Author: BBDN

Have you recently been told by your General Practitioner (CP) or gastroenterologist that you have “diverticulosis” and wonder how you should be eating differently to keep it from getting worse?

What is “diverticulosis”?

Diverticulosis is where your colon (large intestine) has small “pockets” in it called diverticula which can cause a number of symptoms or in some people, no symptoms at all.

Diverticula can vary in number from one to literally hundreds. Generally, diverticula increase in number and size over time and range in size from 0.5-1 cm (0.2-0.4 inch) in diameter to 2 cm (0.8 inch)[1]. Diverticulosis occurs in about 5% of adults younger than forty years old, but rise to at least 50% of those older than sixty, with 65% of those who older than 85 having diverticulosis[1].

These little pouches were once thought to be cause by a diet that was too low in fiber[1] which caused the stools to move too slowly though the colon, resulting in constipation. Based on this “fiber hypothesis”, the remedy was thought to be to eat a diet high in fiber; including whole grain bread, unprocessed wheat bran, porridge and fruit. For the last 50 years or so, increased fiber intake has been the recommendation for treatment of diverticulosis, including by the GI Society of Canada and the American Gastrolenterology Association recommends at least 25 g of fiber per day[2,3]. It was thought that increased fiber would increase the volume of the stool and thus require less straining to move the bowels and prevent weakening of the bowel wall, reducing the occurrence of these “pouches”.  Unfortunately, several recent studies have shed doubt on the “fiber hypothesis” [4-8].

Not only did a 2012 study find no association between a low fiber diet and diverticulosis [9], the study found that increasing total fiber intake in the form of grains, insoluble fiber and soluble fiber actually increased the prevalence of diverticulosis!

“People with the lowest fiber intake were 30% less likely to develop diverticula than people whose diets included the most fiber.” [9]

Subsequent studies have either found no association between the amount of fiber intake and diverticulosis [10] or that there was no association between diverticulosis and constipation symptoms [11].

These findings left researchers and clinicians with little evidence for continuing to recommend a high fiber diet in diverticulosis, but no alternative options.

ADDENDUM (July 17 2019): There are a number of hypotheses as to what causes diverticulosis with many thinking it could be related to colonic aging weakening of the smooth muscle bands, motor dysfunction, increased luminal pressure, as well of lack of dietary fiber.

Eating foods with soluble and insoluble fiber and drinking sufficient fluid is good, however the source of that fiber is now thought to be important, as I will outline below.

Logical Hypothesis for Diverticulosis

A recent hypothesis is that the increased pressure in the colon that resulted from the intake of so much fiber; particularly the types of fiber that are easily fermented by gut bacteria is what weakens the colon wall, resulting in these ‘pockets’ or diverticula.

What seemed to add credibility to this hypothesis is that historically (prior to WWII) diverticula were seen in a specific region of the colon (proximal colon) in people in Asian countries, with the condition only affecting the right side. This has been explained by the high prevalence of lactose intolerance (inability to digest the sugar in milk and dairy) which exists in Asians.  As well, the incidence of this right-sided diverticulosis has been lowest in European populations, where lactose intolerance is very low [12]. Similarly, in Western countries, most of the diverticula are on the left side of the colon, which is thought to be associated with the higher ingestion of wheat, compared historically to Asian countries [12]. 

Both lactose and the fructans in wheat are carbohydrates that are easily fermented by gut microbes and which results in high amounts of water being drawn into the colon, resulting in increasing pressure on the colon wall from the gas produced by the microbes, possibly leading to the creation of these diverticula. 

Of interest, consumption of wheat in Japan and in South Korea has increased considerably since WWII and there is now a considerably higher incidence of left colon diverticula now being observed there, as well [12].

Use of a low-FODMAP Diet in diverticulosis

FODMAPS is an acronym for fermentable oligosaccharides, disaccharides, monosaccharides and polyols (sugar alcohols) which are the specific types of carbohydrate that are fermented by the gut bacteria, resulting in increased gas production, abdominal pain, bloating and either diarrhea and constipation or a combination of both. These are very similar symptoms as are observed in Irritable Bowel (IBS) Syndrome and a low-FODMAP diet has long been used to minimize the symptoms in IBS, and is now being used to reduce the same symptoms in diverticulosis.

It is thought that use of a low-FODMAP diet in those with diverticulosis may reduce the occurrence of diverticulitis; which is painful inflammation of these diverticula that often requires medical treatment ranging from antibiotics and pain medication, to bowel resection as is common in Inflammatory Bowel Disease (IBD), such as Ulcerative Colitis and Crohn’s disease.

I offer a Diverticulosis Option for those who want to have specific nutrition education to help them reduce their symptoms and lower the likelihood of their disease progressing to diverticulitis.

Even if you are already following a low-carbohydrate diet and not eating wheat, foods with lactose or fruit, it’s important to know that there are a number of low carbohydrate vegetables that also contain some of these fermentable carbohydrates, as do many of the sugar alcohols many people following a low carb diets use. Reducing the intake of these specific vegetables and sticking to sweeteners that are low FODMAP can greatly help!

More Info

If you would like a Meal Plan designed just for you in light of your diagnosis, as well as specific nutrition education services on how to minimize the symptoms of diverticulosis and lower the likelihood of it progressing to diverticulitis, please click on the Diverticulosis Option, under the Services tab to learn more.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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. GI Society, Canadian Society of Intestinal research, https://badgut.org/information-centre/a-z-digestive-topics/diverticular-disease/
2. Painter NS, Diverticulosis of the Colon and Diet. Br Med J. 1969 Jun 21;2(5659):764-5.
3. American Gastroenterological Association. A Patient Guide: Managing Diverticulitis. Gastroenterology. 2015;149:1977—1978
4. Tan KY, Seow-Choen F. Fiber and colorectal diseases: separating fact from fiction. World J Gastroenterol. 2007;13:4161—4167. 
5. Unlu C, Daniels L, Vrouenraets BC, Boermeester MA. A systematic review of high-fibre dietary therapy in diverticular disease. Int J Colorectal Dis. 2012;27:419—427. 
6. Peery AF, Sandler RS. Diverticular disease: reconsidering conventional wisdom. Clin Gastroenterol Hepatol. 2013;11:1532—1537. 
7. Tursi A, Papa A, Danese S. Review article: the pathophysiology and medical management of diverticulosis and diverticular disease of the colon. Aliment Pharmacol Ther. 2015;42:664—684. 
8. Elisei W, Tursi A. Recent advances in the treatment of colonic diverticular disease and prevention of acute diverticulitis. Ann Gastroenterol. 2016;29:24—32.
9. Peery AF, Barrett PR, Park D, Rogers AJ, Galanko JA, Martin CF, Sandler RS. A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology. 2012;142:266—272
10. Peery AF, Sandler RS, Ahnen DJ, Galanko JA, Holm AN, Shaukat A, Mott LA, Barry EL, Fried DA, Baron JA. Constipation and a low-fiber diet are not associated with diverticulosis. Clin Gastroenterol Hepatol. 2013;11:1622—1627
11. Braunschmid T, Stift A, Mittlbí¶ck M, Lord A, Weiser FA, Riss S. Constipation is not associated with diverticular disease – Analysis of 976 patients. Int J Surg. 2015;19:42—45.
12. Uno Y, van Velkinburgh JC. Logical hypothesis: Low FODMAP diet to prevent diverticulitis. World J Gastrointest Pharmacol Ther. 2016;7(4):503—512. doi:10.4292/wjgpt.v7.i4.503

An analysis was published last week in the British Medical Journal which raised several important concerns about the World Health Organization (WHO)’s draft guidelines on fatty acids; including saturated fat.

The international group of 16 nutrition experts who wrote the paper are concerned as “many governments consider the WHO dietary guidelines to be state of the art evidence, translating them into regional and national dietary guidelines” [1].

In fact, this is exactly the case in Canada. The new Canada Food Guide that was just released on January 22, 2019 relied extensively on the WHO’s 2017 Guidelines for it’s policy regarding decreasing dietary saturated fatty acids (SFA), as indicated by the table below from pg. 5 of Health Canada’s Interim Evidence Update 2018 [2]. 

“These guidelines have potential health implications for billions of people, so the consistency of the science behind such recommendations and the validity of the conclusions are crucial”.

The authors state that the WHO, in their draft guidelines released in May 2018 “excluded some important aspects and studies” concerning evidence linking saturated fat intake and cardiovascular (CVD) risk.

“They [WHO] recommend reducing intake of total saturated fatty acids to less than 10% of total energy consumption and replacing with polyunsaturated fat and monounsaturated fat to reduce incidence of cardiovascular disease and related mortality. But this fails to take into account considerable evidence that the health effects vary for different saturated fatty acids and that the composition of the food in which they are found is crucially important.”[1]

The authors point out that the composition of the food in which the fatty acid is found has a substantial effect on lipid digestion, absorption, as well as the amount of emulsified fat that is found in the blood after a meal (postprandial lipemia), which “is an independent risk factor for cardiovascular disease.”[1]

The authors point out that recently there have been several meta-analyses of observational studies and randomized controlled trials (RCTs) that found that total saturated fat is NOT associated with coronary heart disease, cardiovascular disease, and all cause mortality (i.e. deaths). In addition they report that a Cochrane analysis found no significant association between reducing saturated fatty acids and total mortality, cardiovascular disease deaths, fatal and non-fatal myocardial infarction (MIs), stroke, coronary heart disease events, and coronary heart disease deaths.

Continued Reliance on Surrogate Endpoints

The authors note that the WHO draft guidelines continue, as they have in the past to (1) rely heavily on “surrogate endpoints” of the effect of dietary saturated fat intake on the level of lipid and lipoproteins in the blood — and (2) ignores the food source of the saturated fat.

They raise three key points;

1. Not all saturated fatty acids are equal; the amount and even the direction of the effects (raises or lowers) both surrogate and long term endpoints vary, depending on which fatty acid is involved.

2. Influence of the food source that the fatty acid is found in; the authors note that it has still not been determined whether any changes in blood lipoproteins translates into a lowering of cardiovascular risk and death, regardless of food source.

“Most trials included in the meta-analysis did not investigate whole food sources of saturated fat.”[1]

That is, the studies that WHO considered compared the effect of diets supplemented with fats rich in saturated fatty acids — not the effect of saturated fats in a specific food matrix.

One example of saturated fat in a whole food matrix cited in the paper is one of eggs; where there is “no association with coronary heart disease, and there is a reduced risk of stroke, and that randomized control trial data show that two eggs a day has beneficial effects on cardiovascular disease biomarkers“. (table 1, [1]).

3. Using LDL cholesterol concentration as a marker for cardiovascular disease risk. As I’ve written about in several previous articles, the authors note that the degree to which LDL particles are atherosclerotic is determined by, among other things, their size.

“Small and medium LDL particles show the strongest association with risk of cardiovascular disease, whereas large particles show no association.” [1]

in fact, the authors point out as I did in a recent article about red meat and white meat “raising cholesterol”, that a rise in serum LDL cholesterol concentration from total saturated fat consumption has been linked to a parallel increase in particle size “so it might not translate into an
increased risk of cardiovascular disease.”[1]

Excluding Observational Studies and Prospective Cohort Studies

The authors point out that the WHO draft guidelines exclude two types of studies from consideration; observational studies and prospective cohort studies because they argue that the quality of the evidence is lower than from
analyses of RCTs, and that it was not possible to assess the potential differential effects of replacing saturated fatty acids with different nutrients.

The problem with this is that (1) observational studies enable assessing the association between saturated fat and cardiovascular disease  rather than simply looking at the association between surrogate endpoints” (i.e. saturated fat and LDL-c) and (2) observational studies enable examining of the actual foods that people eat, rather than just individual nutrients, as

“Longstanding evidence indicates that the food matrix is more important than its fatty acid content for predicting the effect of a food on risk of coronary heart disease.”

The authors concluded;

“A recommendation to reduce intake of total saturated fat
without considering specific fatty acids and food sources is not
evidence based; will distract from other more effective food-
based recommendations; and might cause a reduction in the
intake of nutrient dense foods that decrease the risk of
cardiovascular disease, type 2 diabetes, other serious
non-communicable diseases, malnutrition, and deficiency
diseases and could further increase vulnerability to nutrient
deficiencies in groups already at risk.

Final thoughts

This analysis adds a critical academic “voice” to the concern of limited saturated fat intake which may translate a reduction in the intake of nutrient-dense whole foods.

In fact, this was precisely the concern that I raised in my recent article about the Canada Food Guide “Snapshot” which came out at the end of June and which linked an image of ultra-processed foods with the message “limit foods high in sodium, sugars or saturated fat”. After all, meat is high in saturated fat and cheese is high in saturated fat and sodium, but are these really the types of whole, real foods that Canadians should be advised to limit?

More Info?

If you would like more information about choosing whole, real food and limiting ultra-processed foods, I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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. Astrup A, Bertram HCS, Bonjour J-P et al, WHO draft guidelines on dietary saturated and trans fatty acids: time for a new approach? BMJ 2019; 366: l4137 doi: 10.1136/bmj.l4137
2. Health Canada. Food, Nutrients and Health: Interim Evidence Update 2018. Ottawa: Health Canada; 2019.

Note: This article is a combination of a Science Made Simple article, with the references below and an editorial which provides my opinion.

Dietary advice ⁠— especially National Dietary Guidelines ought to give clear, consistent messages. It would seem that the new Canada Food Guide ‘snapshot’ outlined in the previous article may inadvertently cause considerable confusion as to which foods are healthy and which are not.

