary Recommendations for people to (a) eat no more than 20- 30% of calories from fat and to (b) limit saturated fat to no more than 10% of calories, combined with the recommendations for people to (c) eat 45-65% of calories as carbohydrate was the “perfect storm” that may well explain the current obesity crisis and associated  increase in metabolic health problems that we now see 40 years later.

In subsequent articles I’ll elaborate on why I believe this is the case.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Ramsey, D*., Graham T., The Atlantic. How Vegetable Oils Replaced Animal Fats in the American Diet, April 26 2012 (www.theatlantic.com/health/archive/2012/04/how-vegetable-oils-replaced-animal-fats-in-the-american-diet/256155/)

*Dr. Drew Ramsey, MD is an assistant clinical professor of psychiatry at Columbia University.


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.

 

 

 

Low Carb or Keto – what can you eat?

Most criticism of a low carb lifestyle or ketogenic diet centers around a few common misconceptions including that such a lifestyle is “restrictive”, “imbalanced”, or that it’s “not sustainable”. This article addresses all three.

Firstly, as explained in an earlier post there isn’t a single “low carb” diet but basically 3 styles;

(1) low carb high protein
(2) low carb high fat approach
(3) higher protein lower fat intake during weight loss, then a moderate protein high fat intake during weight maintenance

What makes a low carb diet keto” is the amount of carbohydrate that is eaten.

There are different types of therapeutic ketogenic diets which have different clinical applications, including use in epilepsy and seizure disorder, specific types of cancer, Polycystic Ovarian Syndrome (PCOS), weight loss and improving insulin sensitivity and in each case, the ratio of protein to fat is specific to the condition (and in cases of weight loss and improving insulin sensitivity, to the individual).

While our bodies have an absolute requirement for essential amino acids, and essential fatty acids, as covered in detail in an earlier article, according to the Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005) there is no essential need for dietary carbohydrate provided that “adequate amounts of protein and fat are consumed”.

That is, a low carb or ketogenic diet can be ‘complete’ as long as it supplies adequate amounts of protein (with all essential amino acids) and fat (with the essential fatty acids) and also provides the other nutrients the body requires (such as vitamins and minerals).

This is where I can help. I’ll design a nutritionally adequate Meal Plan specifically for you, in light of any clinical conditions you may have and factoring in your goals in choosing to eat this way.

Let me address the common (but unfounded) misconceptions that a low carb or ketogenic diet is “restrictive”, “imbalanced” or “not sustainable”.

A Low Carb or Keto Diet is “restrictive”, “imbalanced” or “not sustainable”

Usually, when people make comments like these, they have absolutely no idea that there are different types of low carb and keto diets. Ketogenic diets used in epilepsy and seizure disorder are very specific, as are ketogenic diets used for those with specific types of cancer. Ketogenic diets used to target insulin resistance associated with Type 2 Diabetes or pre-Diabetes are different again.

Foods and ratios of foods eaten when following a low carb diet targeting insulin resistance based on Dr. Jason Fung’s approach will differ somewhat from a low carb diet based on Dr. Eric Westman’s approach. A low carb diet based on Dr. Stephen Phinney and Dr. Jeff Volek’s approach will be different during the weight loss phase than during weight maintenance. As well, some low carb diets target protein and others target fat. Some promote unrestricted saturated fat in all forms, including bacon and cream, while others don’t. For example Dr. Fung’s approach does not limit eggs, cream and bacon and for weight loss, Dr. Westman’s approach does.

Low Carb Food Categories (based on a diagram from Dr. Ted Naiman)

In my practice, I focus on whole, unprocessed foods that are naturally low in carbohydrates and that come from a wide range of food categories, including non-starchy vegetables, plant fats, low sugar fruit, meat fish poultry and seafood, and animal fat.

I encourage people to eat the fat naturally found in the flesh of animal protein, but to trim meat of extraneous visible fat.

If people enjoy eating bacon from time to time, I’d encourage them to obtain one that is naturally cured and smoked and to eat it on occasion rather than daily.

From my perspective, it makes no sense for someone seeking weight loss to ‘add fat’ to foods for the sake of adding fat (e.g. ‘bulletproof’ coffee or ‘fat bombs’).  If people want to have a bit of cream in their coffee or a touch of butter on their asparagus there’s no reason why not, as there is nothing intrinsically ‘dangerous’ about fat, even saturated fat (more on this in upcoming blogs!). However from my perspective, adding coconut oil and butter to coffee for the sake of “adding fat” makes no sense, even for those following a “ketogenic” diet. I encourage folks to pursue health, not ketones.

Note: There are very few physiological conditions that require very high fat intake such as specialized diets for epilepsy or seizure disorder or for specific types of cancer as an adjunct to treatment.

To address the misconceptions that a low carb or ketogenic diet is restrictive, imbalanced or in any way unsustainable, below are some photos of types of foods that I prepare and eat. Everybody has different types of foods that they enjoy, these are simply some of mine.

Keep in mind that in some photos, only the main course is shown not the large salad or side of cooked vegetables which almost always accompanies it. As well, many of the servings shown are of one of my young adult son’s plates, rather than mine (my serving sizes are different because my nutritional needs are different).

I am showing these photos to dispel the myth that eating a low carb diet is in any way “restrictive”, “imbalanced” or “not sustainable” and I hope they give you some ideas of the wide range of whole, delicious food that is available to be enjoyed when pursuing a low carb or keto lifestyle.

Shakshuka is weekend breakfast or brunch food, that I usually serve with a huge mixed green salad or cucumber and tomato salad.

Shakshuka for three
individual serving of shakshuka

Another favourite on the weekend is Vanilla Bean Pancakes – which one of my young adult sons loves to smother in butter (too much butter for me!). That day, he had poached eggs on the side and a mixed green salad with pumpkin seeds and pomegranate arils on top, drizzled with cold-pressed olive oil.

One of my young adult son’s helping of Vanilla Bean pancakes and butter
a close up of a Vanilla Bean pancake

This is one of my favourite breakfast or brunch salads:

Greek salad with mini marzano tomatoes, mini cukes, goat feta and kalamata olives with a drizzle of cold pressed olive oil, rubbed oregano and fresh lemon

Below is a totally decadent plate that I made this past Sunday from the other half of my rib steak that I cooked the night previously (way too much meat for me!!), that I sliced thinly and warmed with stir fried asparagus, roasted peppers (also from the previous night’s supper) and a few thin slices of melted brie on top. This was shared between two for brunch, and served along with a mixed green salad.

Brunch plate made with leftover steak, roasted peppers and asparagus, with melted brie
BBQ’d burgers on a lettuce bun with grilled asparagus and a small side salad

Here’s how we eat “burgers” for dinner.

 

 

 

…and a close up of one of my son’s plates:

BBQ’d cheese burgers served on a lettuce bun

The burgers look bigger than they are, because they are served on a smaller diameter “lunch” plate, rather than a “dinner” plate. The burgers in this case were served with a large mixed green salad, with a few raspberries on top, a light sprinkling of roasted pumpkin seeds along with a drizzle of cold- pressed olive oil.

Below is one of my son’s plates of lamb souvlaki that I also made this past weekend, and served with homemade tzatiki, grilled asparagus and a small Greek salad on the side (my plate had less lamb and a smaller piece of feta and more asparagus – again, because my nutritional needs are different).

a son’s plate of lamb souvlaki with homemade tzatiki, grilled asparagus and small Greek salad

…and finally, this is a popular weekend Middle Eastern style brunch in warmer weather:

Homemade Maza for weekend brunch

Want “noodles”? Sure!  See the “Recipe” tab for details.

low carb broad noodles

These can be cut (or bought pre-cut) in thinner slices like linguine and are wonderful topped with spaghetti sauce or pesto.

Eating low carb or keto need not involve this much cooking, either! One can make a simple piece of grilled, broiled or pan-fried fish or chicken, some cooked veggies in the microwave and/or a salad.  I happen to enjoy cooking (and my sons enjoy eating!) so this is something I do to relax.

Whether the meals are simple with little cooking required or elaborate, there is nothing “restrictive” about eating low carb.

As for eating this way being “imbalanced”, someone would be hard-pressed to demonstrate that eating this way doesn’t provide adequate nutrients. There is cheese and other dairy, nuts, seeds, fruit, vegetables and a wide variety of meat, fish and poultry. The diet provides all essential amino acids, essential fatty acids and ample vitamin and minerals – certainly no less than the average Canadian diet provides!

As for eating this way being “not sustainable”, what is not sustainable about eating fresh, healthy, whole foods that can be eaten with a minimum of preparation or as elaborate as one’s imagination allows?

I know of people that have been eating this way for 15 or 20 years and I personally have been eating this way for just over a year now (see “A Dietitian’s Journey” tab) and there is nothing that I miss!

If I want something, I make it!

When it was blustery out, I wanted to make “Shepherd’s Pie”, so I made it, substituting cut up green and waxed beans with cubed carrot for the usual vegetable medley and topping with mashed cauliflower, instead of mashed potato.

low carb Shepherd’s Pie

Another time, I felt like lasagna so I made it with thinly sliced Chinese eggplant in place of pasta and it was delicious!

low carb lasagna

Oh and bread? No worries!

One of my son’s wanted a “grilled cheese” and so I made him this.

low carb grilled cheese

What if you want a kaiser bun for a sandwich, or a hamburger bun? No problem (see “Recipes” tab).

Low carb kaiser bun sandwich
freshly baked low carb hamburger buns

Crispy, yeasty pizza? Sure! Yes, the full recipe is available on the “Recipe” tab.

crispy, yeast pizza

While “keto pizza” is higher fat than I personally would ordinarily eat as an ‘everyday food’ (because I follow the third type of low carb style of eating and am still in the weight loss phase), if I really wanted a pizza, I’d make it! I can plan for it ahead of time or adjust my eating for a little while afterwards to compensate, but eating this way does NOT involve food restriction.  It does require making some adaptation to prepare it differently, but there are plenty of websites geared to supporting those following a low carb lifestyle that have wonderful recipes.

I hope this post encouraged you that following a low carb or keto lifestyle is entirely doable, provides adequate essential nutrients from a wide variety of food categories. It is certainly not restrictive or nutritionally imbalanced and can be sustained for as long as someone desires to eat this way.

Want to get started, but need some help designing a Meal Plan just for you? I’d be glad to help.

Whether you live here in the Lower Mainland or live far away, the identical services and prices are available in-person or via Distance Consultation.

Have questions?