The new Canada Food Guide ‘snapshot’ released last week shows a photo of ultra-processed products as foods to avoid, yet the label beneath the photo reads “limit foods high in sodium, sugars or saturated fat” (see circled part of photo, below).

In fact, when the image of these processed foods is clicked on the Health Canada website, it brings the reader to a page listing the “Benefits of Limiting Highly Processed foods” and has paragraphs below for Sodium, Sugars, and Saturated Fat. 

In my opinion, this conflates two issues. 

Advising people to limit ultra-processed food is not the same as advising them to limit saturated fat, sodium and sugar. 

There are many whole unprocessed foods and minimally processed foods such as meat, eggs, cheese, yogourt, olives and berries that have sustained humans through thousands of years of history that contain these elements and are unlikely to be responsible for our current epidemics of obesity, diabetes, hypertension and cardiovascular disease that we now face.

As mentioned in an earlier article about distinguishing between food and food-like products there is a big difference between the three categories of food as defined by the NOVA food classification system [2,3,4]. Unprocessed Foods such as meat, chicken, fish and eggs are whole, real food in their original state and Minimally Processed Foods such as cheese, yogourt or pickled and cured fish or meat or olives are foods that have been preserved in some fashion by curing, smoking or soaking in brine. Foods such as meat, eggs, cheese and olives may be high in saturated fat or sodium but have been part of the human diet for thousands of years without compelling evidence that these pose a risk to human health.

It may be helpful to recommend that people consume pickled, cured meat and fish in smaller quantities, not because these foods are high in saturated fat or sodium, but because many are now made in less traditional ways that involve the use of chemical additives.

The primary health concern that I see it is that Ultra Processed Foods is making up more than 50% of the Canadian (and American) diet and really isn’t food at all. These are manufactured products made from a combination of refined carbohydrates (including sugar) and seed oils and are convenient, hyper-palatable and cheap — and displace real food from the diet. In fact, some of the most addictive foods available to us are ultra processed foods; including breakfast cereal, muffins, pizza, cheeseburgers, French fries and fried chicken — and desserts such as chocolate, ice cream, cookies and cake, as well as the soda we wash them down with [5]. These ultra processed foods are full of “empty calories” / have little nutritional value, and full of refined fats and refined carbs. It is for this reason ultra processed should be limited — not because it is high in saturated fat and sodium. 

Even though fruit as we now know it has been bred over the last 50-100 years to be hyper-sweet, for metabolically healthy people there is still no comparison between natural whole fruit such as berries or an apple, and sugary pop. One is real, whole unprocessed food and the other is ultra processed.

In my opinion, it makes good sense for Health Canada to show a photo of ultra-processed foods as they had (above)with advice to limit them — but because they are ultra processed, not because they are high in saturated fat or sodium.

Shifting the Focus off Saturated Fat Based on the Evidence

As covered in several previous article on this site, while research does indicate that dietary saturated fat raises low density lipoprotein cholesterol (LDL-cholesterol) in the blood, distinction in these studies isn’t made between the small, dense LDL sub-fraction which is atherosclerotic, and the large, fluffy LDL which is not. This recent study makes this distinction; demonstrating that saturated fat from red meat and poultry raises the large, fluffy LDL and cardio-protective HDL, but not the small dense (atherosclerotic) LDL.

Epidemiological studies that do exist provide a very mixed picture of any possible association between saturated fatty acids and cardiovascular disease (heart disease and stroke); with recent studies finding no association [6,7]. Even more compelling, the data from the Prospective Urban and Rural Epidemiological (PURE) Study which was the largest prospective epidemiological study to date involving many different countries found that dietary saturated fat was actually beneficial; with those who ate the largest amounts of saturated fat having significantly reduced death rates and that those that ate the lowest amounts of saturated fat (6-7% of calories) had increased risk of stroke [8].

In addition, according to the Canadian Heart and Stroke Foundation position statement titled ”Saturated Fat, Heart Disease and Stroke” released in September 2015 [9], different saturated fatty acids (e.g. lauric, stearic, myristic and palmitic acids) have different effects on blood cholesterol, so we can’t simply lump all saturated fats together.

Focus on Where Change is Needed

I believe that national guidelines such as Canada’s Food Guide should focus on eliminating ultra-processed foods from the diet because these form almost half of caloric intake with little nutrients and displace real, whole nourishing food from the diet.

This makes good sense.

In my opinion, the linking of ultra processed foods to saturated fat and sodium as has been done in this most recent Canada Food Guide ‘snapshot’ will end up confusing the public that things like fried chicken and cheese are both equally unhealthy because they are high in saturated fat and salt.

It would be far more helpful to highlight the benefits of whole, unprocessed foods and minimally processed foods while encouraging the public to limit ultra processed foods.

More Info?

If you would like more information about limiting ultra-processed foods, while including whole, real foods (plant-based and animal-based), I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019  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. Health Canada Snapshot: https://food-guide.canada.ca/en/?utm_source=canada-ca-foodguide-en&utm_medium=vurl&utm_campaign=foodguide
2. Moubarac JC, Batal M, Martins AP, Claro R, Levy RB, Cannon G, et al. Processed and ultraprocessed food products: Consumption trends in Canada from 1938 to 2011. Can J Diet Pract Res. 2014 Spring;75(1):15-21.
3. Monteiro CA, Moubarac J-C, Cannon G., Ng SW, Popkin B. Ultra-processed products are becoming dominant in the global food system. Obes Rev. 2013
4. Moubarac JC. Ultra-processed foods in Canada: consumption, impact on diet quality and policy implications. Montréal: TRANSNUT, University of Montreal; December 2017Nov;14 Suppl 2:21-8. doi: 10.1111/obr.12107.
5. Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959
6. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of dietary, circulating and supplement fatty acids with coronary risk: A systematic review and meta-analysis. Ann Internal Medicine 2014;160:398-406.
7. Sri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nut 2010;91(3):535-546.
8. 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
9. Heart and Stroke Foundation of Canada, Position Statement ”Saturated Fat, Heart Disease and Stroke, September 24, 2015, https://www.heartandstroke.ca/-/media/pdf-files/canada/position-statement/saturatedfat-eng-final.ashx

Note: This article is a combination of a Science Made Simple article with references below and an editorial which provides my opinion.

This past Monday, Health Canada released the Canada’s Food Guide “snapshot”[1] in 28 languages which is not intended to be a stand-alone resource, but to be used as a tool to guide people to the Canada’s Food Guide website.

Canada’s Food Guide includes Canada’s Dietary Guidelines[2], the healthy eating recommendations[3], and all of the other resources and information on the Canada’s Food Guide website. Links to the guidelines and healthy eating recommendations are available in the References, below.

The “Snapshot”

The main message of the “snapshot” is that “healthy eating is more than the foods you eat” ⁠— which I think is an excellent way of summarizing the guidelines and recommendations and encouraging the public to want to learn more. From that point of view, the snapshot is successful in that it is likely to guide people to the website.

The main points on the Snapshot are;

1. Be mindful of your eating habits
2. Cook more often
3. Enjoy your food
4. Eat meals with others
5. Use food labels
6. Limit foods high in sodium, sugars or saturated fat*
7. Be aware of food marketing

Each of these points link to the sections of Canada’s Food Guide which address those points and in my opinion are all very helpful, except for one elaborated on below.

For example, under “Be mindful of your eating habits” is and encouragement for Canadians to be aware of;

• how you eat
• why you eat
• what you eat
• when you eat
• where you eat
• how much you eat

Being mindful can help you:

• make healthier choices more often
• make positive changes to routine eating behaviours
• be more conscious of the food you eat and your eating habits
• create a sense of awareness around your every day eating decisions
• reconnect to the eating experience by creating an awareness of your:
  • feelings
  • thoughts
  • emotions
  • behaviours

As the Snapshot re-iterates, these are factors that are “more than the food you eat” and helpful for people to keep in mind.

My only issue with the “Snapshot” is the use of the image for “Limit foods high in sodium, sugars or saturated fat“, circled below.

Here is that image by itself;

What I see when I look at this image is ultra-processed food (what I refer to in a previous article about the NOVA Food Classification System as “food-like products“.

These are not whole, real food, but are creations of the food industry that are intended to displace real, whole food from the diet (you can read more about that by clicking here). These are products that are “branded assertively, packaged attractively, and marketed intensively“.

In fact, this picture shows some of the most addictive foods listed in a 2015 study including chocolate, muffins, pizza, pastry and soda pop[4].

If the intention is for Canadians to “limit foods high in sodium, sugars and saturated fat” (not that I think there is solid, scientific evidence that healthy individuals necessarily need do so with all sources of saturated fat and sodium), in my opinion the following photo would be a more accurate reflection of that principle;

Cheese, eggs and meat are high in saturated fat, and cured meats are high in sodium and saturated fat, and dates are certainly very high in sugar, but are not ultra-processed foods. Are these really foods that all Canadians should limit?

Is there irrefutable scientific evidence that healthy people should limit eggs, real cheese and whole fresh meats and poultry? Is it “unhealthy” for metabolically well folks to eat dates, which are very high in sugar? Or are we conflating whole, real food with ultra-processed food?

Using the NOVA food classification (outlined in the article linked above) that foods such as cheeses, cured meats and olives or anchovies are minimally processed foods that have been processed to make them ore durable and palatable, but they are not “ultra-processed foods” akin to hot dogs, pizza and pop!

I don’t believe that it is helpful to lump “ultra-processed food” and whole, real food that are high in saturated fat, sodium and sugar, together.

In my opinion, it would far better for the image in the Snapshot to read like this;

It makes good sense to advise Canadians to limit ultra-processed food⁠ because they are high in refined carbohydrates and refined fats, and low in nutrient density ⁠— but when ultra-processed food is labelled with the advice “limit foods high in sodium, sugar or saturated fat”, whole, real foods are conflated with food-like products which displace real, whole food from the diet.

More Info?

If you would like more information about limiting ultra-processed foods, while including whole, real foods that are both plant-based and animal-based, I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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. Health Canada Snapshot: https://food-guide.canada.ca/en/?utm_source=canada-ca-foodguide-en&utm_medium=vurl&utm_campaign=foodguide
2. Health Canada, Canada’s Dietary Guidelines, https://food-guide.canada.ca/en/guidelines/
3. Health Canada, Healthy Eating Recommendations, https://food-guide.canada.ca/en/healthy-eating-recommendations/
4. Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959

The maintenance of blood sugar is very tightly regulated; with a healthy person’s blood glucose being kept in the range from 3.3-5.5 mmol/L (60-100 mg/dl) between meals, however a new study indicates that it may be newer variant of a gene that determines how well (or not) we are able to maintain these levels.

After eating, the higher levels of blood glucose that comes from the broken-down carbohydrate-based food triggers the release of insulin by the pancreas, which in turn causes the release of a special transporter called GLUT4.  The GLUT4 transporter acts like a taxi to remove excess glucose from the blood, taking it into muscle and fat tissue.

Newer Variant of an Older Gene

Between meals and with the help of a special protein (CHC22) produced by the CLTCL1 gene, the GLUT4 glucose transporter remains inside muscle and fat, so that some blood sugar will continue to circulate.

A newly published study [1] by research specialists in population genetics, evolutionary biology, ancient DNA and cell biology analyzed the human genomes to understand how the gene producing CHC22 has changed over human history [2].

By examining the genomes of 2,504 people from the global 1000 Genomes Project compared to the genomes of ancient humans, researchers found that almost half of the people in various ethnic groups have a variant of CHC22 protein that is produced by a new variant of the CLTCL1 gene that became more common as humans moved away from being hunter-gathers and began farming and raising crops. Researchers postulate that the increased consumption of carbohydrates may have been the selective force driving this genetic adaptation.

Researchers found that the newer CHC22 variant of the gene is less effective at keeping the GLUT4 glucose transporter inside muscle and fat tissue between meals, which means that the transporter can more readily clear glucose out of the blood*.

As a result, people with the newer variant of the gene will have lower blood sugar than those with the older variant of the gene.

“The older version of this genetic variant likely would have been helpful to our ancestors as it would have helped maintain higher levels of blood sugar during periods of fasting, in times when we didn’t have such easy access to carbohydrates, and this would have helped us evolve our large brains”[2] — lead author Dr Matteo Fumagalli

*Note: It’s important to keep in mind that only GLUT4 transporters are insulin-dependent. There are other glucose transporters that allow glucose into the cell that don’t involve insulin, such as the GLUT1 transporter that works on a concentration gradient. That is, the effect of this gene is not on all glucose regulation, but only glucose regulation in adipose and muscle cells that use GLUT4 transporters.

The higher carbohydrate diets that came as a result of the advent of agricultural meant that this newer variant of the gene could be advantageous, as it moves the excess blood sugar from the blood into the muscle and fat tissue and having the older variant of the gene may make people more likely to develop Diabetes and may also make worse the insulin resistance that underlies the process of developing Diabetes.

“People with the older variant (of the gene) may need to be more careful of their carb intake, but more research is needed to understand how the genetic variant we found can impact our physiology”[2] — co-author Dr. Frances Brodsky 

Along with the 2015 study from Israel[3] that demonstrated substantial differences in blood glucose response between both healthy individuals and those with Diabetes predictable by their gut microbiome, this new research adds to the knowledge that multiple factors are involved with determining whether people can tolerate specific dietary carbohydrate loads.