Please send me a note using the “Contact Me” form and I’ll reply as soon as possible.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


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

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

Sugar Industry Paid Researchers that Blamed Saturated Fat as Cause of Heart Disease

A year ago, I found out from a fellow Dietitian that a recently published article in the Journal of the American Medical Association revealed that the sugar industry had secretly funded a group of renowned Harvard researchers to write an influential series of articles which downplayed, discredited or outright ignored research known at the time, and which demonstrated that sugar was a contributor to heart disease.

I read the article and was stunned at its significance.

As I am in the midst of a new series of articles on the role of saturated fat and polyunsaturated fat in health and disease, I felt it’s important that people understand the sugar’s industry involvement in potentially skewing of the scientific evidence at the very time that the original 1977 low-fat high carb Dietary Guidelines were being formulated and so I researched further and wrote this article.

Two of the prominent Harvard researchers that were paid by the sugar industry and who wrote articles dismissing that sugar was a significant contributor to heart disease and implicating saturated fat as the cause were the late Dr. Fredrick Stare, chair of Harvard’s School of Public Health Nutrition Department and the late Dr. D. Mark Hegsted, a professor in the same department [2].

POST PUBLICATION NOTE (March 12 2018): Dr. Hegsted, one of the 3 Harvard researchers paid by the sugar industry to write these review articles was directly involved in developing the 1977 US Dietary Guidelines [6].

[Note: April 1, 2021: see this article for documentation.]

 

A commentary in the Journal of Accountability in Research [4] summarized the significance of those articles as follows;

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

In the mid-1960’s, the Sugar Research Foundation (which is the predecessor to the Sugar Association) wanted to counter research that had been published at the time which suggested that sugar was a more important cause of atherosclerosis than dietary fat. The Sugar Research Foundation invited Dr. Stare of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board and then approved $6,500 in funds ($50,000 in 2016 dollars) to support a review article that would respond to the research showing the danger of sucrose[2].  Letters exchanged between the parties were brought to light in the November 2016 article published by Kearns et al [1] maintained that the Sugar Research Foundation tasked the researchers with preparing “a review article of the several papers which find some special metabolic peril in sucrose [sugar] and, in particular, fructose [3].”

This would seem akin to the tobacco industry having secretly funded articles demonstrating that something other than smoking was responsible for lung cancer.

In August 1967 the New England Journal of Medicine published the first review article written by Drs. Stare, Hegsted and McGandy titled “Dietary fats, carbohydrates and atherosclerotic vascular disease”[3] which stated;

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

The report concluded;

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

The Harvard researchers went on to say;

“there can be no doubt that levels of serum cholesterol can be substantially modified by manipulation of the fat and cholesterol of the diet.”

The Harvard researchers concluded;

“on the basis of epidemiological, experimental and clinical evidence, that a lowering of the proportion of dietary saturated fatty acids, increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit.”

Stare, Hegsted and McGandy did not disclose that they were paid by the Sugar Research Foundation for the two-part review [4].

In response to Kearns et al article in the Journal of the American Medical Association in November 2016 [1], the Sugar Association responded [5] by stating that it;

“should have exercised greater transparency in all of its research activities, however, when the studies in question were published funding disclosures and transparency standards were not the norm they are today.” [5]

Some final thoughts…

The reviews written by these influential Harvard School of Public Health Nutrition Department researchers and paid for by the sugar industry have the appearance of being a deliberate manipulation of the perception of the scientific evidence known at the time. 

Whether deliberate or inadvertent, the fact that such sponsorship occurred at the very period in time when the Dietary Guidelines were under revision to emphasize that saturated fat intake must be reduced and carbohydrate consumption must be increased cannot be understated — a move which certainly benefited the sugar industry.

POST PUBLICATION NOTE (March 12 2018): Discovered after publication of this article, one of the three Harvard researchers funded by the sugar industry, Dr. D.M Hegsted was one of the scientists that worked on the 1977 US Dietary Guidelines[6].

[Note: April 2, 2021: See this article for documentation.]

How has this turned out for us?

For the last 40 years, Americans and Canadians have diligently eaten more carbohydrate (including foods containing sucrose and fructose) and more polyunsaturated fats (especially soybean and canola oil) just as the Harvard researchers paid for by the sugar industry recommended — and to what end?

Obesity rates have gone from ~10% in the 1950’s and 60’s in both countries to 26.7% in Canada (2015) and ~34% in the US (2017) and Diabetes and high blood pressure (hypertension) rates have risen exponentially.

What’s going on?

Could it be that the shift to a diet abundant in omega-6 polyunsaturated fat (such as soyabean oil) and which supplies 45-65% of daily calories as carbohydrate created the ‘perfect storm‘ which inadvertently fueled the obesity and health epidemic we now see?

This will be the subject of future articles.

Have questions?

I provide both in-person and Distance Consultation services (via telephone or Skype) can help you learn a better and easier way to eat, while you achieve and maintain a healthy body weight long term.

Please send me a note using the “Contact Me” tab above and I will reply shortly.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


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

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

References

  1. Kearns C, Schmidt LA, Glantz SA, et al. Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med. 2016 Nov 01; 176(11):1680-1685.
  2. Husten, L, How Sweet: Sugar Industry Made Fat the Villain, Cardio|Brief, 2016 Sept 13.
  3. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242–47
  4. Krimsky, S. Sugar Industry Science and Heart Disease, Accountability in Research. 2017 Oct 07; 24:2, 124-125.
  5. Sugar Association, The Sugar Association Statement on Kearns JAMA Study, 2016 Sep 12
  6. Introduction to the Dietary Goals for the United States – by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF

PART 2 of 2: The Evolving Hypothesis of Obesity – how polyunsaturated fat makes us fat

This content of this post is based largely on a presentation titled “A New Hypothesis for Obesity” given by Dr. Michael Eades at the Low Carb Breckenridge Conference, Breckenridge Colorado, Sunday, March 4, 2018 with some details filled in from his website. Dr. Eades has been in full time practice of bariatric, nutritional and metabolic medicine since 1986 and is the Director of Medi-Stat Medical Clinics, a chain of ambulatory out-patient family care clinics in central Arkansas. I have added the Canadian data for the benefit of my readers. This article is Part 2 in the two-part series The Evolving Hypothesis of Obesity. Part 1, which lays the groundwork for this article can be read here.

In the 1970’s the Dietary Guidelines in both the US and Canada advised us to eat more grains, vegetables and fruit and to eat vegetable fat, instead of saturated fat in butter, eggs, whole milk and red meat.

The US has dutifully complied, as indicated by the following graph;

US per capita consumption of grains, vegetables and fruit and vegetable oils compared to red meat, whole milk, eggs, animal fats and butter – Nina Teicholtz via – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Similar types of increases and decreases have been observed in Canada. According to Statistics Canada;

“In the past two decades, Canadians have shifted towards a diet which includes more fruits and vegetables, cereal products, and nuts and beans. During this time, poultry consumption has increased, while beef and pork consumption has continued to decline.”

In 2016, per capita consumption of beef, pork, lamb and veal in Canada was 47.7 kg (105 lbs) per person per year down from the 73.2 (161 lbs) per person per year it was in 1980. Egg consumption also dropped from 21.96 dozen per person per year in 1980 to 19.93 dozen in 2016. The last time it was measured nationally in 2009, total fresh vegetable intake (excluding potatoes) rose to a record 40.7 kg (89.7 lbs) per person and the amount of potatoes including as french fries was 27.9 kg (61.6) per person, making total vegetable consumption 68.6 kg (151 lbs) per person per year. Total fresh fruit consumption also rose to a record 39.3 kg per person.

The Canadian Canola Growers Association reported that in 2012, 600,000 tonnes of canola oil and soybean oil was consumed by Canadians either as grocery store items or food-service products, including margarine, cooking oil, mayonnaise and salad dressing. In the twelve months ending July 2012, 2.8 million tonnes of Canadian vegetable oil was exported to the US and China, accounting for another 2.4 million tonnes.

In 2012, Sean McPhee, President of the Vegetable Oil Industry of Canada said;

“The vegetable oil industry is an important part of Canada’s growing agri-food sector. The industry’s processing capacity in 2012 is nearly double the capacity of 2007, and it is anticipated that further expansion will increase capacity 50 per cent by 2015.”

As saturated fat intake has declined, carbohydrate intake has continued to increase from the mid-1960s onward.

Decrease in saturated fat consumption, increase in carbohydrate consumption (US data) – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

The Evolving Hypothesis of Obesity

The most significant change since 1976-1980 is that we are eating a great deal more linoleic acid found in soybean, canola and corn oil while simultaneously eating significantly less saturated fat and overall eating more calories.

Three factors together are thought to have produced the “perfect storm” which has resulted in the massive increase in obesity from 1980 until the present;

(1) the vilification of saturated fat
(2) the encouragement to eat industrially produced vegetable oils
(3) the increased consumption of refined carbohydrates.

Simply put, the evolving hypothesis of obesity states that in addition to the (a) increasing amount of carbohydrate in the diet since ~1980, things are made significantly worse by (b) large amounts of industrially-produced  polyunsaturated fats which promote obesity simultaneous to the (c) decrease in naturally occurring saturated fats which protect against obesity.

Dr. Eades credits much of the mechanism for the linoleic hypothesis to Dr. Petro Dobromylskyj, whose is a doctor of veterinary medicine and who writes a technical blog called Hyperlipid which I referred to in order to fill out my understanding in writing this article.

The difference between how the body processes saturated fats versus polyunsaturated fats

To understand the mechanism, the only chemistry you need to understand is the difference between a saturated fat and an unsaturated fat.

Saturated fats are ones where all the carbons in the chain are saturated with hydrogen atoms and there are no double bonds in the middle of the fatty acid chain. Palmitic acid (a 16 carbon fat) is an example of a saturated fat – and is one that our body synthesizes.

Saturated fat – palmitic acid

When a saturated fat is broken down (called “beta oxidation”), 2 carbons are cleaved off at a time, until the fat is completely broken down.

Beta Oxidation of a Saturated Fat – e.g. palmitic acid

Glucose is processed anaerobically in the cytosol of cell, but fatty acids are metabolized inside organelles called mitochondria (the ‘powerhouse of the cell’). All our food (regardless what it is) is metabolized to a combination of FADH2 and NADH.

The NADH and FADH2 enter the Electron Transport Chain at different complexes. NADH enters at Complex I (CI), while FADH2 enters at Complex II (CII).

 

Saturated fat has a feedback mechanism called the Reverse Electron Transport which keeps the cell from taking in too much energy – – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

The lower the FADH2:NADH ratio is, the lower the local insulin resistance is and the higher the FADH2:NADH ratio, the higher the local insulin resistance.

A saturated fat generates a higher FADH2:NADH ratio, so saturated fat increases local insulin resistance which serves to keeps more carbs in the blood.  A process called Reverse Electron Transport is initiated which results in the making of a signalling molecule known as a superoxide (SO) molecule. This signalling molecule tells the body to stop insulin signalling by inducing local insulin resistance. This way, the cell doesn’t take up too much energy.

An unsaturated fat, on the other hand (such as palmitoleic acid or linoleic acid) has double bonds in the middle of the chain which changes the way the body processes it.

Beta oxidation of Palmitoleic acid (unsaturated fatty acid)
Polyunsaturated fat provide NO feedback mechanism (no Reverse Electron Transport) so there is nothing to keep the cell from taking in too much energy – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

When fat cells (and other cells) are metabolizing an unsaturated polyunsaturated fat (PUFA) such linleoic acid from soybean oil, corn oil or canola oil, they generates a lower FADH2:NADH ratio, so an unsaturated fat reduces local insulin resistance, which means they allow plenty of glucose into the cells along with the PUFA.

These n-6 PUFAs generate energy all the way through the Electron Transport Chain and the Reverse Electron Transport is not triggered, so NO (superoxide) signalling molecule to tell the body to stop insulin signalling (i.e. there is no localized insulin resistance caused). The cell just keeps taking in more and more energy even though it doesn’t need any more!  This means the fat gets driven into the fat cells and is stored there, making it unavailable for use for energy.

Once fat gets stored in the fat cells, the body can only break it down when no more energy is coming in (such as when fasting), so the only way the body can get more energy is to eat more. The glucose is driven into the cells because of the decreased insulin resistance caused by the n-6 PUFAs oils, which results in glucose level falling. This causes the body to produce a strong signal to eat; in other words, it makes you hungry.

Along with carbohydrates, n-6 PUFA vegetable oils have increased dramatically in the typical American and Canadian diet since the 1970s and this mechanism explains why we’ve been getting fatter and fatter since then.

So much of our eating now takes place away from home, or with food made away from home, that much of the fat intake in the diet is n-6 PUFA vegetable oils that signal glucose to come right in along with them.

French Fries then and now

In the 1960’s French fries were fried in beef tallow (which is a saturated fat), and the stearic acid from the beef fat and the glucose (from the broken down potato) would be processed by the fat cell (adipocyte).

When the cell had enough energy, Reverse Electron Transport would kick in and create the signalling molecule (superoxide molecule), which would tell the body that it didn’t need any more energy. This would result in a decrease in hunger and an increase in energy expenditure.

Think of the superoxide molecule as a “bouncer” at a night club.  When there are enough people inside, the “bouncer” simply won’t admit any more people until some leave.

When French fries are fried in polyunsaturated vegetables oil, the linoleoic acid (from the soybean oil or canola oil) and glucose (from the broken down potato) are processed by the fat cell. The problem is, that even when the cell has more than enough energy, Reverse Electron Transport does NOT kick in and there is NO signalling molecule (superoxide) produced. The body doesn’t get any message that it doesn’t need any more energy, and the person doesn’t get any signal that they’re full, so they just keep eating.

In the case of eating foods made with polyunsaturated fat, it would be like a night club that has no “bouncer”.  Even when the club is jam-packed with people, everybody is admitted until there is no room to move!

The absence of a feedback mechanism in processing unsaturated polyunsaturated fats results in fat cells getting bigger and bigger – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

The mechanism simply explained

Fat cells (adipocytes) bind more insulin at a given level of exposure when eating polyunsaturated fats such as soybean oil, canola oil and corn oil, than fat cells bind when eating saturated fat such as butter, lard or beef tallow.

Since insulin has to bind to its receptor to work and more insulin is bound when eating a diet rich in polyunsaturated fats, significantly more glucose is taken up into a fat cell in a diet high in polyunsaturated fats than in a diet rich in saturated fat. That is, the cells are more sensitive to insulin when eating a diet rich in polyunsaturated fats than a diet rich in saturated fat, so polyunsaturated fats allow too much glucose in to cells.

When fat cells and other cells are metabolizing saturated fat they make a superoxide (SO) molecule as a result of Reverse Electron Transport which is used to stop insulin signalling. When fat cells and other cells are metabolizing polyunsaturated fats, there is NO Reverse Electron Transport, so they are unable to generate the  superoxide molecule that is needed to stop insulin signalling. This is because there is too little FADH2 being delivered to ETF.

Saturated fats, such as Palmitic acid have a higher FADH2: NADH ratio and it is believed that this is what drives Reverse Electron Transport (RET).

The FADH2 to NADH Ratio (also called the F:N ration – different with saturated fats and unsaturated fats – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Oleic acid, the monounsaturated fat found in olive oil drives Reverse Electron Transport (RET) somewhat, but to a lesser degree than a saturated fat.

Unsaturated polyunsaturated fats such as Linoleic acid (found in soybean oil, corn oil and canola oil) have too small a FADH2: NADH ratio which prevents it from initiating Reverse Electron Transport (RET). It is thought that because polyunsaturated fats have such a low FADH2: NADH ratio, they are treated by the body similarly to glucose.

There are two consequences to eating fats with this low FADH2: NADH ratio.

  1. the fat cells (adipocytes) get over-stuffed with fat (because there is no “off switch”)
  2. When these fat cells get over-full they are unable to keep the fat contained as they should, and as a result free fatty acids are released and eventually find their way into other places where fat is not supposed to be found, such as in the liver, pancreas, even muscle and bone cells.  This is known as ectopic fat and the condition that results is called metabolic syndrome.

Summary

What happened after the 1950s and 1960s that caused overweight and obesity to suddenly explode in the 1970’sand just keep rising?

The answer is the types of fat we started eating.

Even though we were eating the same total amount of fat as before, these new industrially-produced polyunsaturated fats (such as soybean oil, canola oil and corn oil) do NOT provide the feedback mechanism that natural fats (such as butter, lard and beef tallow) do, so there is nothing in these manufactured fats to signal us that we are “full”.

This is why we began eating 240 more calories per day in carbohydrates –because the polyunsaturated fat that accompanied the carbs don’t tell us we’ve had enough!

The (1) the vilification of saturated fat, the (2) encouragement to eat and our acceptance and adoption of industrially produced vegetable oils and the (3) increased consumption of refined carbohydrates created the “perfect storm” and which taken together, certainly provide a reasonable mechanism with explains the massive increase in obesity from 1980 until the present.

Final Thoughts…

The different way the body processes natural saturated fats (such as butter, lard and beef tallow) versus the way it processes industrially-produced polyunsaturated fats (such as soybean oil, canola oil and corn oil) explains the mechanism by which the prevalence of obesity graph so closely mirrors the consumption of vegetable oil graph.

Trends in obesity among US Adults Aged 20-74 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018
Added fats and oils compared with trends in obesity among US Adults Aged 20-74 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Given that (1) total fat consumption has not changed since the 1960’s, only the type of fat we are eating has and (2) given that the body manufactures saturated fat in the form of palmitate, these naturally occurring saturated fats should not be thought of as “dangerous” or to underlie obesity.

As occurred late in the game with trans fats, it is time that these industrially-produced polyunsaturated fats be examined much more closely.

We ought to ask ourselves if we should even be eating oil from crops not thought of as fat-containing. If we squeeze an olive and fat comes out or we crush a nut and oil comes out, these are natural fats. Fats such as cold pressed olive oil, macadamia nut oil and walnut oil (to name a few) are natural sources of largely monounsaturated fats that are foods our ancestors (or other people’s ancestors) knew.

If “oil” needs to be produced under high pressure, high heat and with the use of solvents and deodorizers, is this even “food”? I think not.

Have questions?

Want to understand how to best nourish your body explained by someone who can make the science simple?  Please feel free to send me a note using the “Contact Me” form above.

To our health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

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

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

Reference

Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4, 2018 (NOTE: here is a similar talk given a Low Carb Down Under on August 11, 2018 and published on YouTube, called A New Hypothesis of Obesity.)

PART 1 of 2: The Evolving Hypothesis of Obesity – the role of polyunsaturated fats

This content of much this post is based on a presentation titled “A New Hypothesis for Obesity” given by Dr. Michael Eades at the Low Carb Breckenridge Conference, Breckenridge Colorado, Sunday, March 4, 2018. Dr. Eades has been in full time practice of bariatric, nutritional and metabolic medicine since 1986 and is the Director of Medi-Stat Medical Clinics, a chain of ambulatory out-patient family care clinics in central Arkansas. I have added Canadian data and photos for Canadian readers. This article is Part 1 of two on The Evolving Hypothesis of Obesity.

The current ‘obesity epidemic’ is often understood in terms of the change in the percentage of obese people in the US or Canada from the early 1950’s, through the early 1970s until today. In Canada in the early 1960s the obesity rates were 10.2% (~8% of men and ~12% of women) and in the US, obesity rates at that time were 10.7%. From 2007 to 2009, obesity in Canada rose to 24.1% and in the US, rose even more to 34.4%.

In addition to statistics, another way to understand the obesity epidemic is through historical photos. Below is a sorority photo from Louisiana from the 1950s (one of the US States that currently has one of the highest rates of obesity).

Louisiana sorority, 1950s

What about Canada?

Here’s a photo of what people looked like in 1967, riding the subway in Toronto.

toronto subway rush hour

As can be seen in another photo (below) from a Toronto rush hour, young adults, middle aged adults and older people were very slim compared to today’s standards.

toronto subway rush hour

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

What happened?  What changed?

What caused overweight and obesity to all of a sudden explode in the 1970’s – and just keep rising?

A clue is in the macronutrient intake between 1971 and 2010.

Macronutrient Intake 1971-2010 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

The graph on the left above shows macronutrients (protein, fat and carbohydrate) as a percentage of calories. After 1980, carbohydrate intake went up, fat intake went down and protein remained about the same.

As carbs intake went up and fat went down (protein intake stayed about the same), people began to gain weight. But what caused people to start eating more carbs?

The graph on the right above is much more telling as it shows the macronutrient intake in grams eaten per person per day. There are only two lines on the graph because the amount of fat and the amount of protein are superimposed over each other and appear as one line. The amount of fat (in grams) and the amount of protein (in grams) is approximately 75 g  each however keep in mind that fat has 9 calories per gram and protein only has 4 calories per gram. The top line on the graph shows carbohydrate intake in grams and as can be seen around ~1976-1980 carbohydrate intake suddenly skyrocketed by ~ 240 calories per day

What made people start eating 240 calories more per day in carbohydrate?