Nutritional guidelines for maintaining healthy blood glucose levels are portrayed as universally applicable, however this new study and the 2015 Israeli study demonstrates that blood glucose varies significantly between individuals based on genetics as well as on gut microbiota composition, which necessitates the need for personalized nutrition in managing blood glucose levels.

More Info

If you are interested in a personalized approach aimed at helping you gain control of your blood sugar levels, I can help.

I offer both in-person services in my Coquitlam, British Columbia office as well as remote services via Distance Consultation. You can find more information about my packages under the Services tab or in the Shop and if you would like to learn more about how Distance Consultation services work, you can click here.

Have Questions?

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
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Copyright ©2019 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. Matteo Fumagalli, Stephane M Camus, Yoan Diekmann, Alice Burke, Marine D Camus, Paul J Norman, Agnel Joseph, Laurent Abi-Rached, Andrea Benazzo, Rita Rasteiro, Iain Mathieson, Maya Topf, Peter Parham, Mark G Thomas, Frances M Brodsky. Genetic diversity of CHC22 clathrin impacts its function in glucose metabolism. eLife, 2019; 8 DOI: 10.7554/eLife.41517
2. University College London. “Gene mutation evolved to cope with modern high-sugar diets.” ScienceDaily. ScienceDaily, 4 June 2019, https://www.sciencedaily.com/releases/2019/06/190604084857.htm
3.  Zeevi D, et al. Personalized nutrition by prediction of glycemic responses. Cell. 2015;163:1079—1094.
4. Noecker C, Borenstein E. Getting Personal About Nutrition. Trends Mol Med. 2016;22(2):83—85. doi:10.1016/j.molmed.2015.12.010

INTRODUCTION: There much debate in the health community about the effect of dietary fat — especially saturated fat on cholesterol levels and whether there is an association between dietary saturated fat intake and cardiovascular disease.

In the first part in this two-part series titled High Cholesterol and the Risk of Cardiovascular Disease, I explained what cholesterol is, the different types of cholesterol (HDL-C, VLDL, LDL-C and triglycerides (which are not actually cholesterol), what their role is, and what “high cholesterol” is.

In this article which is Part 2 in the two-part series, I will explain the association between dietary intake of saturated fat and higher levels of total LDL, and whether reducing total LDL — whether through the use of statin medication or diet lowers the risk of cardiovascular disease.

Dietary Saturated Fat and LDL

When people are told that they have “high cholesterol”, what is meant is that they have high total LDL. They are told they have high “bad” cholesterol, with no regard that there are different sub-fractions of LDL.

It is well known that eating foods high in saturated fat can raise LDL-C (total LDL cholesterol, but as covered in Part 1 of this two-part series, the first question one should ask when told they have “high LDL cholesterol” is “which LDL? The small dense ones or the large fluffy ones?”[1].

More often than not, the clinician that breaking the ‘bad news’ to the patients has absolutely no idea that there are different sub-fractions of LDL and that it is only the small, dense ones that are atherosclerotic [1].

Furthermore, there is almost a knee-jerk reaction on the part of many clinicians to prescribe statin medication in order to lower their LDL, on the assumption that lowering LDL will lower their risk of cardiovascular disease. In fact, aggressive treatment to lower total LDL-C has been at the (pardon the pun) heart of preventative cardiology for decades.

While statin medication (e.g. Lipitor®, Crestor®, etc.) is well-documented to reduce LDL-C levels, these are only surrogate markers (not direct markers) of cardiovascular disease (CVD). The assumption of an association between high LDL levels and CVD goes back as far as Ansel Keys and the Seven Country Study, and that the Diet Heart Hypothesis (covered in several previous articles) is simply an “establish fact”. But it is?

What evidence is there that lowering total LDL with statin medication lowers one’s risk of cardiovascular disease (CVD)?

The brand new guidelines on cholesterol management issued by the American Heart Association (AHA) and American College of Cardiology (ACC) which has just been published online ahead of print[2], places a renewed focus on LDL-C as a means to assess risk. In fact, these guidelines propose that non-fasting lipids be adopted as a screen in the general population, including “non-adults” (children and youth) [2]. As has been the case for decades., this is based on the assumption that total LDL (LDL-C) is an accurate surrogate marker for elevated cardiovascular risk, but does lowering LDL-C really lower CVD?

Of particular interest, the new American Heart Association (AHA) and American College of Cardiology (ACC) guidelines state that the traditional Friedewald equation which is used to calculate total LDL (i.e. LDL-C) as covered in Part 1 of this series of articles has been “prone to inaccuracy …at low-LDL-C and high triglyceride levels” — yet decades of statin treatment has been based on the previous “inaccurate” Friedewald equation. The new guidelines promote the use of a new Martin/Hopkins LDL-C calculation method which is said to “perform better in these settings”. The question remains ‘does lowering LDL-C lower the risk of cardiovascular disease?’.

There are 44 randomized controlled trials of drug or dietary interventions to lower total LDL ( LDL-C) published in the literature which show no benefit in lowering rates of death [3] and most did not reduce CVD events [4].

Furthermore, despite a 37% drop in LDL-C and a 130% increase in HDL-C (so-called “good cholesterol”), the ACCELERATE double-blind randomized control  trial showed no significant reduction in CVD or death [3.4].

In addition, there does not appear to be a clear reduction in CVD deaths in Western European countries either as a result of using statins for prevention [5].

This begs the question as to whether using statin medication to aggressively lower LDL-C has any benefit.

A 2018 article published in Expert Review of Clinical Pharmacology concluded;

“For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.” [6]

What about lowering the intake of dietary saturated fat? Does that lower the risk of cardiovascular disease?

A 2014 meta-analysis of data of 72 studies involving more than 600,000 participants from 18 countries published in the journal Annals of Internal Medicine in 2014 [7] concluded that total saturated fat; whether measured in the diet or in the bloodstream showed no association with heart disease [7].

Take away: While eating dietary fat may raise the level of total LDL cholesterol (LDL-C), lowering its intake does not show any benefit in reducing the incidence of heart disease, nor does lowering LDL-C using statin drugs.

Which LDL?

A brand new study published June 4, 2019 in the American Journal of Clinical Nutrition sheds some very helpful light [8].

The study enrolled 113 people and randomized them to either a high saturated fat diet (40% carbs, 24% protein, 35% fat; 14% saturated fat) or a low saturated fat diet (40% carbs, 24% protein, 35% fat; 7% saturated fat replaced by monounsaturated fat).

Each group changed their diet every 4 weeks from (a) a high red meat diet (mostly from beef), (b) a high white meat diet (chicken and turkey) and (c) a non-meat protein diet (legumes, nuts, grain and soy).

Researchers found that LDL cholesterol and Apolipoprotein B (explained in the first part of this article) were higher with red and white meat alike and that the increase “was due primarily to increases in large LDL particles” with no change in the small particles and no significant change in the total cholesterol to HDL ratio.

This is highly significant!

What this means is that yes, eating meat; whether it’s red meat (such as beef, lamb or goat) or white meat (such as chicken or turkey) DOES increase LDL —but it’s the large, fluffy LDL particles that are increased; the ones that are not associated with cardiovascular disease[1]!

In fact, in the paper, the researchers acknowledge;

“Large LDL particles, measured by several different methodologies, have not been associated with CVD in multiple population cohorts in contrast to the associations observed for concentrations of medium, small, and/or very small LDL… Thus, the estimated impact of red meat, white meat, and dairy-derived saturated fatty acids (SFA) on CVD risk as reflected by their effects on LDL cholesterol and ApoB concentrations may be attenuated by the lack of their effects on smaller LDL particles that are most strongly associated with CVD.

Essentially, there has been on over-reliance on total LDL cholesterol (LDL-C) as a marker of cardiovascular disease, without distinguishing the atherosclerotic small, dense LDL from the non-atherosclerotic large, fluffy LDL.

The authors conclude;

“…the impact of high intakes of red and white meat, as well as saturated fatty acid (SFA) from dairy sources, which selectively raised large LDL sub-fractions may be overestimated by reliance on LDL cholesterol, as is the case in current dietary guidelines.”

This means that eating red meat (such as beef or lamb) or white meat (such as chicken or turkey) or eating saturated fat from full-fat dairy (such as full fat milk, cheese and yogurt) are associated with increased levels of the large, fluffy LDL sub-fraction and based on multiple population studies the large, fluffy LDL subfraction has not been found to be associated with cardiovascular disease.

Simply put, this means that eating foods high in saturated fat does not raise small LDL particles (which are the atherosclerotic sub-fraction) and results in no change to the total cholesterol to HDL ratio, and increases the large, fluffy LDL-subfraction (which are NOT found to be associated with cardiovascular disease)!

While this is a small pilot study, it adds further evidence that eating saturated fat does not increase cardiovascular risk.

Note: high levels of the small, dense LDL sub-fraction is thought to be genetic, but is also associated with intake of trans fatty acids and high intake of refined carbohydrates. More on that in future articles.

More Info?

If you would like to learn more about my services, you can find more information under the Services tab or in the Shop and if you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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.

1. Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
2. Cao J, Devaraj S, Recent AHA/ACC guidelines on cholesterol management expands the role of the clinical laboratory, Clinica Chimica Acta 495 (2019) 82—84, Available online 03 April 2019.
3. DuBroff R. Cholesterol paradox: a correlate does not a surrogate make. Evid Based Med,2017;22(1):15—9. doi: 10.1136/ebmed-2016-110602
4. Demasi M, Lustig RH, Malhotra A, The cholesterol and calorie hypotheses are both dead — it is time to focus on the real culprit: insulin resistance, Clinical Pharmacist, 14 July 2017.
5. Vancheri F, Backlund L, Strender L et al. Time trends in statin utilisation and coronary mortality in Western European countries. BMJ Open 2016; 6(3):e010500. doi: 10.1136/bmjopen-2015-010500
6. Ravnskov U, de Lorgeril M, Diamond DM, et al, LDL-C does not cause cardiovascular disease: a comprehensive review of the current literature, Expert Review of Clinical Pharmacology, 2008;11:10, 959-970, DOI: 10.1080/17512433.2018.1519391
7. Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, et al. Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis. Ann Intern Med. 2014;160:398—406. doi: 10.7326/M13-1788

INTRODUCTION: There is much debate in the scientific community about the effect of dietary fat — especially saturated fat on cholesterol levels and risk of cardiovascular disease. To best understand this complex topic, I have broken the subject into two articles. In this first part, I explain the different ways cholesterol values are assessed, what they are used for and what they mean. In the next part I will explain whether lowering LDL and dietary saturated fat lowers the risk of cardiovascular Disease.

What is Cholesterol?

INTRODUCTION: National dietary guidelines in both Canada and the US focus on the variety of foods available in each of several defined ‘food groups’ and make recommendations about “healthy eating” based on how much of particular nutrients are in specific foods.  In Canada for example, foods that are rich in saturated fat, sodium or sugar are said to undermine health. This type of classification results in dishes rich in cheese and fried chicken both being deemed as unhealthy, as both are high in saturated fat and sodium. 

This article outlines an internationally established way of classifying foods that is based on the degree of food processing they have undergone — which I believe provides a better framework to help people to choose which foods they should aim to eat most often.

Many of us have heard the alarming health statistics in both the US and Canada, but they are worth repeating.

Obesity has risen in Canada from < 10% in 1970-1972 to almost 15% in 1989, to over 23% in 2004 [1,2]. That is, in the early 1970s, only one in 10 people in Canada was obese and now almost 1 in 4 people in Canada are obese [3]. The prevalence of obesity among American adults is almost 40% as of 2015-6 [4]. 

And it’s not only adults.

As of 2015, over 10% (1 in 10) children between the ages of 5 and 17 years of age in Canada were obese[3] and that figure rises to 20% (1 in 5 kids) in the United States [4]. 

It’s not only obesity.

As of 2015,  >25% of Canadians adults have been diagnosed with high blood pressure[3] and as of 2013, >30% of American adults have high blood pressure [5]. That’s 1 in 4 in Canada and 1 in 3 in the US [4] with hypertension; a major risk factor for heart attack and stroke.

Over 8% in Canada have been diagnosed with coronary heart disease (CHD) [3] and in the US, coronary heart disease accounts for ~13% of deaths as of 2016 [6] and over 8% of Canadians has diabetes [3] and in the US, almost 9.5% of Americans has diabetes [7].

What has changed over this time period to account for this? 

Too Many Carbs?

When I first started writing articles about obesity and the increased rates of metabolic diseases ~ 4 years ago, I thought it was largely related to the increased in carbohydrate content of the diet due to changes in the national dietary guidelines that occurred in Canada and the US in 1977. To some degree there is a relationship between these, but it is not as clear-cut as I once thought.

Industrial Seed Oils (Polyunsaturated Vegetable Oil)

With further reading in the scientific literature, I came to believe that it was the inclusion of novel “seed oils” (also called “polyunsaturated vegetable oil”) including canola, soybean, corn and cottonseed oil — along with too much carbohydrate in the diet that lay at the root of obesity and metabolic disease and while this is certainly part of the story, I was still missing a vital piece of the puzzle.

Manufactured Food-like Products

As national dietary guidelines in both Canada and the US in 1977 focused on reducing dietary intake of fat — especially saturated fat, food manufacturers sought to fill the gap left by the removal of butter, cream, lard and tallow (saturated fats) from the diet, and began to manufacture products that were made up of both refined carbohydrate and industrial seed oils (“polyunsaturated vegetable oils”). The food industry heavily marketed these manufactured products and promoted them as being “low in saturated fat”, which was perceived by the general public as being equivalent to “healthy”.

Since the mid-1980s, the food supplies of high-income countries such as Canada, the US, Australia and the UK have been dominated by pre-packaged, ready-to-eat “convenience foods” [13]. In fact, the percentage of energy (calories) in the diet of Canadians of these “ultra-processed foods” rose from <25% in 1938 (when manufactured products such as Crisco and soy oil were first created) to almost 54% in 2011 (9). Similar trends have been observed worldwide (10-12).

It is my now my conviction that it has been the over-consumption of these ultra-processed “convenience foods” that are high in both refined carbohydrate and seed oils which precipitated the huge deterioration of the Western diet, and which has fueled the concurrent epidemics of obesity, diabetes and other chronic diseases, such as hypertension and coronary heart disease [8].

Hundreds of thousands of people in Canada, and millions worldwide are metabolically unwell because the bulk of the diet has centered around eating these manufactured food-like products — from our morning sweetened cereal or spreads on toast to the burger with ‘plastic cheese’ and French fries we grab in place of real food.

So how do we distinguish real food from food-like products?

The NOVA Food Classification system – defining “processed food”

From the time food is harvested to when it is eaten, most food is processed in some way. Some of this processing may be as simple as peeling and chopping it, to cooking it, but food doesn’t become “unhealthy” just because it is processed. The issue is how much it is processed.

NOVA is a food classification system developed in Brazil and used in the US, Canada and other countries around the world to define the level of food processing.

The NOVA definition of types of food processing are as follows [13]:

Minimally processed foods are defined as ”unprocessed foods altered in ways that do not add or introduce any new substance (such as fats, sugars, or salt) but often involve removal of parts of the food.”  Examples of these include fresh, dry, or frozen vegetables, root vegetables, grains and legumes, fruits and nuts, and meats, fish, seafood, eggs, and milk [13]. For the most part, minimal processing is what’s involved in preparing it for eating and/or improving its palatability.

Processed foods are defined as ”foods made by adding fats, oils, sugars, salt, and other culinary ingredients to minimally processed foods to make them more durable and usually more palatable, and by various methods of preservation“.  They include simple breads and cheeses; salted, pickled or cured meats, fish and seafood; and vegetables, legumes, fruits and animal foods preserved in oil, brine or syrup.

Canned fish in oil would fall in this category, as would hummus (ground chickpeas with sesame seed butter, garlic and lemon juice), as well as bacon and sausages.

These foods can be part of a healthy diet, depending on how they are prepared and used in dishes and meals [13] and how much of these are eaten at a time.

Ultra processed foods are defined as ”not modified foods, but formulations of industrial ingredients and other substances derived from foods, plus additives. They mostly contain little if any intact food. The purpose of ultra-processing is to create products that are convenient (durable, ready-to-eat, -drink or -heat), attractive (hyper- palatable), and profitable (cheap ingredients). Their effect all over the world is to displace all other food groups. They are usually branded assertively, packaged attractively, and marketed intensively.“

Foundations for Healthy Eating using Degree of Food Processing

I like to define foods as being either “everyday foods” or “sometimes foods”.  The issue is how much and how often we eat them.

“Everyday Foods”

Choosing foods to make up a meal should aim to include mostly unprocessed foods (whole foods in their original state) and minimally processed foods. This is how our grand-parents and great-grandparents ate (when obesity, hypertension and diabetes rates were a fraction of what they are now!).

Another way to determine what foods to include in a meal is to eat food that your great-grandparents would recognize as food.

“Sometimes Foods”

For people who are metabolically healthy, eating “processed foods” such as breads and cheese,  salted, pickled or cured foods (including meat, fish, seafood, vegetables, legumes) and whole foods preserved in oil or brine are perfectly fine to add to unprocessed foods (whole foods in their original state) and minimally processed foods to make up a meal.

For those who are already overweight or metabolically unhealthy, focusing on making up a meal of real, whole foods in their original state (i.e. unprocessed foods) and minimally processed foods is best, while limiting processed foods. How much bacon, olives, bread and cheese can be eaten really depends on a person’s metabolic health. This is where having a Meal Plan designed by a Dietitian is helpful because everybody’s needs are different.

Ultra-Processed Food

Ultra-processed food isn’t food. They are products made from a combination of refined carbohydrates (including sugar) and seed oils. These are convenient, hyper-palatable and cheap, and displace real food in the diet.

According to a 2015 study, some of the most addictive foods are in this category; including breakfast cereal, muffins, pizza, cheeseburgers, French fries and fried chicken — as are the desserts that often eaten with them including chocolate, ice cream, cookies and cake, and the soda we wash them down with. Even our favourite snacks like popcorn and chips are really nothing more than a combination of refined carbs and industrial seed oil eaten in place of real food.

These ultra-processed food-like products are intended to displace real food in the diet and as such are not something we should consider as components for making up a meal.

Does that mean we should never eat a slice of pizza or a cheeseburger? Of course not. But let’s be fully aware that this is not real food. It is something we eat in place of real food.

As well, there is a huge difference between a homemade burger with real melted cheddar cheese on top — sandwiched between fresh leaf lettuce and tomato, and what can be picked up at a 1000 drive-throughs in cities around the Western world.

National Food Guidelines as foundations for healthy eating

National food guidelines in both Canada and the US have traditionally categorized food based on the variety available in each food group; including grains and cereals, vegetables &/or fruit. milk and dairy, and meats and alternatives.

In the case of the new Canada Food Guide, it recently eliminated the Milk and Dairy food group and combined those foods with Protein foods. The other two food groups are now Grains and Vegetables and Fruit.

The new Guide centers it’s dietary advice around 3 “Guidelines”.

Guideline 1 of the new Canada Food Guide focuses on eating from the different food groups and stresses that Canadians should eat plant-based foods more often because they lower intake of saturated fat. 

Guideline 2 of the new Canada Food Guide encourages Canadians to limit processed or prepared foods and states the reason is because they contribute excess sodium, sugar and saturated fat.

Based on this definition, dishes made with lots of cheese and fried chicken are high in saturated fat and sodium, and thus are categorize as foods that undermine healthy eating.

Does eating cheese really undermine healthy eating?

Or a rib steak?

Or milk?

As covered in previous articles I’ve written on the new Canada Food Guide,  I am not convinced that there is a compelling reason to limit real, whole food simply because it is high in saturated fat.

Guideline 3 of the new Canada Food Guide encourages Canadians to learn how to prepare and cook their own food and promotes the use of nutritional food labels as a tool to help them make informed choices.

The fact is, there are no nutrition food labels on unprocessed food (real, whole foods).

Choosing Healthy Food

As I’ve said in prior articles, Canadians can use the new Canada Food Guide to make up healthy meals by focusing on the part of Guideline 1 which encourages them to eat “real, whole food” and on the part of Guideline 2 which encourages them to “limit processed or prepared foods” — and by defining “processed foods” using the NOVA category of “ultra-processed foods” given above. In this way they will be able to design meals with a wide range of healthy and interesting foods.

Defining what is healthy based on how much a food is processed makes good sense. In this way people are free to add bread and cheese,  and salted, pickled or cured foods (including meat, fish, seafood, vegetables, legumes) to their unprocessed foods (whole foods in their original state) and minimally processed foods to make up an interesting and healthful meal.

Furthermore, categorizing food using the NOVA categories based on the degree of food processing avoids lumping foods made with lots of real cheese with fried chicken as those that undermine healthy eating, based on their saturated fat and sodium content.

More Info?

If you would like to have a Meal Plan designed to meet your health and nutritional needs, I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 BetterByDesign Nutrition Ltd.

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

some image(s) © https://traineracademy.org/

References

1. Public Health Agency of Canada, Canadian Institute for Health Information. Obesity in Canada. A joint report from the Public Health Agency of Canada and the Canadian Institute for Health Information. Ottawa: Public Health Agency of Canada & Canadian Institute for Health Information; 2009. 62 pages.
2. Katzmarzyk PT. The Canadian obesity epidemic: an historical perspective. Obes Res. 2002, Jul;10(7):666-74.
3. Public Health Agency of Canada. Canadian Chronic Disease Indicators, Quick Stats, 2017 edition. Ottawa: Public Health Agency of Canada; 2017. 4 pages
4. NCHS Data Brief, Prevalence of Obesity Among Adults and Youth: United States, 2015-2016, https://www.cdc.gov/nchs/data/databriefs/db288.pdf
5. American Heart Association, Statistical Fact Sheet 2013 Update, High Blood Pressure, https://www.heart.org/idc/groups/heart-public/@wcm/@sop/@smd/documents/downloadable/ucm_319587.pdf
6. American Heart Association, Heart Disease and Stroke Statistics-2019 At-a-Glance, https://healthmetrics.heart.org/wp-content/uploads/2019/02/At-A-Glance-Heart-Disease-and-Stroke-Statistics-%E2%80%93-2019.pdf
7. Centers for Disease Control and Prevention, New CDC report: More than 100 million Americans have diabetes or prediabetes, https://www.cdc.gov/media/releases/2017/p0718-diabetes-report.html
8. Liu AG, Ford NA, Hu FB, Zelman KM, Mozaffarian D, Kris-Etherton PM. A healthy approach to dietary fats: understanding the science and taking action to reduce consumer confusion. Nutr J. 2017 Aug 30;16(1):53. doi: 10.1186/s12937-017-0271-4.
9. Moubarac JC, Batal M, Martins AP, Claro R, Levy RB, Cannon G, et al. Processed and ultraprocessed food products: Consumption trends in Canada from 1938 to 2011. Can J Diet Pract Res. 2014 Spring;75(1):15-21.
10. Monteiro CA, Moubarac J-C, Cannon G., Ng SW, Popkin B. Ultra-processed products are
    becoming dominant in the global food system. Obes Rev. 2013 Nov;14 Suppl 2:21-8. doi: 10.1111/obr.12107.
11. Moodie R, Stuckler D, Monteiro C, Sheron N, Neal B, Thamarangsi T, et al. Profits and pandemics: prevention of harmful effects of tobacco, alcohol, and ultraprocessed food and drink industries. The Lancet. 2013 Feb 23;381(9867):670-9. doi: 10.1016/S0140-6736(12)62089-3.
12. Baker P, Friel S. Food systems transformations, ultra-processed food markets and the nutrition transition in Asia. Global Health. 2016 Dec 3;12(1):80.
13. Moubarac JC. Ultra-processed foods in Canada: consumption, impact on diet quality and policy implications. Montréal: TRANSNUT, University of Montreal; December 2017.
14. Schulte EM, Avena NM, Gearhardt AN (2015) Which Foods May be Addictive? The Roles of Processing, Fat Content and Glycemic Load. PLoS ONE 10(2); e0117959. https://doi.org/10.1371/journal.pone.0117959

Note: this article is both an editorial (expressing my personal opinion on the subject) as well as an article rooted in the literature.

The new Canada’s Food Guide (CFG) hangs on three Guidelines and unfortunately many people discount the Guide entirely because of the caveats to which they are linked. In my opinion, this is a little bit like “throwing the baby out with the bath water”. The essence of the three Guidelines are sound and worth considering.

I have elaborated at length in previous fully reference articles (such as here and here) as to why I believe that one of these caveats, the insistence that dietary saturated fat is associated with heart disease is less than clear. Even the Canadian Heart and Stroke Foundation position statement titled ”Saturated Fat, Heart Disease and Stroke” released in September 2015 concludes the same, but that does not mean that the Guidelines themselves should be entirely discounted or discarded.

I have also explained in a few previous articles (such as this one and this one) why I believe that a diet that is highly carbohydrate-centric may not be suitable for the vast numbers of people that are already metabolically unwell (88% based on a recent US study) and that a meal pattern that has a lower percentage of carbohydrate would be better suited to those who are insulin resistance, or who are already pre-diabetic or have Type 2 Diabetes already. That said, the three Guidelines on which the new Canada’s Food Guide is based are largely correct.

In this article, I will highlight what I feel the new Canada Food Guide got entirely right.

Guideline 1 – Real, whole food

Guideline 1 of the new CFG is that nutritious foods are the foundation for healthy eating and the Guide defines nutritious foods as vegetables, fruit, whole grains and protein foods that include fish, shellfish, eggs, poultry, lean red meat including wild game, milk, yogurt, kefir and cheese, as well as legumes, nuts, seeds, tofu and fortified soy beverages.

The caveat to this advice that plant-based should be chosen more often and that animal-based foods be lower in fat and sodium and this is based on the enduring belief that foods containing saturated fat and/or sodium contribute to heart disease. As mentioned above, I’ve already addressed the saturated fat issue in several previous articles and the concern about excess carbohydrate-based foods for those who are metabolically unwell, but it is true that nutritious foods as vegetables, fruit, whole grains and protein foods that include fish, shellfish, eggs, poultry, lean red meat including wild game, milk, yogurt, kefir and cheese, as well as legumes, nuts, seeds, tofu and fortified soy beverages are nutritious foods.

Yes!

Whole vegetables and whole fruit, and a variety of animal based and even plant-based protein foods and even unrefined grains are nutritious foods and suitable for healthy individuals.

How much and what types of fruit and how much and what type of carbohydrate-based foods a given person should consume will vary depending on a their specific metabolic health, however there is no reason to vilify any whole food as being unhealthy.

For more information about why I don’t believe that carbohydrates are inherently “evil” please read my previous article titled Carbohydrates Are Not Evil located here.