More on this in Part 2, but the clue is in the type of fat that people began to eat.

The graph below shows the change in the type of fat that people ate from 1970 to 2010. While the total amount of fat remained relatively constant from 1970 – 2010, there was a significant change in the type of fat that people ate. From 1970 onward, there is a huge increase in the consumption of polyunsaturated vegetable oils.

Added fats and oils – 1970-2010 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Breaking these vegetable oils down into specific types of oils, one can see that there is a huge increase in the consumption of soybean oil over this period.

Increase in soybean oil consumption 1949 – 1999 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Where does good old Canadian “canola oil” place?

Image result for consumption of rapeseed oil 1970 to 2010
Clinical and Metabolic Effects of Altering Omega-3 and Omega-6 Fatty Acids – Dr. Doug Mann MD, Professor of Neurology, University of North Carolina, February 21 2014

The graph at the top of the illustration below is the same graph as the one above and shows that soybean oil consumption reaches 12 kg per person per year. Looking at the graph below that one, canola oil is less than 1 kg per person per year.

It’s important to remember that the per person consumption of these oils is not only the fats that people buy and use at home, but include the oils used in the food that people eat at restaurants and in pre-made foods, including baked goods. Most oils sold as “vegetable oil” are soybean oil and it finds its way into things we’d never expect to find it in. Read labels more closely and you’ll find it everywhere. It’s in peanut butter and infant formula, most  commercial salad dressings, crackers and baked goods, such as muffins.  Its what your mayonnaise is made of (even if it says that its “olive oil mayonnaise”) because soybean oil can turn two ounces of olive oil into 500 ml bottle of ‘olive oil’ mayo or salad dressing. These vegetable oils are what potato chips and tortilla chips are fried in and it’s the fat in almost all commercial bread you eat – from burger buns to wraps.  It’s everywhere!

While the total amount of fat in the diet hasn’t change over time (1970-2010), the type of fat being eaten is very different! We’re eating MUCH more vegetable oils just as the Dietary Guidelines in Canada and the US have encouraged us to do since the 1970s and at the same time, we’re eating less saturated fat from beef, pork, eggs, butter etc. As will be developed in the second part of this article, this increase in the consumption of vegetable oils and decrease in eating saturated fat has served as two sides of a dual-edged sword that has contributed to the obesity epidemic.

One of the reasons for the huge increase in the consumption of vegetable oils is the number of meals that are eaten away from home, as opposed to cooked at home. In the 1950’s and 1960’s people rarely ate out at restaurants unless there was a special occasion, or they were travelling away from home. Meals at home were cooked from scratch (there were very few ‘convenience foods’) and before the creation of vegetable shortening (Crisco®) people used lard (a saturated fat) in their pies and butter in their cakes.  Butter (also a saturated fat) was the used on potatoes and as a spread on bread but with the rationing during World War II, margarine came into use – as did vegetable shortening, which was inadvertently created when extracting fats for the industrial production of soap.

Restaurants in the 1950s and 1960s used either beef tallow or lard in their deep fat fryers, but with the change in the Dietary Guidelines in the 1970s which told us ‘saturated fat was bad for our health’, these natural fats were replaced with industrially produced soybean oil and canola oil which are extracted under high heat and pressure, with the use of solvents, bleaches and deodorizers.

Note: you can squeeze a soybean all day long and you’re not going to get any ‘oil’ out of it – same with a corn kernel or canola (rapeseed).  Gently pressing olives or nuts between one’s fingers will extract some oil so one can easily see that these are rich sources of fat. Soybeans, corn and canola require hours of industrial processing (heat, pressure and solvents) to extract ‘oil’. It has long been known that polyunsaturated omega-6 fats compete for binding sites with anti-inflammatory omega-3 fats (from fatty fish and flax seed) and as a result PUFA oils such as soybean oil, corn oil and canola oil promote inflammation in the body.

Approximately 1/2 of meals now are eaten away from home.  These could be grabbing a coffee and a pastry at Starbucks® or Tim Hortons®, eating lunch at the work or school cafeteria or picking up ready-made sandwiches at a grocery store.  Of course, this amount includes order in pizza and Chinese food, a quick bowl of Pho and any number of snacks bought away from home. The issue with these is the fat used in cooking these foods is now out of our control. Most often, soybean oil is used and behind that, canola.

Let’s take a closer look at these vegetable oils.

Linoleic content of canola oil, soybean oil compared to beef fat – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

As can be seen from this chart, canola oil is 32% polyunsaturated fatty acids (PUFAs), soybean oil is 61% polyunsaturated fatty acids and beef tallow is only 4% polyunsaturated fatty acids. The issue with oils (which will be presented in part 2 of this article) is that canola oil and soybean oil are very high in linoleic acid.

Reflective of the linoleic content of our diet is that the linoleic acid content of human body fat has also increased in a dramatic linear fashion over the last 50 years. The following graph was created by researcher Dr. Stephan Guyenet, PhD (neurobiology) based on various US studies, each of which is represented by an orange dot.

Linoleic Acid in US Body Fat 1961-2008 – Dr. Stephan Guyenet

This graph indicates that as we’ve been eating a lot more linoleic acid in our diet, this is showing up as an increasing amount of linoleic acid in our bodies.  Why these polyunsaturated fatty acids (PUFAs) are being taken up so readily will become clear in Part 2 of this post, which will show the proposed mechanism.

Let’s look at the prevalence of obesity among US adults aged 20-74 from 1960-2010. In 1960-1962, obesity rates in the US were 10.7% which is very comparable to the Canadian obesity rates referred to above. From 2007 to 2009 the prevalence of obesity in the US was 34.4%, which is 10% higher than the obesity rate in Canada which was 24.1%.

[www.statcan.gc.ca/pub/82-625-x/2011001/article/11411-eng.htm]

Trends in obesity among US Adults Aged 20-74 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

Now let’s compare the above graph on obesity rates to the increased use of vegetable oils over the same period.

Added fats and oils compared with trends in obesity among US Adults Aged 20-74 – Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4 2018

The parallel rise in the intake of polyunsaturated fats over the same period is striking, and while we know that “correlation is not causation” (i.e. two things being related does not mean that one causes the other) one must wonder if these two factors are related, and if so, how.

The proposed mechanism between the rise in obesity and the rise in the use of polyunsaturated fats (such as soybean oil, canola oil and corn oil) is covered in Part 2,  The Evolving Hypothesis of Obesity – how polyunsaturated fats (PUFAs) make us fat.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

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

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

Reference

Dr. Michael Eades – A New Theory of Obesity, Low Carb Breckenridge, March 4, 2018 (NOTE: here is a similar talk given a Low Carb Down Under on August 11, 2018 and published on YouTube, called A New Hypothesis of Obesity.)

The Role of Protein in the Diet – importance in adults and older adults

This article is Part 3 in a three-part series on Protein and 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).

People understand it’s important for children to eat enough protein because they’re growing but adults and older adults need to eat enough protein each day, as well.

After youth have finished growing, they are at their maximum physical capacity between age 20 and 30 years old and after the age of 30 years old, adults begin to lose muscle mass at the rate of 1% per year [1].

We’ve come to expect that as people age, they will gain more fat, loose bone mass and that they’ll have decreased muscle strength and that in time, these will lead to difficulty getting around, a greater risk of falls and eventually to physical disability. We commonly see older people with spindly legs and bony arms and we think of this as ‘normal’, but as discussed in a recent “A Dietitian’s Journey” article, we’ve mixed up what is “common” with what is “normal”.  When we look at seniors in Okinawa, Japan for example, we don’t see this. They continue to do manual jobs and practice martial arts well into their 80’s and 90’s. Aborigine elders in Australia also remain lean, fit and active as seniors. This is normal.

The physical deterioration that we associate with aging including weak bones (osteoporosis) and the loss of skeleton muscle mass (sarcopenia) don’t develop suddenly, but take place over an extended period of time – brought on by less than optimal practices in early middle age.

The Recommended Dietary Allowance (RDA) for protein is set at 0.8 g protein/kg per day and describes the minimum quantity of protein that needs to be eaten each day to prevent deficiency. Protein researchers propose that while sufficient to prevent deficiency, this amount is insufficient to promote optimal health as people age[2].

There have been several recent “position statements” issued by those that work with an aging population indicating that protein intake between 1.0 and 1.5 g protein / kg per day may provide optimal health benefits during aging [3, 4]. This seems at odds with the 2010 Dietary Guidelines Advisory Committee report [5] which states that ‘protein intake in the US is more than adequate’ and that ‘inadequate protein intake is rare’ [5]. These seemingly contradictory positions are largely due to a difference in terms of how protein adequacy is determined.

The RDA – more specifically the Estimated Average Requirement (EAR) is the minimum amount of protein intake required to prevent deficiency and is based on nitrogen balance studies (since nitrogen is the main component of the amino acids which make up proteins). The EAR is set at the amount of protein that allows the body to achieve nitrogen balance (protein making and protein breakdown is equal) and evaluates overall protein intake.  Evaluation of optimal protein intake not only considers total amount of protein eaten, but also evaluates the metabolic roles of individual amino acids. While the EAR may be enough protein for healthy younger adults, higher intakes of specific Essential Amino Acids (ones the body can’t make, e.g.  Leucine and Isoleucine and Valine) have been reported to improve body composition (muscle mass and increased strength) in older adults.

Another factor is that nitrogen balance studies look at the total amount of protein eaten in a day but don’t look at the amount of protein eaten at each meal [6,7] nor the role of the Essential Amino Acid Leucine which is  required to be present for protein synthesis to begin (including synthesis of new protein for muscle and bone)[6].  Leucine is an indispensable amino acid in the making of all types of protein, but has a unique role in signaling the beginning of muscle protein synthesis. Much research has been done with large doses of free leucine, however a 2012 animal study[6] found that in small meals with limited protein intake (often the case for older adults), that there was a specific minimum amount of Leucine required to be be present, before protein synthesis took place. This “Leucine threshold” had to be met or exceeded before the body would even begin the energy-expensive process of making new proteins!

Typically, the average American eats only 10 g protein for breakfast, 15 g protein for lunch and has most of their daily protein at supper (65 g protein at supper) and since the minimum amount of Leucine that needs to be present in a meal (i.e. “Leucine Threshold”) is not enough at breakfast and lunch with this pattern of protein intake, protein synthesis is only triggered after the evening meal. As elaborated on below, it is recommended that this change.

A 2013 study of muscle protein synthesis in adults in their late 30’s found that when the amount of protein is distributed evenly throughout the day (30 g protein at breakfast, lunch and supper) that significantly more muscle protein was made. Of importance, the (a) making of new protein and (b) the threshold at which protein will be triggered to be made differ with age – with older people needing a higher intake of protein and specifically the amino acid Leucine, than younger adults [8]. This reduced muscle protein synthesis has been called “anabolic resistance” (anabolic means to ‘build’) and studies have shown that this “anabolic resistance” can be overcome with meals containing higher amounts of Essential Amino Acids and appears to be related to the Leucine content of the meal [8]. These findings led to Dietary Recommendations for older adults that emphasize a minimum of 20 g of protein per meal containing more than 2.3 g Leucine to optimize the building of new muscle protein [4].

Final Thoughts…

It is not only growing children and youth that need to eat adequate protein daily, but older adults as well. In many Indigenous cultures, the Elders eat first and eat the best of the animal proteins – which may factor in to the preservation of bone and muscle mass we see in many of these cultures.

The average protein intake for men >20 years old in the US is ~98 g per day and for women it is 68 g per day which may be adequate in total for healthy young adults, but is considered imbalanced in terms of distribution, as a minimum amount of Leucine is required for protein synthesis (specific amount in humans has not yet be determined). Dr. Layton recommends that until further research is conducted and the optimal amount of Leucine is determined that young adults and middle aged adults distribute their protein evening throughout the day with ~25 g (women) -30 g (men) of animal-based protein at each meal. The reason high biological value proteins from animal sources (meal, poultry, fish, egg, dairy) are recommended is because these are high in Leucine (rather than having only 10 g protein for breakfast, 15 g protein for lunch and 65 g protein at supper).

The recommendations above for older adults to eat 1.0 – 1.5 g protein / kg per day distributed evening over three meals which would be on average ~30-40g of animal-based protein at each meal to provide for optimal muscle protein synthesis, preventing sarcopenia – the muscle loss we’ve come to see as ‘normal’ in aging.

How much is too much protein?

According to Dr. Layman, the Upper Limit of Protein according to the Recommended Daily Allowance for Protein is set at ~ 2.5 g protein / kg per day which would put the maximum amount for most adult men at ~200 g protein per day.

Recommended Daily Allowance (RDA) for Protein [slide from Dr. Donald Layman, PhD – The Evolving Role of Dietary Protein in Adult Health]
Have questions?

Need help determining how much protein you should optimally be eating at each meal and from what sources? Please send me a note using the “Contact Me” form and I will reply as soon as possible.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


References

  1. Keller K, Engelhardt M. Strength and muscle mass loss with aging process. Age and strength loss. Muscles, Ligaments and Tendons Journal. 2013;3(4):346-350.
  2. Volpi E, Campbell WW, Dwyer JT, et al. Is the optimal level of protein intake for older adults greater than the recommended dietary allowance? J Gerontol A Biol Sci Med Sci. 2013 Jun;68(6):677-81
  3. Fielding RA, Vellas B, Evans WJ, Bhasin S, et al, Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences. International working group on sarcopenia. J Am Med Dir Assoc. 2011 May;12(4):249-56
  4. Bauer J1, Biolo G, Cederholm T, Cesari M, et al. Evidence-based recommendations for optimal dietary protein intake in older people: a position paper from the PROT-AGE Study Group. J Am Med Dir Assoc. 2013 Aug;14(8):542-59
  5. U.S. Department of Agriculture and U.S. Department of Health and Human Services, Dietary Guidelines for Americans, 2010. 7th Edition, Washington, DC.
  6. Norton LE, Wilson GJ, Layman DK, et al. Leucine content of dietary proteins is a determinant of postprandial skeletal muscle protein synthesis in adult rats. Nutr Metab (Lond). 2012 Jul 20;9(1):67
  7. Mamerow MM, Mettler JA, English KL, et al. Dietary Protein Distribution Positively Influences 24-h Muscle Protein Synthesis in Healthy Adults. The Journal of Nutrition. 2014;144(6):876-880.
  8. Layman DK, Anthony TG, Rasmussen BB, et al. Defining meal requirements for protein to optimize metabolic roles of amino acids, The American Journal of Clinical Nutrition, Volume 101, Issue 6, 1 June 2015, Pages 1330S–1338S

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.

Unreliability of Many Blood Glucose Monitors – cause for concern

Yesterday morning, as I always do, I tested my morning fasting blood glucose with my glucometer. As someone with Type 2 Diabetes, this helps me understand the effect that the food I had for supper may have had and also helps guide me as to whether I may begin the day with time-delayed eating. For Type 1 Diabetics or insulin-dependent Type 2 Diabetics however, the accuracy of this information is critical! They base the dosage of insulin they take on this data and count on it being reliable and accurate.

Accuracy is how close the reading on the meter is to the actual blood glucose value and reliability is the likelihood of repeating the measure with the same meter at the same time and getting the same result.

Yesterday, I swabbed by thumb with an alcohol wipe, let it dry and took my blood glucose reading at 5:27 am and got a reading of 4.8 mmol/L (86 mg/dl) and thought “that can’t be!“, as I know that is a blood sugar reading that I only obtain after more than 18 hours of fasting.

 

I got another test strip from the same vial (recently opened and not expired) and tested the same thumb in a location immediately beside where I had just tested and got a reading of 5.8 mmol/L (105 mg/dl) and thought “that seems more reasonable, but what’s with the meter?”.

Ironically, only several hours prior a physician-friend sent me the link a report from August 14, 2017 that indicated that only 6 out 18 blood glucose meters tested passed the standard for meter accuracy which is for them to be within 15% or 15 mg/dl (0.8 mmol/L) of the laboratory value in 95% of 100 trials. That means there was only a 1/3 pass rate!

Naturally, the first thing I did was look up to see how my meter – actually both my meters (which are identical) ranked.  It failed!

 

Even though I had brought my glucometer to the lab with me in July when I last had my fasting blood glucose measured and it matched the lab results exactly, my meter failed the test because when tested 100 times, it was NOT accurate 95% of the time.  

To pass a meter had to match or be within 15% or 15 mg/dl (0.8 mmol/L) of the laboratory value on 95/100 trials.

I only tested my meter against the lab value ONCE and assumed it to be accurate. It was accurate on that one occasion, but it was not reliable, because when repeating the measure 100 times with the same meter it did not produce results within the 15% acceptable variation.

At 5:27 AM my blood glucose reading was 4.8 mmol/L and 2 minutes later with a new strip it was 5.8 mmol/L – on the same meter. That is a huge amount of variation, although depending on what the lab value actually would have been at that time, the results may or may not have fallen with range (see box below).

NOTE: The average of the two readings, 4.8 & 5.8 is 5.3 mmol/L and a ±15% tolerance would be ± 0.795 or ~ ± 0.8, for a range of 4.5 mmol/L to 6.1 mmol/L, so the readings would be within that range, ASSUMING the AVERAGE is the CORRECT result. While 0.8 is +16.7% more than the lower result and -13.8% less than the higher result, the actual ± 0.5 deviation from the mean is +10.4% and -8.6% of the lower & upper results. If either one result was correct, then 4.8 x 1.15 = 5.52 mmol/L, while 5.8 x 0.85 = 4.93 mmol/L, so the other would be erroneous. But, 4.8 ÷ 0.85 = 5.65 mmol/L, and  5.8 ÷ 1.15 = 5.04 mmol/L, so if the laboratory serum reading fell between 5.04 and 5.65 mmol/L then the meter’s two readings would be accurate to within ±15%. Now ± 15% is 30% of the value which means that (a) A serum glucose of 3.5 mmol/L (low end of normal) could mean a glucometer reading range of 1.05, or 3.04 mmol/L to 4.12 mmol/L A serum glucose of 11 mmol/L (way too high!) would be a 3x larger range of 3.3, or 9.56 mmol/L to 12.94 mmol/L. [thanks to Dr. L De Foa for the calculations]

Unfortunately, I know that my device(s) are not reliable based on this study data and for people who are insulin-dependent Type 1 or Type 2 Diabetics, they rely on the readings from their blood glucose monitors in order to dose their insulin. When their meters have been proven unreliable, it is cause for major concern.

I am reproducing the main data from this study because it is imperative that people know whether the monitor they are relying on is indeed, reliable.

Overall Results of Blood Glucose Monitoring Systems – Diabetes Technology Society 2018

The full testing protocol and results can be found here.

The rated accuracy from Bayer of the number one rated meter above, the Contour Next USB is 100% within ±0.56 mmol/L for glucose < 5.55 mmol/L and 98.1% within ±10% and 100% within ±15% for blood glucose > 5.55 mmol/L and it was accurate 100% of the time in the tests.

As for me, I have gone back to using a glucometer that I had on hand (which also tests blood ketones), as it is one of the models that passed.

While I am left with almost 1/2 a package of new test strips from the unreliable meter, how much worse could it be for someone who is dosing insulin based on unreliable blood glucose meter reading.

Type 2 Diabetes?

If you have Type 2 Diabetes and have struggled to lower your HbA1C or achieve your weight loss goals and have wondered whether a low carb approach might be helpful for you, why not have a read through some of my other articles documenting the science behind this type of lifestyle.

Eating low carb for Diabetics is hardly a new “fad” but was the standard approach before the discovery of insulin, and has proven to be a very safe and effective approach.

Have questions?

Please send me a note using the “Contact Me” form above and I’ll be happy to reply.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/


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

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

New Low Fat versus Low Carb Diet Study – when a tie is not a win

A new one-year study from Stanford University[1] was released February 20, 2018 and reports that low carb diets are no better than low fat diets for losing weight. On one hand, such a conclusion seems like progress when the debate used to be whether low carb diets were “dangerous” – now it’s whether low fat diets are as good as low carb diets.

The conclusion that there was no significant difference in weight loss between a low fat diet and a low carbohydrate diet sounds good on the surface, however closer examination of the methodology indicates that the ‘low carb’ intervention group was only low carb  (≤ 20 g of carbs per day) for the first 8 weeks of a the one year study. After that subjects were instructed to “add carbs back in until they reached the lowest level they believed they could maintain indefinitely. This resulted in subjects in the ‘low carb group’ eating ~100 g carbs per day at 3 months and at the end of the study were averaging 130 g carbs per day ; hardly a ‘low carb’ diet!

The American Diabetes Association (ADA) in its Clinical Practice Recommendations [3] and  Standards of Medical Care in Diabetes [4]  already approves of a 130 g / day intake of carbohydrate as a weight-loss option for those with Type 2 Diabetes in what it calls a ‘low carbohydrate’ diet (more in this article).