Vegetarians can choose their protein as tofu, nuts and seeds, yogurt, kefir, eggs and cheese, whereas pescatarians can include fish and seafood, and omnivores can include meat, including wild game — and all can include whole vegetables and fruit. Inclusion of “healthy whole grains”, as well as how much and how often really depends on which meal patterns someone has chosen, as well as their metabolic health. As to the matter as whether one can exclude an entire food group is addressed in this article on my affiliate low carb website.

Regardless of a person’s chosen meal pattern — be it whole-food plant-based, whole-food pescetarian or omivore, Mediterranean or low carbohydrate, whole, real food is nutritious food.

I decided to pull some food out of my own fridge and take a picture of what whole, real, food looks like in my own meal pattern (low carbohydrate omnivore), but this by no means defines or limits what nutritious food can look like for you!

Perhaps the idea of buying a chicken the way I choose to doesn’t appeal to you and you’d prefer to buy your boneless and skinless wrapped in plastic on a Styrofoam tray. Go for it! It’s still nutritious, real food.

Buying a whole rotisserie chicken at the store is totally good, too!

So is buying pre-made salad or veggies that are already cut up and frozen or packed ready-to-cook!

If it looks like something your grandparents or great grandparents would recognize as real food, it has a greater chance of falling in what is “nutritious food”.

Guideline 2 – Limit Processed or Prepared Food

Guideline 2 of the new Canada Food Guide is that processed or prepared foods should not be consumed regularly, as these undermine healthy eating.

The caveat to this advice is that these contribute to excess sodium, free sugars or saturated fat which are believed to pose a risk to health and while I’ve previously addressed some of these in earlier articles, regardless of meal pattern processed foods make more energy available for absorption than the whole food from which they are made. In the case of those who have pre-diabetes or Type 2 Diabetes, they also make more carbohydrate available for ready digestion, contributing to a higher insulin response and higher blood sugar response. More information is available in this article as well as this one).

Regardless of the type of meal pattern a person follows, processed or prepared foods ought to be “sometimes foods” and not “everyday foods” — and it doesn’t matter if the processed food is a bake-and-eat frozen pizza, a low carb fat-head pizza or a pre-prepared fake meat burger. These aren’t real, whole foods. Sure, they are nice for an occasional treat but as elaborated on in several previous articles (links above), foods prepared from refined, processed foods have a very different impact on blood sugar response and insulin response than the whole foods from which they are made. 

Remember, real, whole foods are usually ones that your grandparents or great-grandparents would recognize as real food.

Guideline 3 – Know How to Prepare and Cook Food

Guideline 3 of the new Guide is that food skills such as buying, preparing and cooking are needed to navigate the complex food environment and support healthy eating.

I agree.

Unfortunately, it is my experience that many people lack the basic skills to buy foods as simple as raw vegetables such as whole broccoli, or a whole squash and know how to prepare them for eating.

In fact, so many young people lack basic food preparation skills such as how to prepare a simple meal that some school districts have toyed with the idea of bringing back “home economics” to the secondary school curriculum.

Of course, not everyone needs to know how to cut up a chicken (such as I did to the one above) but knowing how to cut up chicken legs into drumsticks and thighs, cut up broccoli or cauliflower or prepare a salad can save people money and increase their availability to eating nutritious (real, whole) food.

Some Final Thoughts…

I said in one of my earlier articles that I consider myself a “nutritional centrist” — that I don’t feel it is necessary to be “tribal” about food allegiances.

People choose different types of meal patterns for all kinds of reasons; from vegetarianism for religious or ethical reasons, to low carb for health reasons, and my role as a Dietitian is to help support them in eating healthy, nutritious food that fits the meal pattern they have chosen.

While I have two specific misgivings about the new Canada’s Food Guide (1) their continued insistence that saturated fat is associated with heart disease and (2) a carbohydrate-centric meal pattern approach when much of the public is already metabolically unwell, there are three things the new Guide got right;

1. Real, whole foods are nutritious and should be foundational for healthy eating
2. It is preferable to limit processed and prepared foods
3. Food skills such as buying, preparing and cooking are needed to support healthy eating

More Info?

If you would like to learn how the essence of these Guidelines can be adopted to you, I can help.

You can learn more about my services under the Services tab or in the Shop. If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
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Copyright ©2019 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. Health Canada, What are Canada’s Dietary Guidelines? https://food-guide.canada.ca/en/guidelines/what-are-canadas-dietary-guidelines/
2. Health Canada. Food, Nutrients and Health: Interim Evidence Update 2018. Ottawa: Health Canada; 2019.
3. Health Canada. Evidence review for dietary guidance: technical report, 2015. Ottawa: Health Canada; 2016.

People who eat a low carb or ketogenic diet often ask about calculating “net carbs” and are surprised by my reply, as it differs from what they’ve read online. The commonly held advice is to subtract “fiber” from the total amount of carbohydrate on the label to arrive at “net carbs” can lead to an underestimation of nutrient intake, as well as possibly an underestimation of the effect of the food on blood glucose and insulin release when those foods are processed into other foods by grinding and/or heating.

As with other evidence-based meal patterns, a “whole foods” approach when following a low-carb lifestyle, is preferable. That doesn’t mean that people shouldn’t enjoy the occasional low-carb treat, as long as they understand that a baked good prepared from almond flour is not equivalent in terms of nutrient availability to the whole almonds from which it is made.

“Net Carbs” and the Perils of Food Processing

In a two-part series of articles posted in March 2018 on my dedicated low-carb website that were titled The Perils of Food Processing, I showed that both the amount and type of food processing applied to a food impacts the amount of nutrients available for absorption by the body, as well as having varying effects on the body’s insulin and blood sugar response. 

“Food processing” in this context means that amount that a food undergoes cutting or grinding and/or cooking in some way, including baking.

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

The availability of carbohydrate and energy is different for whole, raw almonds versus ground almonds such as almond flour — a staple in low carb and keto baking. More on that, below.

Changes in Insulin and Blood Glucose Response Resulting from Food Processing

As covered in the first article linked to above, mechanical processing of a food doesn’t change the amount of carbohydrate that is in it. That is, when we compare 60 g of whole apple with 60 g of pureed apple or 60 g of juiced apple, there is the same amount of carbohydrate in each. The Glycemic Index of these three are very similar so this isn’t very helpful to inform about the blood glucose response to actually eating these different foods.

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

As can be seen by the graph on the right, in healthy individuals blood insulin level goes very high with the juiced apple and in response, blood glucose then goes very low, below baseline. The response seen with the juiced apple is typical of what is seen with ultra-processed carbohydrates.

The same effect that is true for fruit is true when grain is ground; plasma insulin response increases the smaller the particle size of the grain.

Whole grain releases less insulin than the same amount of cracked grains, which is less than the same amount of course flour. The highest amount of insulin is released in response to eating the same amount of fine flour.

What is true for wheat is also true for rice and of interest, there isn’t a big difference between the insulin response with brown rice versus white rice.

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

Also as outlined in the previous articles (links above), the amount of fiber that was in the grain did not make a difference in the amount of insulin released, only the amount of mechanical processing of the grain. So, eating brown rice versus white rice won’t change the amount of insulin that is released.

Remember, insulin is a hormone that signals the body to store energy (calories), so increased insulin response in response to grinding food is important.

In short, it is the amount of cell disruption caused by grinding that increases insulin and glucose response; not the specific amount of carbohydrate in the whole food, nor the amount of fiber in the food.

For those with Type 2 Diabetes or pre-diabetes, applying “net carb” calculations to foods that have been ground is a problem; as it does not take into account the increased insulin release and resulting change in glucose response, as well as the change in energy availability caused by the grinding.

NOTE (June 2 2019): The fiber in the whole food and the ground food remains unchanged and is indigestible by the body, although it is digested by the gut microbiome into fatty acids. While fiber may slow the gastric emptying of the ground product (compared to the same product with the fiber removed), in and by itself the presence of fiber in the ground product compared to the whole food does not reduce the impact on insulin and glycemic response that the grinding causes. 

The Effect of Cooking on Nutrient Availability

Also as documented in the first of the two articles on food processing, cooking also has an effect on nutrient availability. When grains are cooked they become much more digestible — meaning that more of the nutrients are available to be absorbed. In the case of potatoes, there is double or triple the amount of energy (calories) available to the body when they are cooked versus when they are raw and these calories are now available to the body where they weren’t when they were raw.

When foods that are high in fat (lipid) such as peanuts are cooked, the amount of energy the body is able to derive from the food, increases.

Does Food Processing Affect Almonds?

Yesterday, in preparing to write this article, I was curious if there was any information available specifically about almonds as almond flour is used in most low-carb and “keto” baked goods. 

I went looking and found a September 2016 article in the International Journal of Food Science and Technology titled “A review of the impact of processing on nutrient bioaccessibility and digestion of almonds” [1] which documents the most common processing technique used on almonds and their effect on the digestion of nutrients.

In short, lab studies and animal and human studies demonstrate that there are marked differences in the way various forms of almonds (whole raw, whole roasted, blanched, milled flour) are digested and the amount of different macronutrients that are absorbed.

What is true with grinding grain, apples and peanuts holds true for almonds.

It is reasonable to assume that the body’s release of insulin and the corresponding glucose response is similarly changed by the increased bioavailablity of nutrients in those processed foods.

Ultra-processed foods, whether fruit, grains, or nuts are not treated by the body the same as whole, unprocessed foods. The macronutrient availability (i.e. amount of carbohydrate and energy) in whole, unprocessed foods is not the same as in the same foods that have been ground and/or heated, and the amount of insulin released and glucose absorbed can differ too.

Final Thoughts on “Net Carbs”

One cannot simply subtract the fiber that is contained in the whole, unprocessed food from the total carbohydrate content of the processed food and arrive at “net carbs” because the amount of macronutrient absorption of the food is increased due to the cell disruption of grinding and heating. For those with Type 2 Diabetes or pre-diabetes, one also needs to factor in the differential impact on insulin and blood glucose release that results from the food processing.

One can subtract the fiber in whole, raw almonds and arrive at “net carbs” on the assumption that the fiber is indigestible by the body and that the other nutrients listed on the label apply to the food in it’s current form, but roasting and grinding those same almonds into almond butter or grinding those almonds into almond flour and then baking (i.e. cooking) them into a host of low carb or keto ‘treats’ on the basis of their low “net carb” content can significantly underestimate their total macronutrient content. 

Should one choose to use the idea of “net carbs”, it should be applied only to whole, unprocessed (not ground or heated) foods.

Ultra-processed foods, irrespective of the carbohydrate content of the original whole, unprocessed foods from which they are made are not equivalent in nutrient availability or the body’s response to them as to whole, unprocessed foods.

While low-carb and keto ‘treats’ may be nice as “sometimes foods”, they are not ideal as “everyday foods” if weight loss and lowering blood glucose and insulin response are goals.

More Info?

If you would like to know more about following a low carbohydrate lifestyle or to adopt it for health reasons, I can help. You can learn more about my services under the Services tab or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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

1. Grundy MM, Lapsley K, Ellis PR. A review of the impact of processing on nutrient bioaccessibility and digestion of almonds. Int J Food Sci Technol. 2016;51(9):1937—1946. doi:10.1111/ijfs.13192

The infographic below has been making the rounds recently on social media and is based on the idea that high Glycemic Index (GI) foods can be represented by the effect those foods have on people’s blood sugar, compared to teaspoons of sugar.

The infographic below is one that I designed to explain the work of Dr.  David Unwin who communicates the concept of Glycemic Index (GI) & specifically Glyemic Load (GL) in terms of how they impact blood sugar compared to teaspoons of ordinary table sugar, as outline in this post on my affiliate web site.

Here is one of Dr. Unwin’s infographics which describes the effect each food has on blood glucose based on Glycemic Index (1). 

The problem is, these tools are only as useful as Glycemic Index is reliable, so the question is, is GI (and GL which is derived from it) reliable for predicting blood sugar response?

If the Glycemic Index (GI) values (1) change between individuals for the same amount of the same food or (2) if they change value within the same individual when they are assessed at different times, then they cannot be relied on to predict blood sugar response in an individual.

Is Glycemic Index Reliable for Predicting Blood Sugar Response?

A study published in  the American Journal of Clinical Nutrition (2) reported that individual response to individual carbohydrate-containing food vary so much that Glycemic Index values may not be useful in indicating blood sugar response in individuals.

The Study

Randomized, controlled, repeated tests on 63 healthy adults participated in 6 testing sessions over a twelve week period and fasted and abstained from exercise and alcohol before each session.

During each session participants ate either (1) white bread (test food) or (2) a standardized glucose drink (reference control).

Blood sugar values were measured at several points over the next 5 hours, and Glycemic Index was derived by testing the test food and reference in the same participant according to standard method. This is usual practice to control for the variability between people which may be caused by biological differences.

Results

Out of the 63 participants, in 22 participants blood sugar response was classified as “low”, in 23 participants it was classified as “medium” and in 18 participants it was classified as “high’ for the same amount of bread.

That is, white bread fell in all three Glycemic Index categories with different individuals. In addition, responses within the same individual varied by as much as 60 points between tests.

Interpretation of the Results

The study indicated that blood glucose response is affected by differing physical structure of similar foods, the effect of food processing and preparation methods, as well as meal consumption patterns (single or mixed meals).

The study authors concluded that the high inter- (between people) and intra-individual (within the same person) variation that was observed in the GI value of foods essentially resulted in the results being of no practical value.

“In summary, our data indicate substantial variability in GI value  determinations for white bread despite the use of standardized methodology and multiple testing in a large number of healthy volunteers. The high degree of variability demonstrates that there is potential to misclassify foods into the 3 commonly used GI categories (low, medium, and high), which would result in the inability to distinguish between foods, thus invalidating the practical applicability of the GI value.“

The authors also indicated that this variability was also partly explained by differences in baseline HbA1c (i.e. glycated hemoglobin) which is an estimate of 3 month average of blood glucose control, as well as the insulin index (the differing insulin response to foods) both affect the GI value.

Individual Glycemic Response

It should be noted that inter-individual and intra-individual variation in glycemic response isn’t only to white bread, as in the above small study.

A 2015 study from Israel(3) involving 800 people who were monitored with continuous glucose monitors (CGMs) indicates that there isn’t a universal’ blood sugar response to either low Glycemic Index foods or high Glycemic Index foods, and that glycemic (blood sugar) response is very individual.

“We continuously monitored week-long glucose levels in an 800-person cohort, measured responses to 46,898 meals, and found high variability in the response to identical meals, suggesting that universal dietary recommendations may have limited utility”.

Some Final Thoughts…

One cannot reliably predict that a specific amount of carbohydrate-based food will raise a person’s blood sugar the same amount as a certain number of teaspoons of sugar, because each carbohydrate based food will have different effects on different people, and different effects within the same individual, at different points in time.

More Info?

If you would like to know how to determine how you respond to specific carbohydrate-based foods and how to know which carbohydrate-based foods spike your blood sugar and which don’t, I can help.

You can learn more about my services including individual appointments and packages above under the Services tab or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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

1. Unwin D, Haslam D, Livesey G. It is the glycaemic response to, not the carbohydrate content of food that matters in diabetes and obesity: The glycaemic index revisited. Journal of Insulin Resistance. 2016;1(1), a8. http://dx.doi.org/10.4102/jir.v1i1.8
2. Matthan NR, Ausman LM, Meng H, Tighiouart H, Lichtenstein AH. Estimating the reliability of glycemic index values and potential sources of methodological and biological variability. Am J Clin Nutr. 2016;104(4):1004—1013. doi:10.3945/ajcn.116.137208
3. Zeevi D, Korem T, Zmora N, et al. Personalized Nutrition by Prediction of Glycemic Responses. Cell. 2015 Nov 19;163(5):1079-1094.

A new study published today in Preventive Medicine estimates that excess body weight, including overweight and obesity is expected to become the second leading cause of preventable cancer in Canada, after tobacco over the next 20 years.

Cancer Rates Expected to Triple

The results of the new ComPARe study (Canadian Population Attributable Risk of Cancer) stemming from research conducted by the Canadian Cancer Society and a Canadian team of experts in epidemiology, biostatistics, cancer risk factors, and cancer prevention provides estimates of the number and percentage of more than 30 cancer types in Canada. 

It found that if current trends continues, it is expected that new cancer cases related to overweight or obesity will triple over the next 20 years, from the current 7,200 cases per year to 21,200 cases per year. These figures are due to overweight and obesity alone and do not include the increase number of cancer cases that are expected due to smoking, physical inactivity / sitting too much or alcohol consumption.

Excess body weight increases the risk of esophageal and endometrial cancer by about 50% and increases the risk of kidney, gallbladder, stomach and liver cancers by 20-30%.  Achieving and maintaining a healthy body weight can substantially lower the risk of these, and other cancers. The study estimates that if Canadians maintained a healthy body weight (BMI ⩽  25), that approximately 110,600 cancer cases could be prevented by the year 2042.

UPDATED (May 8, 2019 5:00 PM): It is not body weight per se that increases the risk of cancer. There are several proposed mechanisms where excess body weight may increase cancer risk, including alterations in the levels of hormones and growth factors, chronic inflammation, excess insulin and leptin. It is thought that excess insulin may help promote cancer cell growth and cause insulin resistance, which
increases the risk of colon, endometrial and kidney cancers in particular.

If you’d like to know how I can help you with symptoms of overweight or obesity (or some of the metabolic disorders that often accompany them), please let me know.

You can learn more about my services and their costs above under the Services tab or in the Shop and if you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To our good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright 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.

In its recently published Consensus Report (April 18, 2019), the American Diabetes Association confirmed something that I have written about in several previous articles, including most recently in Part III of Carbohydrates are Not Evil and that is that it isn’t biologically essential to eat carbohydrate containing foods in the diet. From the top of page 4 of the Consensus Report:

“The amount of carbohydrate intake required for optimal health in humans is unknown. Although the recommended dietary allowance for carbohydrate for adults without diabetes (19 years and older) is 130 g/day and is determined in part by the brain’s requirement for glucose, this energy requirement can be fulfilled by the body’s metabolic processes, which include glycogenolysis, gluconeogenesis (via metabolism of the glycerol component of fat or gluconeogenic amino acids in protein), and/or ketogenesis in the setting of very low dietary carbohydrate intake.”

That is, the body can make all the glucose the brain needs from the glycogenolysis (which is the breakdown of glycogen to glucose), via  gluconeogenesis (which is the generation of glucose from glycerol or glucogenic amino acids) and via ketogenesis(which is from ketones generated in a very low dietary carbohydrate [ketogenic] diet). In short, dietary intake of carbohydrate is not essential. While there is no biological need to eat carbohydrate-based food, one certainly can and there are many good reasons to include some types of carbohydrate-containing food in the diet.

Because there is no essential need to eat carbohydrate because the body can make all the glucose it needs itself, the American Diabetes Association includes among its eating patterns both a low carbohydrate pattern (26-45% daily calories as carbohydrate) and a very low carbohydrate (ketogenic) eating pattern (20-50 g carbohydrate / day). How much carbohydrate is a major consideration for those who are pre-diabetic or Diabetic because as the ADA stated in this new consensus report;

“Carbohydrate is a readily used source of energy and the primary dietary influence on postprandial blood glucose.

That is, it is the carbohydrate in a meal that is the biggest predictor of how high blood sugar will rise after a meal, and how quickly. For those who want to improve their blood sugar levels (glycemia) the same report also makes it clear that;

“Reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia* and may be applied in a variety of eating patterns that meet individual needs and preferences.”

For those adults with Type 2 Diabetes who are not meeting their blood sugar targets or who need to, or want to have their physician reduce their need for Diabetes medications, a low carbohydrate or very low carbohydrate (keto) eating pattern is a viable option;

“For select adults with type 2 diabetes not meeting glycemic targets or where reducing anti-glycemic medications is a priority, reducing overall carbohydrate intake with low or very low- carbohydrate eating plans is a viable approach.”

Remember, carbohydrate-based foods are not necessary for your brain because your body can make all the glucose it needs from the metabolic processes listed above. That’s not to say one has to avoid carbohydrate-based foods, but how much and how often can and is best determined based on people’s individual needs and glycemic response to carb-based foods.  I recently outlined in another article based on the American Diabetes Association’s Consensus Report and which was posted on my affiliated low carbohydrate-focused website, that in the US a well-designed low carb or ketogenic diet to lower blood sugar need not have all the same foods or food groups as a diet based on The Dietary Guidelines for Americans because it is used as Medical Nutrition Therapy (i.e. is a therapeutic diet).

While these are the guidelines in the US, in Canada individuals have the right to choose a low carbohydrate lifestyle if that is their personal preference.

If you would like some professional support to begin eating this way or to continue eating this way,  I can help. I provide Registered Dietitian services to those in any province in Canada (except PEI), and for those in the US, I can provide nutrition education to help you know how to eat according to a low carb eating pattern.

You can learn more about my services including individual hourly appointments and sessions as well as packages above under the Services tab or in the Shop and if you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

Here are the links to other articles that I wrote about the new ADA Consensus Report:

April 24, 2019 – ADA Eating Patterns Differ from The Dietary Guidelines for Americans April 23, 2019 –  ADA includes use of a Very Low Carb (Keto) Eating Pattern in New Report

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

Reference

Evert, AB, Dennison M, Gardner CD, et al, Nutrition Therapy for Adults With Diabetes or Prediabetes: A Consensus Report, Diabetes Care, Ahead of Print, published online April 18, 2019, https://doi.org/10.2337/dci19-0014 Copyright

©2019 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

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

On April 18, 2019, the American Diabetes Association published a new Consensus Report which not only includes the use of a low carbohydrate eating pattern of 26-45% of total daily calories as carbohydrate, but in this report also includes the use of a very low carbohydrate (ketogenic) eating pattern of 20-50 g carbs per day. The report is clear that there is no “one-size-fits-all” eating pattern for the prevention or management of diabetes, and that it unrealistic to expect that there should be just one eating pattern for everyone; especially given the wide variety of people affected by diabetes and pre-diabetes, including their varied cultural backgrounds, personal preferences, co-occurring conditions and the variety of socio-economic backgrounds from which they come.

“Reducing overall carbohydrate intake for individuals with diabetes has demonstrated the most evidence for improving glycemia (blood sugar) and may be applied in a variety of eating patterns that meet individual needs and preferences.”

“reducing overall carbohydrate intake with low- or very low- carbohydrate eating plans is a viable approach.”

Yesterday, the headlines screamed out from around the world that a new study from Oxford University found that there is a 20% higher chance of developing colorectal cancer from eating as little as one strip of bacon per day. This sounds terrible, but is it true? To understand what this study is reporting, it is important to understand the difference between relative risk and absolute risk.

Absolute Risk

It was known before this study, that regardless what people eat, there is approximately a 5% chance of developing colorectal cancer in a person’s lifetime (whether they eat bacon every day or not). This is known as the absolute risk.

A 5% likelihood means that for every 100 people, 5 will get colorectal cancer regardless what they eat.

Illustrated, this looks as follows;

Relative Risk

The study reported that there is a 20% higher chance of developing colorectal cancer by eating as little as one strip of bacon per day.

This means that compared to not eating bacon daily, eating it daily results in one more person per 100 people developing colorectal cancer in their lifetime.

This is known as relative risk and illustrated that looks as follows:

Headlines as click-bate

It wasn’t only the American media that reported this, Canadian new outlet CTV did also.

Each individual person’s increased risk of getting colorectal cancer by eating as little as 1 strip of bacon per day is NOT 20%! Their increased absolute risk of getting colorectal cancer (*based on this study) is 0.08%.

*this study was an epidemiological study, not a clinical study and can only show if there is an association between two factors and cannot make any conclusions about cause. The difference is explained below.

The study found that for every 10,000 people who ate 21g a day of red and processed meat, 40 were diagnosed with colorectal (bowel) cancer, and a single slice (or rasher) of bacon is ~23g.

i.e. 40 / 10,000 = 0.4%

The study also found that for every 10,000 people who ate 76g a day of red and processed meat, 48 were diagnosed with colorectal (bowel) cancer.

i.e. 48/10,000 = 0.48%

The actual chance of a person getting colorectal cancer (i.e. absolute risk) from eating bacon daily is the difference between these two numbers; i.e. 0.4% – 0.48% = 0.08%

Association is not Causation

This was an epidemiological study based on population data, and was not a clinical study.

Epidemiological studies are the study of diseases in populations and are helpful for researchers to know which areas warrant clinical studies.

It is important to know that epidemiological studies cannot attribute “cause” of disease or death. When an epidemiological study finds an “association” between two factors  such as bacon and higher colon cancer rates — this does NOT mean that eating bacon ’causes’  heart disease.

Based on this study, all that can be said is that there was an increase in the association between eating bacon and absolute rates of colon cancer of 0.08%.

Not so impressive now, is it?

If you are having trouble sifting through all the information you read and in knowing if it is accurate, or even says what it seems to be saying, I can help. Sometimes people start by booking an appointment just to ask me those types of questions, because they want credible answers.

You can learn more about my services including individual hourly appointments and sessions as well as packages above under the Services tab or in the Shop.

If you have questions, please feel free to send me a note using the Contact Me form above and I will reply as soon as I can.

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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

Kathryn E Bradbury, Neil Murphy, Timothy J Key, Diet and colorectal cancer in UK Biobank: a prospective study, International Journal of Epidemiology, , dyz064, https://doi.org/10.1093/ije/dyz064

A newly published large-scale epidemiological study has reported that taking vitamin and mineral supplements does not reduce the risk of cardiovascular disease such as heart attack and stroke, cancer rates or other causes of health-related death. The study published Tuesday, April 9, 2019 in the Annals of Internal Medicine analyzed US nutritional data from 30, 899 adults over the age of twenty from the NHANES survey between 1999 to 2010 and linked it to mortality data from the National Death Index [1]. During the six year follow-up period there were 3613 deaths; of which 945 were cardiovascular-related and 805 were from cancer.

Vitamin and Mineral Supplement versus Nutrient Intake from Food

The study found that use of vitamin and mineral supplements was not related to improved outcomes in rates of death from cardiovascular disease, cancer or all-cause health related death. Adequate intake of vitamin A, vitamin K, magnesium, zinc and copper was associated with reduced rates of cardiovascular disease and death from all health-related causes, but these improved associations only applied to those who obtained these nutrients from food.

Calcium Supplements – too much of a ‘good’ thing

So many adults take calcium supplements, however  calcium intake from supplements of ≥ 1000 mg/day (which many adults take!) was associated with increased risk of death from cancer.

Want to Live Longer? Eat Whole, Real Food

Based on this large-scale epidemiological study, eating foods rich in vitamin A, vitamin K, magnesium, zinc and copper was associated with reduced rates of cardiovascular (CVD) disease and death from all health-related causes. Good news! All of these nutrients are widely available in whole, real foods that also happen to be low in carbohydrate.