The ‘low fat’ intervention group in this study ate an almost equivalent amount of fat and carbohydrate (48% carbohydrate and 29% fat) as the standard ‘low fat diet’ recommendation of the American Diabetes Association, so the fact that they didn’t find a difference between the two groups should come as no surprise, given that the ADA has already concluded that both are equally effective for weight loss (see quotations below).

Keep in mind when you read the quotes below, what the American Diabetes Association defines as “a low carbohydrate diet” is 130 g carbohydrate per day, which is the same as the average intake of carbohydrates at a year in this study. The amount of 130 g carbs per day is a moderate-low carbohydrate diet when compared with the the intake of the first 8 weeks in the study (≤ 20 g carbs / day) and in light of the fact that the average adult US intake is almost 300 g carbs per day.

“The evidence is clear that both low-carbohydrate* [i.e. moderate low carbohydrate] and low-fat calorie restricted diets result in similar weight loss at one year. We’re not endorsing either of these weight-loss plans over any other method of losing weight.  What we want health care providers to know is that it’s important for patients to choose a plan that works for them, and that the health care team support their patients’ weight loss efforts and provide appropriate monitoring of patients’ health.”

– Dr. Ann Albright, RD, President, Health Care & Education, American Diabetes Association, Clinical Practice Recommendations [3]

“For weight loss, either low-carbohydrate* [i.e. moderate low carbohydrate] or low-fat calorie-restricted diets may be effective in the short-term (up to 1 year).”

– Summary of 

In actuality, this “new study” didn’t find anything “new”.

Both the ‘low fat’ and ‘low carb’ [i.e. moderate low carb] groups were instructed to “avoid sugar and refined carbohydrates” but the absolute level of carbohydrate in the ‘low fat’ diet group was not held constant. The
‘low fat’ group actually lowered its carbohydrate intake over the course of the year-long study – from ~242 g carbohydrate per day at the beginning to between 205 g and 213 g carbohydrate per day. This means that the difference  between the two study groups when it came to the level of carbohydrate was decreasing. No wonder there was no significant difference found.

DIETFITS – carbohydrate intake between groups

Final thoughts…

This was not really a study between a ‘low carbohydrate’ diet and a ‘low fat’ diet with fixed grams per day of carbohydrates in each group. This was a study between a flexible moderate carbohydrate diet and a flexible moderately-low carbohydrate diet.

In fact, this “new study” ended up comparing the two diets that have already been approved by the American Diabetes Association and which the ADA has already concluded that neither is more effective than the other for weight loss.

Hardly new.

You can follow me at:

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References

  1. Gardner CD, Trepanowski JF, Del Gobbo LC, Hauser ME, Rigdon J, Ioannidis JPA, Desai M, King AC. Effect of Low-Fat vs Low-Carbohydrate Diet on 12-Month Weight Loss in Overweight Adults and the Association With Genotype Pattern or Insulin Secretion – The DIETFITS Randomized Clinical TrialJAMA. 2018;319(7):667–679.
  2. American Diabetes Association, Adjusting the Meal Plan, http://www.diabetes.org/mfa-recipes/2017-07-adjusting-the-meal-plan.html
  3. Dairman T., Diabetes Self-Management, ADA’s New Guidelines OK Low-Carb Diets for Weight Loss, 2008 Jan 7,  www.diabetesselfmanagement.com/blog/adas-new-guidelines-ok-low-carb-diets-for-weight-loss/

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.

 

Curious About Keto?

There isn’t one “keto diet” but rather there are a few different approaches to eating low carb diet that can each be done ketogenically (or “keto”).

Ketogenic diets are used for a variety of clinical conditions, including seizure disorder and epilepsy, specific kinds of cancer, Polycystic Ovarian Syndrome (PCOS), non-alcoholic fatty liver (NAFL) as well as insulin resistance associated with Type 2 Diabetes and Pre-diabetes. It is also sometime prescribed by people’s physicians for use prior to or following bariatric surgery or for weight loss prior to other kinds of surgery.  A well-designed ketogenic diet is not for ‘rapid weight loss’ but for gradual, sustainable long-term weight loss.

Ketosis is the state where a person is burning primarily fat and using ketones to fuel their body rather than using primarily glucose from carbohydrate for that purpose. There are essential fatty acids (fats) and essential amino acids (building blocks of protein) but there are NO essential carbohydrates. The little bit of glucose that the body needs can easily be made from fat or protein in the diet. Ketosis is hardly an usual state, but something everyone experiences when there is a long gap between meals or when they are sleeping.

What makes a low carb diet “keto” is the amount of carbohydrate in grams compared to the amount of total energy in the diet. Since each person’s toleration of carbohydrate is different, how much one can eat and be in “ketosis” varies.

Not all Keto diets result in weight loss

People mistakenly assume that a “keto” diet is automatically a weight loss diet and that’s incorrect. The ketogenic diets that are used in seizure disorder, epilepsy and in the treatment of specific type of cancer and in some forms of dementia that are designed to not result in weight loss.

What makes a diet ketogenic is the amount of carbohydrates, however the amount and types of protein eaten and the amount and types of fat eaten have a large effect on the amount and speed of weight loss. Depending on a person’s health goals and the presence of any medical or metabolic conditions, the ratio of protein to fat will vary.

Is a keto diet one-size-fits-all?

Outside of the clinical application in seizure disorder, epilepsy and cancer , ketogenic diets also have application in Type 2 Diabetes and pre-Diabetes. In these situations, each person’s ability to tolerate carbohydrate is different depending whether they are insulin sensitive, insulin resistant or Type 2 Diabetic. How much carbohydrate each person can eat and still be in ketosis also varies, too.  Someone who is insulin sensitive for example, can eat considerably more carbohydrate than someone who is insulin resistant  without causing a spike in their blood glucose level, accompanied by the release of insulin. For those who are Type 2 Diabetic, both the degree of insulin resistance and the length of time they’ve been Type 2 Diabetic will affect the amount of carbohydrates they can tolerate.

I like to use the analogy of ‘lactose intolerance’ to explain how some people can tolerate more carbohydrate than others.  Some people who are lactose intolerant can manage to drink and eat milk products, provided the  quantities are small and the person doesn’t have it too often. Others who are lactose intolerant can’t even tolerate a small amount of lactose without symptoms. Carbohydrate intolerance is similar.  People who are insulin sensitive or only mildly insulin resistance will be able to tolerate more carbohydrate than those who are very insulin resistant or have had Type 2 Diabetes a long time.

The average intake of carbohydrate in the Canadian and American diet is ~ 300 g per day, which is a lot!  People who are insulin sensitive or mildly insulin resistance may do very well lowering their carbohydrate amount to a moderate ~130 g per day where as others who are ore insulin resistant will very likely need to eat less than that in order to begin to see an effect.

Factors that can affect how much carbohydrate a person beginning to eat a low carb diet include gender (whether they are men or women) and whether they are insulin sensitive or insulin resistant (IR) and to what degree, and whether they have Type 2 Diabetes (T2D). How long a person has been insulin resistant or Diabetic also factors into how much carbohydrate they may be able to tolerate.

Everyone is different and because of this, there is no one way to “keto”.

Different ways to “keto”

There are a few different approaches to eating low carb diet that can each be done ketogenically or “keto”. Three common approaches are;

(1) low carb, higher protein, high fat
(2) a low carb, moderate protein, high fat approach

(3) a higher protein lower fat intake during weight loss, then a moderate protein high fat intake during weight maintenance

Each of the above types of low carb diets can each be done “keto”- with the amount of carbohydrate being individualized based on a person’s gender (male or female) and whether they have any metabolic conditions (including IR or T2D). What is appropriate for each person depends on their clinical conditions, health goals and will vary person to person, depending on their personal food preferences.

Going at it alone

While some people set out to “eat keto” on their own or by following a ‘diet book’ they’ve bought, it can be dangerous for people taking any kind of medication to manage blood sugar or blood pressure to do this. Decreasing carbohydrates suddenly can result in a dramatic drop in blood sugar and/or blood pressure which, depending on the medication that people may be taking, can be very risky. Some types of medication for blood sugar may result in blood sugar dropping too low when following a low carb diet and for people taking medication for high blood pressure, blood pressure can become too low. For people taking these kinds of medications eating a low carb or ketogenic diet must be done with a doctor’s oversight and should ideally be done with a knowledgeable Dietitian such as myself who can decrease carbohydrates gradually, while the person monitors their blood sugar and/or blood pressure daily.

Even for those not on medication, it is also important that people ensure that they are eating a nutritionally adequate diet, not just a low carb or ‘keto’ one. This is where having the help and support of a Dietitian such as myself comes in.

A little bit about me…

I’ve been helping others eat a low carb diet for about 3 years now through my private practice, BetterByDesign Nutrition Ltd. which has been in business for more than a decade providing in-person and remote services to people in the Lower Mainland of Vancouver and beyond.

Since March 5, 2017, I have been eating a low carb (and more recently a keto diet) myself and in May of last year, I opened the LCHF-Dietitian division  to focus on helping people manage a number of health conditions by following a low carb or ketogenic lifestyle.

The photo collage below is of me. The frame on the left was what I looked like when I first learned about a low carb diet, the middle frame is of me in October of 2017 and the frame on the right is what I look like now.
Me on the left 2 1/2 years ago, 4 months ago in the middle, on the right now

I used to be an obese Dietitian with high blood pressure, high cholesterol and 10 years as a Type 2 Diabetic and am now in partial remission from these, as I continue my weight loss journey. You can read my personal story under “A Dietitian’s Journey” on the blog, under the Food for Thought tab.

Also in the blog are articles written about the science behind following a low carb and ketogenic lifestyle, under the category Science made Simple.

Have questions about how I can help you?

Please send me a note using the “Contact Me” form.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

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

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

New Study: Reversal in T2D Symptoms can be Sustained Long Term

In June of 2017 results of a 10-week outpatient study using a  ketogenic diet intervention  were published and demonstrated significant improvements in subject’s body weight, glycated hemoglobin (HbA1C) and medication usage. One year follow-up data has just been published demonstrating that reversal of Type 2 Diabetes symptoms is sustainable over the long term, as participants continue to eat a ketogenic diet.

Participants

There were 238 participants  enrolled in the continuous care intervention at the beginning of the study and all had a diagnosis of Type 2 Diabetes (T2D) when the study began, with an average HbA1c of 7.6% ±1.5%.

Participants ranged in age from 46 – 62 years of age (mean age = 54 years). Sixty-seven (67%) of participants were women and 33% were men.

Weight ranged from 200 pounds to 314 pounds (117±26 kg), with an average weight of 257 pounds (117 kg).  Average Body Mass Index (BMI) was 41 kg·m-2 (class III obesity) ±9 kg·m-2, with 82% categorized as obese.

The majority of participants (87%) were taking at least 1 glycemic control medication at the beginning of the study.

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

Intervention

Each participant received an Individualized Meal Plan for nutritional ketosis, behavioral and social support, biomarker tracking tools, and ongoing care from a health coach with medication management by a physician.

Subjects typically required <30 g·day−1 total dietary carbohydrates. Daily protein intake was targeted to a level of 1.5 g·kg−1 based on ideal body weight and participants were coached to incorporate dietary fats until they were no longer hungry. Other aspects of the diet were individually tailored to ensure safety, effectiveness and satisfaction, including consumption of 3-5 servings of non-starchy vegetables and enough mineral and fluid intake. The blood ketone level of β-hydroxybutyrate was monitored using a portable, handheld device.

Ten Week and One Year Outcomes

Medication Use

At baseline, 87% of participants were taking at least one medication for Diabetes and at 10 weeks, almost 57% had one or more Diabetes medications reduced or eliminated.

After one year, Type 2 Diabetes medication prescriptions other than metformin declined from 57% to just below 30%.

Insulin therapy was reduced or eliminated in 94% of users and sulfonylurea medication was entirely eliminated in the  continuous care intervention group.

Glycosylated Hemoglobin (HbA1C)

At baseline, the average HbA1c level was 7.6% ±1.5%, with less than 20%  of participants having a HbA1c level of <6.5% (with medication usage).

After 10 weeks, HbA1c level was reduced by 1.0% and the percentage of individuals with an HbA1c level of <6.5% was 56%.

Average HbA1C Reduction after One Year [from Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.]
On average after 1 year, participants in the intervention group lowered HbA1c from 7.6% to 6.3% – which is in the sub-Diabetes range.

Weight Loss

At 10 weeks, mean body mass reduction was 7.2% from a baseline average of 117 kg (257.4 pounds) ±26 kg / 57 lbs.

Average Weight Loss at One Year [from Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.]
At one year, mean body mass reduction of participants was  12% of their initial body weight.

Other Metabolic Markers

At 10 months, participants experienced a 20% reduction in triglycerides and after one year, reduction in triglycerides was at 24%.  After one year, LDL increased on average by 10% however HDL increased on average by 18%. Serum  creatinine and liver enzymes (ALT, AST, and ALP) also declined.

Conclusion

This intervention study demonstrated that individualized nutrition care plans that encourage nutritional ketosis can significantly resukt in reduced weight, HbA1c and medication use within 10 weeks, and that these outcomes can be sustained, or even improved on  over the long term, as participants continue to eat a ketogenic diet.

Do you have questions about how a carefully-designed low carbohydrate or ketogenic diet can help you improve symptoms of Type 2 Diabetes?

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

To our good health,

Joy

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

McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD, A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, JMIR Diabetes 2017;2(1):e5, URL: http://diabetes.jmir.org/2017/1/e5, DOI: 10.2196/diabetes.6981

Hallberg, S.J., McKenzie, A.L., Williams, P.T. et al. Diabetes Ther (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.  https://doi.org/10.1007/s13300-018-0373-9

PART 2: The Role of Protein in the Diet – Evolutionary Exposure to Macronutrients

This article is Part II in a series titled The Role of Protein in the Diet and looks at macronutrients in our diet from an evolutionary perspective.

Over the course of man’s existence, there have been a number of major shifts in the human diet and with that change, came the necessity of the body to adapt by producing enzymes capable of digesting and absorbing nutrients from these novel foods. This required the human genome (our genes) to adapt, evolve and change [1].  This takes time.

In the ~4.4 million span of mankind’s existence, solid evidence for use of human-controlled fires, which would have given us the ability to cook our meat is only about 800,000 years old [2] with less certain sites dating back 1,500,000 years [3,4].

The origin of domestication of animals is considered to be ~10,000 – 12,000 years and represent another relatively recent shift in the human diet [1], moving mankind from a hunting and gathering species, to an agricultural one. With this shift came the need to domesticate crops, which dramatically changed the human diet. The innovation of human agriculture greatly reduced diversity in the human diet. Instead of ‘food’ being what hunter-gatherers were able to find, ‘food’ was what each group grew and raised.

Of even more  significance, it is estimated that 50%–70% of calories in the agricultural diet are from starch (carbohydrates) alone [5]. The advent of animal domestication and an agricultural diet may also resulted in an over-abundance of starch-based calories, which exceeded growth and energetic requirements [1].

The remainder of 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).

Looking at it from the perspective of man’s evolutionary history, the appearance of cereal grains is very recent. Cereal grains as food were non-existent in the evolutionary diet. Same with legumes, such as chickpeas and lentils.  These too were non-existent in the evolutionary diet. Refined sugar (made up of sucrose) was also non-existent in the evolutionary diet. Humans would eat wild fruit (fructose) and on the rare occasion when available they would eat honey (half glucose, half fructose), but this idea of a diet centering around sucrose and fructose was simply non-existent.

Consumption of dairy products and alcohol are also very recent in terms of human history. We didn’t milk wild animals, we ate them. Fermentation of fruit for wine is also very recent in terms of the evolutionary diet.

Our body did not evolve to see cereal grain, legumes, refined sugar, dairy foods and alcohol and all of these are very rich in carbohydrate.

We are exposed to carbohydrate in a way that were never evolved to see.

Our bodies developed metabolism patterns around our dietary intake of protein and fat.

We have very extensive and elaborate pattern for handling protein; for digesting and metabolizing it. We also have developed a very high ‘satiety’ (feeling full) to protein, such that we simply won’t over eat it.  It is the only macronutrient that provides sufficiently strong feedback such that we can’t over eat it.

Fat, contrary to common belief is a very passive nutrient. It has very little direct effect on our body. We store it effectively and this ability to store excess intake as fat is what enabled us to survive as hunter-gatherers.

The macronutrient that is at odds in this picture is carbohydrate.

We have very little evolutionary exposure to carbs; in fact the body responds to it has if it were highly toxic. Carbs have to be rapidly cleared after we eat it because our body must maintain our blood sugar within a very narrow range between 3.3-5.5 mmol/L (60-100 mg/dl). When we eat carbohydrate,  the body breaks it down to simple sugar (glucose) and insulin takes the extra sugar out of the blood and moves it into cells. Our only mechanism to protect us from carbohydrate is insulin. The problem is, when we eat carbohydrates every few hours, the ability for insulin to respond becomes overwhelmed.

We have a biological system for handling carbohydrate and the traditional teaching is that carbs are handled in the muscle, which is true if one exercises 2-3 hours per day.  When were were hunter-gatherers and we came across a bee hive, for instance or a fruit tree in season, our muscle was able to process the short spike in glucose load because we were very active. The average North American or European is not typically exercising that much, with ~75%  considered sedentary (inactive).

So where are those carbs going?

They’re going to body fat.

Carbohydrate regulation is very important to think about. Carbs are among some of the most regulated substances in the body. Blood sugar is controlled and kept within an extremely tight range between 3.3-5.5 mmol/L (60-100 mg/dl).

If we don’t burn off the 30 gm of carbs (equivalent to ~ 6 tsp of sugar) we ate for breakfast by the time we have a fruit mid-morning (another 15 gm of carbs / equivalent to 3 tsp of sugar), we have to store the carbs somewhere.  Comes lunch, most people eat another 30 – 45 gm of carbs (~6 – 9 tsp of sugar) if they’re eating a lunch brought from home and even more than that if eating out at the food court. Maybe another fruit is eaten mid-afternoon, and without realizing it, people have consumed the equivalent of 24 tsp of more of sugar, eating what they’ve believed is a healthy diet. As explained in a previous post, the blood can only have at most the equivalent of ~ 1 tsp of sugar in it at any one time, so where does all the sugar go?

It goes to fat stores.

Fatty Acid Processing [slide from Dr. Donald Layman, PhD – Nutrition Forum, June 23, 2013, Vancouver, British Columbia, Canada.]
To synthesize the excess sugar into fat, the glucose (sugar) comes into the liver and is synthesized into free fatty acids.

Our body is constantly pulling out free fatty acids from our fat stores (adipose tissue) when we are sleeping or exercising, for example to use as a fuel source, so the free fatty acids that are coming in from adipose tissue (fat stores) and those that are being synthesized from glucose (the excess carbs we took in our diet) mix in the liver, and are then packaged into very-low-density lipoprotein (VLDL).

Think of these VLDL as “taxis” that move cholesterol, triglycerides and other fats around the body. Once these VLDL “taxis” deliver their payload, 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’.

[Calling LDL ‘bad cholesterol’ 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.]

The origins of high triglycerides is the beginning of Metabolic Syndrome (also called Syndrome X). This is the point at which the body is getting too many carbs and the system is breaking down. The result is high than normal blood sugar after meals (called post prandial glucose), an increase in free fatty acids, and the increase in triglycerides and these together contribute to fatty liver. These are all symptoms Metabolic Syndrome.

If one is eating more than 30 gm of carbohydrates per day then they either need to have very high exercise to account for it, or they’re going to be making fat from it.

With an average carb intake of 300 gm per day and 75% of North Americans sedentary, it is easy to see where the problem of excess fat stores comes from.

Since our only mechanism for dealing with carbohydrate is insulin, by continually overwhelming the body with a steady supply of glucose – way above the small amount of carbohydrate that our genome has adapted to see, the system fails. This is where the origins of the overweight and obesity statistics elaborated on in the first part in this series (located here).

To address this carbohydrate excess, we can lower carbohydrate intake and either raise fat intake or raise protein intake. In Part III of this series, we will shift the focus to the benefits of increasing protein in the diet.

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. Luca F, Perry GH, Di Rienzo A. Evolutionary Adaptations to Dietary Changes. Annual review of nutrition. 2010;30:291-314. doi:10.1146/annurev-nutr-080508-141048.
  2. Goren-Inbar N, Alperson N, Kislev ME, Simchoni O, Melamed Y, et al. Evidence of hominin control of fire at Gesher Benot Ya’aqov, Israel. Science. 2004;304:725–727
  3. Brain CK, Sillent A. Evidence from the Swartkrans cave for the earliest use of fire. Nature. 1988;336:464–466.
  4. Evidence for the use of fire at zhoukoudian, china
    Weiner S, Xu Q, Goldberg P, Liu J, Bar-Yosef O
    Science. 1998 Jul 10; 281(5374):251-3.
  5. Copeland L, Blazek J, Salman H, Chiming Tang M. Form and functionality of starch. Food Hydrocolloids. 2009;23:1527–1534.