Zinc and Copper

Meat and seafood are some of the richest sources of zinc and copper.

Vitamin K

Dark, leafy greens  are excellent sources of vitamin K. Vitamin K is needed to help the body absorb vitamin D and to help with proper calcium utilization.

Magnesium

Nuts and seeds, including cocoa beans (think ‘dark chocolate’!)  are very good sources of magnesium, as are avocados

Vitamin A

…and yellow and orange vegetables are excellent sources of vitamin A.

Final thoughts…

Epidemiological studies (which are the study of diseases in populations) are helpful to know what areas warrant good quality clinical trials, but aren’t useful for attributing “cause” of disease or death. When an epidemiological study finds an “association” between two factors, this does NOT mean that one causes the other.  For that, clinical trials are necessary. That said, eating whole, real foods that also happen to be low in carbohydrate are an excellent way to get all of the nutrients that this study found are associated with lower rates of cardiovascular disease and death from all health related causes and it is pretty difficult to eat too much of any nutrient when eating whole, real food. Since taking vitamin and mineral supplements is not associated with lower rates of disease or death, and in the cases of calcium supplements may even be associated with negative health outcomes, eating a whole-food diet rich in the above foods is the safest way to ensure adequate intake of these nutrients. If you would like more information about how much of these foods you should be eating, I’d be glad to help. Please have a look at the Services tab or the Shop for more information. To your good health! Joy You can follow me on:

Twitter: https://twitter.com/lchfRD Facebook: https://www.facebook.com/BetterByDesignNutrition/
Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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

1. Chen F, Du M, Blumberg JB, Ho Chui KK, Ruan M, Rogers G, et al. Association Among Dietary Supplement Use, Nutrient Intake, and Mortality Among U.S. Adults: A Cohort Study. Ann Intern Med. [Epub ahead of print ] doi: 10.7326/M18-2478

An analogy is a comparison between similar ideas to help illustrate one of them. The featured photo for this post are sugar crystals on a string and the reason for this will become clear. The idea for this article came when someone I follow on social media (Dr. RD Dikeman*) posted the graphic below, which shows complex carbohydrates as long strings of glucose, which starches are. But there are also other types of complex carbohydrates that are long strings of different sugar molecules that can impact blood glucose differently. I thought a simple explanation of what “complex carbohydrates” are, how they are digested and how these can affect blood sugar differently might be helpful, so that is what this article is about.

*Dr. RD Dikeman holds a PhD in Theoretic and Mathematical Physics and has become very knowledgeable in carbohydrate metabolism as a result of his son having been diagnosed in 2013 with Type 1 Diabetes. His son was eating 40-60 g of carbohydrate per meal and was experiencing a “roller-coaster ride” of high and low blood sugars, including an incidence of “ketoacidosis”; which is a life-threatening condition when the body produces high levels of ketones due to an insufficiency of insulin. This should not be confused with “ketosis” where the body switches to using fat stores for energy, such as after an overnight fast. Five years ago, Dr. Dikeman’s son began to follow the low carbohydrate protocol of Dr. Richard Bernstein MD (outlined in his book “Diabetes Solution”) and since that time has been able to maintain normal normal blood sugar levels with the minimum required doses of insulin. 

I liked the analogy of Dr. Dikeman’s graphic and wanted to use it as a ‘jumping off point’ for this article.

Glucose Explain Simply

Glucose (also called dextrose) is the type of sugar found in the blood which is why the common term “blood sugar” and the more clinical term “blood glucose” refer to the same thing. Glucose is one of the two sources of energy (along with ketones) that are used to fuel the body’s cells. Even people that don’t eat “low carb” will make ketones after a night’s sleep, so the body of healthy people runs on both glucose and ketones. The carb-containing foods that we eat are broken down into glucose for energy or the body makes the glucose it needs for the brain and red blood cells from other substances in a process called gluconeogenesis.

The Glucose-Complex Carb Analogy

In the graphic above, Dr. Dikeman questions whether people such as Diabetics that have trouble metabolizing glucose should be eating complex carbohydrates which are essentially just long strings of glucose molecules strung together like beads on a chain. As in Dr. Dikeman’s illustration, some complex carbohydrates such as starch are just long chains of glucose molecules,  however other complex carbohydrates are made up of other sugars such as galactose and fructose, along with glucose. Because of that I wanted to expand on Dr. Dikeman’s illustration.

Simple and Complex Carbs

One way that carbs are sometimes classified is as “simple” or “complex”; with starch and fiber being categorized as complex carbs and all sugars being categorized as simple carbs.

Simple Sugars

There are two types of simple sugars; monosaccharides and disaccharides. Mono means “one” and saccharides means “sugar” so a monosaccharide is just a single sugar molecule. Di means “two”, so a disaccharide is two sugar molecules joined together.

Monosaccharides

As mentioned above, monosaccharides are made up of only a single sugar molecule and examples of these are glucose, fructose and galactose. All three monosaccharides have 6 carbons and the same chemical formula but look entirely different from each other. For example, glucose and galactose are 6-ring sugars and fructose is a 5-ring sugar. Glucose is usually found in food bound either to other glucose molecules, as in Dr. Dikeman’s illustration above, or may be bound to other types of sugar molecules in a disaccharide (2 sugar molecules) or a starch or fiber (long chain of sugar molecules). Fructose is the sugar found in fruit and since it is a 5-ring sugar, it can’t simply be broken down into glucose, which is a 6 ring sugar. Galactose is a six ring sugar that rarely exists on its own in food but that can be broken down in the body through digestion. It is usually found bound to glucose to form lactose, the sugar found in milk and dairy products.

Disaccharides

Disaccharides are two monosaccharide sugar molecules bound together. Sucrose is ordinary table sugar and made up of glucose-fructose. Lactose is the sugar in milk and milk products and is glucuse-galactose Maltose which rarely occurs naturally in foods, is glucose-glucose. Maltose is used in food processing such as the shiny glaze on Chinese roast duck.

complex carbohydrates

Complex carbohydrates are made up of more than two monosaccharides (sugar molecules). Oligosaccharides (where oligo means “scant” or “few”) are made up of 3-10 sugar molecules, whereas polysaccharides are made up of hundred or even thousands of monosaccharides (sugar molecules).

Oligosaccharides

Oligosaccharides are made up of 3-10 sugar molecules and the two most common are some of the complex carbohydrates found in dried beans, peas and lentils[1]. Raffinose is an oligosaccharide made from 3 sugar molecules: galactose-glucose-fructose and stachyose is an oligosaccharide made from 4 sugar molecules: galactose-galactose-glucose-fructose. The body can’t break down either raffinose or stachyose, but this is done by the bacteria in the intestine.

Polysaccharides

Polysaccharides are made up of hundreds or thousands of sugar molecules linked together. When those sugar molecules are only glucose, the polysaccharide is called “starch”. Some polysaccharides form long straight chains while others are branched like a tree. These structural difference affect how these carbohydrates behave when they’re heated or put in water. The way the monosaccharides are linked together makes the polysaccharides either digestible as in starch, or indigestible as in fiber. Polysaccharides found in plant foods such as fiber, cellulose, hemicellulose, gums and mucilages (such as psyllium) are indigestible by the body so won’t be covered in this article, but it should be noted that they can slow down the absorption of digestible carbohydrate.

Starch

Starches are long chains of glucose molecules strung together like beads on a string and are the ones illustrated in Dr. Dikeman’s illustration, above. Starches are found in grains such as wheat, corn, rice, oats, millet and barley as well as in legumes such as peas, beans and lentils* and tubers such as potatoes, yams and cassava.

*Recall as mentioned above that peas, beans and lentils also have the complex carbohydrates called oligosaccharides which are not broken down by the body, but by the bacteria of the gut.

There are two types of starches; the long unbranched chains called amylose and the long branched chain ones call amylopectin. What is important in this context is that the long branched chain starches called amylopectin are more easily digested. The body digests most starches very easily, although those with a high percentage of amylopectin (such as cornstarch) are digested much more easily than those with a high amount of amylose, such as wheat starch [1]. Since starches are just glucose molecules linked together and they are easily broken down to individual glucose molecules, starches can quickly affect the blood sugar of those who are pre-diabetic or have Diabetes. That is the “point” behind Dr. Dikeman’s illustration, above which I have modified slightly, below.

Those who are Diabetic (or pre-diabetic) already have challenges with their blood glucose, so does eating foods such as starches that are nothing more than long strings of glucose really make sense?

Note: While the fiber content of whole grain pasta will slow down its digestion compared to refined pasta, it is still long strings of glucose molecules. Think of whole wheat pasta as a string of pearls with in addition to the pearls, in this case fiber.

Digestion of Carbohydrates

Carbohydrate digestion begins in the mouth where an enzyme in saliva called amylase breaks starch down into shorter polysaccharides and maltose. The acidity of the stomach temporarily stops the effect of the salivary amylase, but the digestion of carbohydrate starts up again in the small intestine where most carbohydrate digestion takes place.

Digestion of carbohydrates begins again when the pancreas secretes pancreatic amylase into the small intestine. In the small intestine, starch is broken down in to many, many individual units of the disaccharide maltose, which are simply two glucose molecules linked together.

Then, enzymes located to the brush border of the small intestine break the alpha bond which holds the two glucose molecules together. It’s easy to understand how starch, which is simply long chains of glucose molecules strung together are so easily broken down when digestion already starts in the mouth and is completed in the small intestine where the disaccharide (maltose) is broken down into 2 glucose molecules.

In the small intestine, other enzymes split other disaccharides into monosaccharides; so for example, the enzyme sucrase splits the disaccharide sucrose into glucose and fructose and the enzyme lactase splits the disaccharide lactose into glucose and galactose.  Note that these other disaccharides are only 1/2 glucose.

Absorption of Carbohydrates

Monosaccharides are absorbed into the mucosal cells of the small intestine and travel to the liver, where galactose and fructose are converted to glucose and the glucose is stored in the liver as glycogen. Glycogen is long, highly branched chains of glucose molecules (similar to amylopectin, but much more highly branched).

When needed, the liver can break down glycogen into glucose at a rate of 100 mg to 150 mg of glucose per minute for up to 12 hours [2]. When glycogen stores of the liver are already full, the glucose from the broken down carbohydrate with the help of the hormone insulin converts the excess glucose into fat and sends to other parts of the body to be stored in adipose tissue.

Carbohydrate-based Foods in the Diet

As covered in previous articles including this one , there is NO requirement for people to eat carbohydrate-based food” provided that adequate amounts of protein and fat are consumed“[3] which are used to provide essential glucose for the brain via gluconeogenesis. This does not mean that I recommend people don’t eat any carbohydrate-based food!

Which carbohydrate-based food people are able to eat and in what quantity without it affecting their blood sugar to any large degree varies considerably from person to person[4], whether or not they are Diabetic.  For those who already have Type 2 Diabetes or are pre-diabetic, a personalized nutrition approach is needed.  This is often called “eating to your meter“; testing a specific quantity of a food by itself, to see how your blood sugar responds. 

Based on research, some people with Type 2 Diabetes can do well eating certain types of legumes (pulses) including black beans, white navy beans, pinto beans, red and white kidney beans, chickpeas and fava beans [5] which is helpful for those who follow a plant-based vegetarian diet. Once people have lowered their HbA1C and fasting blood glucose levels and achieved remission of Type 2 Diabetes symptoms, I work can work with them in determining which foods they can re-introduce into their diet and in what quantities and how often, so as not to adversely impact their blood sugar. Some do better than others.

Over the last 4 years of my clinical practice, I have found that many people with pre-diabetes or Type 2 Diabetes can often manage their blood glucose well while including small servings (1/2 cup / 125 ml) of whole-food starchy vegetables such as winter squash (butternut, acorn, kobacha, etc.), as well as small servings of other starchy whole-food vegetables such as orange or purple yam, or peas. For those eating a moderately-low level of carbs (non-ketogenic) or want to keep eating these foods, I encourage them to choose these more often over starch-based foods such as pasta, rice and bread.

That doesn’t mean that people with Type 2 Diabetes shouldn’t ever eat whole, unmilled brown rice or quinoa but that avoiding refined starches such as white bread, pasta and rice is best preferable. I hope that you found this article helpful to understand what complex carbohydrates are, and why certain types of complex carbs are more of a challenge to those with Type 2 Diabetes or pre-diabetes.

If you have questions about how I can help you eat in a way to lower your blood sugar levels, please send me a note through the Contact Me form above and for information about the types of services I offer, please have a look under the Services tab or in the Shop.

To your good health,

Joy

You can follow me on: Twitter: https://twitter.com/lchfRD Facebook: https://www.facebook.com/BetterByDesignNutrition/ Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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. Chapter 4, Carbohydrates: Simple sugars and Complex Chains, http://samples.jbpub.com/9781284064650/9781284086379_CH04_Disco.pdf
2. Rappaport B, Metabolic factors limiting performance in marathon runners. PLoS Comput Biol. 2010; 6(10). doi: 10.1371/journal.pebi.1000960
3. National Academies Press, Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005), Chapter 6 Dietary Carbohydrates: Sugars and Starches”, pages 265-275
4. Zeevi D, Korem T, Zmora N, et al. Personalized Nutrition by Prediction of Glycemic Responses. Cell. 2015 Nov 19;163(5):1079-1094.
5. Sievenpiper, J.L., Kendall, C.W.C., Esfahani, A. et al. Effect of non-oil-seed pulses on glycaemic control: a systematic review and meta-analysis of randomised controlled experimental trials in people with and without diabetes. Diabetologia (2009) 52: 1479.