 

 

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.

You can follow me at:

 https://twitter.com/lchfRD

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

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

Misconceptions About the Keto Diet

Alarming social media posts cry out dire warnings about the supposed “dangers” of the ‘keto diet’ but are they founded? What is “the keto diet”?

The Keto Diet

There is no one “keto diet”, but many variations of ketogenic diets that are used for different therapeutic purposes.

Some therapeutic ketogenic diets are used in the treatment of epilepsy and seizure disorder and are extremely high in fat. Other types of therapeutic ketogenic diets are used in the treatment of various forms of cancer (those that feed on glucose), such as brain cancer. There are ketogenic diets that are used in the treatment of Polycystic Ovarian Syndrome (PCOS), as well as for weight loss and for increasing insulin sensitivity in those with Type 2 Diabetes and insulin resistance. Even among those using a nutritional ketogenic diet for weight loss and to increase insulin sensitivity, there is no one “keto diet”.  There are ketogenic diets with a higher percentage of fat than protein, with a higher percentage of protein than fat and mixed approaches which may have different ratios of protein to fat – depending on whether the individual is in a weight loss phase or a weight maintenance phase. There are as many permutations and combinations as there are people following a keto diet for these reasons.

What makes a diet ketogenic (or keto) is that the amount of carbohydrate relative to the amount of protein and fat results in the utilization of fat as a primary fuel source rather than carbohydrate. 

Macronutrient Percentages of Keto Diets

Another assumption is that a keto diet used for weight loss (as if there were only one?) is 20% protein, 70% fat and 10% carbohydrate (and such posts are often accompanied by photos of large plates piled high with bacon and eggs), however therapeutic ketogenic diets used for weight loss ranges from those with a higher percentage of fat than protein (which may focus on mono-unsaturated fats and omega 3 fats), a higher percentage of protein than fat (thus no piles of bacon!), and a mixed approach with different ratios of protein to fat depending on whether the individual is in a weight loss phase or a weight maintenance phase.

This idea that a “keto diet” has a specific percentage of fat to protein to carbs in itself is very  confusing, because the percentage of calories of any of these macronutrients will depend on how many calories a person is eating in a day. For example, two different people may be eating ~30% of their calories as protein but one person is eating just over 55 gm of protein on an 800 calorie a day diet, while another person is eating 160 gm of protein on a 2000 calories diet. When discussing macronutrients, we have to specify grams of protein, grams of fat and grams of carbohydrate, otherwise the figures are meaningless.

What makes a diet ketogenic is that the amount of carbohydrate in the diet results in people’s body utilizing fat as its primary fuel and depending on the individual, how insulin resistant (IR) they are, how long they have been IR or had Type 2 Diabetes and whether they are male or female will affect the degree of carbohydrate restriction. Some may do very well with 100 gms of carbohydrate, while others may need to consume less.

Not everyone with lactose intolerance for example, needs to restrict milk to the same degree; some can tolerate 1 or 2 cups whereas other can only tolerate a few ounces. It is the same case with those that have become intolerant to carbohydrate. Different individuals depending on their metabolic state and clinical conditions,  have varying ability to process carbohydrate. That is why there is no “one size fits all” ketogenic diet.

The “Dangers” of Keto Diets

Some articles warn that “ketosis is actually a mild form of ketoacidosis” which is simply not true.

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

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

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

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

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

Final Thoughts…

There is no one “keto diet” but rather  many variations of ketogenic diets that are used for different therapeutic purposes. Depending on the condition for which a person is using a therapeutic ketogenic diet, the number of grams of fat, protein and carbohydrate will vary. Even in those utilizing a ketogenic diet for weight loss or lowing insulin resistance, the number of grams of carbohydrate will vary considerably person to person.

People following a ketogenic diet need to work closely with their doctor. For those on blood sugar- or blood pressure lowering medication this is very important, because clinical studies have demonstrated that the dosage of medication needs to be adjusted downwards as glycemic control is restored.

As with anything we read in magazines or on the internet, a healthy dose of discernment is needed. The person writing the article may not be current with the research in this field and be sincerely operating on an older paradigm. I encourage you to ask questions, read reviews of current studies using ketogenic diet for the condition of relevance (whether on this site or others) and to speak with your doctor. Let your decision will be an informed one, not fueled by dramatic headline with dire warnings and misinformation.

Have questions?

Please send me a note using the “Contact Me” form above.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

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

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

Why Grazing Can Look Like a Scene From Hoarders

INTRODUCTION: Most people know that prediabetes and diabetes is having “high blood sugar” but just how much sugar is actually in the human body? And how does grazing on food, rather than eating set meals affect this?

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” — and it may get this way by them “grazing” all day long, or eating more carbohydrate than their body can handle. 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 type 2 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. But what if the person is grazing all day long? The sugar just keeps on coming!

Some people have the ability to store the excess sugar 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 contributing to type 2 diabetes and fatty liver disease. It is easy to pack away excess carbohydrate when one is grazing instead of eating, because they don’t eat enough at anyone time to feel satiated (full).

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 often is that we never get to access our fat stores because we are grazing on food with carbohydrate in it 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.  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. The grazing continues…

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. Then, believing grazing is better than eating 3 big meals, 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! But isn’t grazing, and eating food we bring from home supposed to be healthier?

What 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 grazing on too much carbohydrate.

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 grazing 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 grazing on 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

https://twitter.com/lchfRD

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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.

The Role of Protein in the Diet – the history of man’s 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 article is part 2 in the series The Role of Protein in the Diet and focuses on the evolutionary history of foods and how we have adapted (or not!) to these foods.

The first article in this series titled The Role of Protein in the Diet – the problem with carbs is located here.

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)

It is almost universally accepted that when man was a hunter-gatherer, we ate largely an animal-based diet and this was distributed as 60% animal protein and 40% plant protein.  Naturally, there was some variation, depending on where people lived.  Those in the tropics tended to eat more plants and fish and the Inuit, who lived in northern climates had less green plants in their diet.

If we look at contemporary agriculture over the past 400-plus years out of the previous past thousands of years, what has absolutely changed is the appearance of cereal grains.

These were totally non-existent in the history of man’s diet previous to the agricultural revolution.

Legumes, such as peas, beans, chickpeas, lentils, etc. were also totally non-existent in the history of man’s diet previous to the agricultural revolution.

Sugars (outside of the little bit in wild honey or in the occasional fruit or berries), plant oils, alcohol and dairy products were simply non-existent before the agricultural revolution.

Our bodies did not evolve to see those things.

What does this means in terms of the foods we eat?

Let’s take fiber as an example. In the past, the plants man ate were very fibrous, both vegetables and fruit. Looking at our current cultivated plants wild cousins, provides some idea:

wild carrot

The earliest known carrots are thought to have been grown in the 10th century in Persia and Asia Minor and are believed to have originally been purple or white with a thin, forked root – like those shown here.

 

Bananas as we know them now are nothing like bananas our ancient ancestors ate. Modern bananas came from two wild varieties, Musa acuminata  and  Musa balbisiana, both of which were very fibrous and had large, hard seeds, like the ones seen in this photo.

The plants we ate traditionally were high in soluble fiber that were easily digested and broken down to form short chain fatty acids (SCFA) which acted in our bodies as prebiotics, as these SCFA are very good fuel for the bacteria in our colon.

The agricultural revolution changed all that, with the domestication of plants, and the shift to a diet high in cereal grains; rice, corn, spelt, etc. Debate rages about consuming more whole grain cereal grains, but those contain largely insoluble fiber, which are not well digested.  They don’t break down easily to SCFA and impact our microbiome (the healthy bacteria that lives in our colon).  These cereal grains typically come with a high Glycemic Index (GI) which means they have a strong effect on a person’s blood glucose level, raising it substantially.

Our bodies developed certain metabolism patterns based on the foods in our ancient diet.

  1. Extensive and elaborate pattern for handling protein: The human body has developed very elaborate patterns for handling protein digestion, metabolism and elimination. We have a very high satiety to protein (the feeling or state of feeling full) such that we won’t over eat it. According to Dr. Layman[1] it’s the only nutrient that causes us to stop eating it.
  2. Fat is a passive nutrient: Contrary to the common belief, fat is a very passive nutrient. It allows what happens to it, without an active response or any mechanism of resistance. Fat in and by itself has very little effect on our body. We store it effectively and break it down effectively and this is what allowed us to survive in the wilderness as hunter-gatherers.The nutrient that is odd in this mix is carbohydrates.
  3. Little evolutionary exposure to carbohydrate: Looking at our dietary history, we have comparatively very little exposure to carbohydrates. According to Dr. Layman, carbohydrates are highly toxic to the bodyGlucose has to be rapidly cleared after we eat it and the only mechanism we have to protect us from carbs is insulin (which acts to move the resulting glucose out of our blood and into our cells).

It’s important to put carbohydrates into perspective in terms of the biological systems that we have for handling them.

The traditional teaching is that carbs are handled in the muscle – which is true, if one exercises 2-3 hours per day.  North Americans are typically exercising that much at in the US, 75% of people are considered sedentary – that is, they have a lifestyle with little or no physical activity.

The carbs we eat at breakfast for example, top up our glycogen stores in our muscle, making us ready for fright or flight.

So let’s say we ate atypical breakfast that has 70 g of carbohydrate in it;

1/2 cup (125 ml) of cold cereal
1 slice of whole grain toast
1 medium orange
1 cup (125 ml) of low-fat milk
2 tbsp (30 mL) peanut butter
coffee or tea

Then, we sat in front of the computer all morning, so chances are we didn’t use any of the carbs from breakfast, and our glycogen stores are still full.

We get to lunch and eat another 100 g of carbs.

Our glycogen stores are still full, so where is that glucose going to? It has to go to fat.

When we have carbohydrates in excess, we make fat out of them.

The matter of carb regulation is very important to think about, because  blood sugar is one of the most tightly regulated substances in the body. We regulate our blood glucose in a very narrow range; between about 3.9-5.5 mmol/L (70-100 mg/dL).

Why does this matter?

Metabolic Syndrome (also called Syndrome X) says it matters a huge amount.

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 – Lewis, Tanya, What Fruits and Vegetables Looked Like Before Domestication, Business Insider, November 16, 2017, https://www.sciencealert.com/fruits-vegetables-looked-before-domestication

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.

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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.