A recently published meta-analysis of 43 cohort or nested case-control studies up until July 1, 2018 [1] did not find that higher saturated fat intake is associated with higher risk of cardiovascular disease (CVD) events. This is the first study to examine the effect of total dietary fat intake and the intake of specific fatty acids on CVDs risk based on dose-response meta-analysis of prospective cohort studies.

It has been proposed that saturated fat (SFA) and trans fatty acids (TFA) contribute to CVD via inflammatory mechanisms and oxidative stress, mediated through the production of reactive oxygen species (ROS) [2,3]. With respect to trans fatty acids, this new study found that dietary TFA intake had a dose-response association with CVDs risk; specifically a 16% increased risk of CVD with an increased TFA intake of 2% of energy per day, however no association was observed between total fat or dietary saturated fatty acid (SFA) intake and the risk of CVDs [1]. In addition, this meta-analysis found no protective effect from the consumption of either monounsaturated fatty acids (MUFA), or polyunsaturated fatty acids (PUFA) and risk of CVDs, except PUFAs showed a protective effect in sub-group analysis followed up for more than 10 years [1].

These findings do not support 2010 recommendations of the WHO / FAO [4] which continue to influence national dietary guidelines around the world to recommend reducing intake of saturated fat in order to lower the rates of CVD.

As well, these new findings call into question the findings of the PREDIMED study [5] and the Lipid Research Clinics Prevalence Follow-up Study [6] that indicate that diets high in polyunsaturated fatty acid (PUFA) and monounsaturated fatty acid (MUFA) and low in saturated fatty acid (SFA) and trans fatty acids (TFA) are associated with reduced CVDs events.

The authors caution that;

“it is possible that the role of dietary fat played in the development of CVDs might be confounded by the fat sources. For instance, vegetables and fruits play protective roles in the development of CVDs. However, we could not investigate the different effects of fat from animal, vegetables and fruit separately in this current meta-analysis.” [1]

Some thoughts…

For almost 50 years it has been believed that dietary saturated fat intake was a risk factor for CVDs based on the assumption that dietary fat can increase low density lipoprotein (LDL) cholesterol and blood pressure and in turn, increase CVDs risk, however this meta-analysis of 43 cohort studies did not find a positive association between total dietary fat intake or saturated fat intake and CVDs risk.

The 2017 Prospective Urban Rural Epidemiological (PURE) study (covered in this earlier article) is the only prospective study to date which covered multiple world regions and which found that total dietary fat and types of dietary fat were not associated with cardiovascular disease or mortality and further, that dietary saturated fat had an inverse association with stroke and a risk of all-cause mortality with higher intake (up to ~14% of energy intake). That is, dietary saturated fat intake was protective.

The findings of the current meta-analysis study, combined with the findings of the 2017 PURE study call into question current dietary recommendations which continue to recommend that people limit dietary saturated fat in order to reduce cardiovascular risk. Such recommendations are included in the most recent Canada’s Food Guide which encourages Canadians to ”choose foods with healthy fats instead of saturated fat” and to ”prepare meals and snacks using ingredients that have little to no added sodium, sugars or saturated fat” (see this article for details) .

Post publication note (April 7, 2019): As I’ve stated in previous articles, I am not opposed to Canada’s new Food Guide. It is a huge improvement over it’s predecessor for many reasons already discussed. My two concerns that I’ve expressed previously remain; (a) that the recommendations for the general population to continue to limit saturated fat because it contributes to CVD has not been conclusively demonstrated. The only thing that has been shown is that saturated fat can raise LDL, but which LDL; the large fluffy sub-fraction, or the small dense sub-fraction? Please see article linked to above for an elaboration. My second concern is that; (b) the amount of carbohydrate in the diet is too high for the large percentage of the population that are metabolically unhealthy. Please see this article for an elaboration.

Author’s Conclusions

The study’s authors concluded that;

“This current meta-analysis of cohort studies suggested that total fat, SFA, MUFA, and PUFA intake were not associated with the risk of cardiovascular disease. However, we found that higher TFA intake is associated with greater risk of CVDs in a dose-response fashion. Furthermore, the subgroup analysis found a cardio-protective effect of PUFA in studies followed up for more than 10 years. Dietary guidelines taking these findings into consideration might be more credible.” [1]

If you would like to learn about the types of fats in your diet and how they may impact your health or those of your family, please send me a note through the Contact Me form on the tab above. You can learn more about the services I provide by clicking on the Services tab or having a look in the Shop.

To your good health,

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD Facebook: https://www.facebook.com/BetterByDesignNutrition/ Instagram: https://www.instagram.com/lchf_rd

Copyright ©2019 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. Zhu Y, Bo Y, Liu Y, Dietary total fat, fatty acids intake, and risk of cardiovascular disease: a dose-response meta-analysis of cohort studies, Lipids in Health and Disease (2019) 18:91, https://doi.org/10.1186/s12944-019-1035-2
2. Sverdlov AL, Elezaby A, Qin F, Behring JB, Luptak I, Calamaras TD, Siwik DA, Miller EJ, Liesa M, Shirihai OS, et al. Mitochondrial reactive oxygen species mediate cardiac structural, functional, and mitochondrial consequences of diet-induced metabolic heart disease. J Am Heart Assoc. 2016;5:e002555.
3. Ruparelia N, Chai JT, Fisher EA, Choudhury RP. Inflammatory processes in cardiovascular disease: a route to targeted therapies. Nat Rev Cardiol. 2017;14:133—44.
4. Nations FaAOotU. Summary of conclusions and dietary recommendations on total fat and fatty acids in fats and fatty acids in human nutrition—report of an expert consultation. Geneva: FAO/WHO; 2010.
5. Estruch R, Ros E, Salas-Salvado J, Covas MI, Corella D, Aros F, Gomez- Gracia E, Ruiz-Gutierrez V, Fiol M, Lapetra J, et al. Primary prevention of cardiovascular disease with a Mediterranean diet. N Engl J Med. 2013;368:1279—90.
6. Guasch-Ferre M, Babio N, Martinez-Gonzalez MA, Corella D, Ros E, Martin-Pelaez S, Estruch R, Aros F, Gomez-Gracia E, Fiol M, et al. Dietary fat intake and risk of cardiovascular disease and all-cause mortality in a population at high risk of cardiovascular disease. Am J Clin Nutr. 2015;102:1563—73.
7. Dehghan M, Mente A, Zhang X, Swaminathan S, Li W, Mohan V, Iqbal R, Kumar R, Wentzel-Viljoen E, Rosengren A, et al. Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017;390:2050—62.

I’ve heard that some types of cancer feed on glucose (the sugar in our blood) and I know of a few people that started a ketogenic diet as adjunct therapy to be used along side surgery and chemotherapy in the treatment of glioblastoma (a form of aggressive brain cancer), but just came across an article that explains why limiting sugar intake can lower one’s risk of cancer. In this article, I explain one biological link between cancer and sugar.

A “Master Switch for Cancer”

In the 1980’s, Dr. Lewis Cantley was a Professor at Tufts University School of Medicine in Boston when he identified a previously unknown enzyme known as phosphoinositide-3-kinase, or PI3K which turned out to a type of ‘master switch for cancer’.

PI3K’s normal function is to alert cells to the presence of the hormone insulin; resulting in the cells pumping in glucose to be used as metabolic fuel for the cell. Signals from PI3K are necessary for normal cell growth, survival and reproduction, however when this enzyme is hijacked by cancer cells, it provides tumors with an over-abundant supply of glucose, which results in their rapid proliferation.

The gene that codes for PI3K is now thought to be the most frequently mutated cancer-promoting gene in humans and is believed to be associated with 80% of cancers, including those of the breast, brain and bladder.

In 2012, Dr. Cantley became the Director of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine, which is the biomedical research unit and medical school of Cornell University, where he is Professor of Cancer Biology. In his work at Weill Cornell, Dr. Cantley has continued to investigate the role of PI3K.

Challenges with some anti-cancer drugs that have been developed that block the PI3K enzyme is that these PI3K-inhibitor drugs are designed to starve the cancer cell of glucose, but also signal the person’s liver that their body is starving for glucose, too.  As a result, the liver would break down glycogen (a storage form of glucose) and send large amounts of glucose into the person’s blood, resulting in their blood sugar spiking and triggering their pancreas to release lots of insulin, as a result. The presence of all of this glucose from the liver and insulin from the pancreas resulted in these patient’s tumors continuing to grow.

Dr. Cantley and his colleagues wondered whether the spike in insulin from the breakdown of glycogen might be countering the effect of the PI3K-inhibiting drugs by reactivating the PI3K pathway in the cancer cells.  Studies first tried giving these patients Diabetes medications to lower their blood sugar and insulin levels, but this didn’t work nearly as well as what they tried next.

The researchers came up with a theory that a ketogenic diet (a diet that is very low in carbohydrate)   could prevent the spikes caused in blood sugar by the  PI3K-inhibiting drugs and might help the drug starve the tumor, while the patient’s blood sugar remained normal because the body would be fueled by breaking down fat and protein for ketones.

They tested the theory using genetically engineered mice that developed pancreatic, bladder, endometrial and breast cancers and treated the mice with a new PI3K inhibitor drug. The study demonstrated that spikes of insulin did indeed reactivate the pathway in tumors, countering the anti-cancer effect of the drug. However, when the researchers put the mice on a ketogenic diet, in addition to the medication, the tumors shrank. The results were published in the journal Nature in July 2018.

Dr. Cantley explains the biological connection between cancer and sugar this way;

“Our pre-clinical research suggests that if somewhere in your body you have one of these PI3K mutations and you eat a lot of rapid-release carbohydrates, every time your insulin goes up, it will drive the growth of a tumor. The evidence really suggests that if you have cancer, the sugar you’re eating may be making it grow faster.”

Some Final Thoughts…

A normal cell function requires the enzyme PI3K that results in the cell pumping in glucose to fuel growth and reproduction and a cancer cell that has a defect in the gene that codes for PI3K may do the same thing. Sugar, in and by itself does not cause cancer, but in those that have a few abnormal cells, sugar can drive the process of tumor development.

According to the World Health Organization, the average American consumes 126 grams of sugar a day, more than people in any other country and the average Canadian eats almost 90 grams (89.1) of sugar per day. Sugar is not required in the diet; in fact, there is no essential need to eat carbohydrate at all, if people eat adequate amounts of healthy fats and protein.

Given that as many as 88% of Americans are already metabolically unhealthy — with likely a smaller percentage of Canadians following suit (due to slightly lower obesity statistics), there is no valid reason* for the average American or Canadian to be eating foods with added sugar. As I’ve written about in many previous articles, high blood sugar and high insulin levels already predispose people to Type 2 Diabetes and obesity and as outlined in this article, are involved in the proliferation of some types of cancer cells.

*(update April 29, 2019): While I say above that there is ”no valid reason” for those who may already be metabolically unwell to eat foods with added sugar — in retrospect, this is not well worded.  I think there are lots of valid reasons for people to eat foods with added sugar, but believe that it may be preferable for those who are already metabolically unwell to limited added sugars.

It would seem to me that a prudent approach for metabolically healthy people (12% of Americans, and perhaps an estimated 25% of Canadians) is to stay healthy by avoiding processed foods that are high in refined carbs and sugar, as well as foods high in “natural sugar” such as 100% fruit juice  in order to reduce the risk of becoming metabolically unwell or inadvertently feeding malignant cells that feed on glucose.

For the large majority of those that are already metabolically unhealthy, a well-designed low carbohydrate diet can help you reverse the symptoms of Type 2 Diabetes, putting the disease into remission, as well as achieve and maintain a healthy body weight.  Not inadvertently feeding tumor proliferation seems like a nice ‘side benefit’, too.

If you would like to know more about how I can help you achieve and maintain a healthy body weight or halt the progression of Type 2 Diabetes and other related metabolic disorders, please send me a note using the Contact Me form on this web page.  If you would like to learn more about the services I offer and their costs, please click on the Service tab or have a look in the Shop.

To your good health!

Joy

You can follow me at:

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Reference

Crawford A, Increasing evidence of a strong connection between sugar and cancer, MedicalXPress, March 20, 2019,  https://medicalxpress.com/news/2019-03-evidence-strong-sugar-cancer.html

Copyright ©2019 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.

If you live almost anywhere in Canada and are looking for a Registered Dietitian with experience in food allergy or sensitivity, including celiac disease and IBS as well as the specific of providing low carbohydrate or ketogenic diet support, I can help.

Whether you live in British Columbia, Alberta, Saskatchewan, Manitoba, Ontario, Quebec, New Brunswick, Nova Scotia, Newfoundland or Labrador, I am now licensed to provide you with services.

I currently can’t provide Dietitian services to Prince Edward Island (PEI) but if I have enough demand, that may change.

Registered in British Columbia since 2002

I have been registered with the College of Dietitians of British Columbia since 2002 as an RD(t) and since 2008 as a full registrant. This registration enables me to provide services to people across Canada, with the exception of  Alberta and PEI but since I’ve had several physicians in Alberta who have asked to refer patients to me as well as individuals from Alberta requesting services, I recently applied to- and was accepted into the College of Dietitians of Alberta.

Provincial Registration Requirements for Virtual Dietetic Practice

As can be seen from the table below, Registered Dietitian such as myself that provide virtual Dietetic practice services (Distance Consultation) to other provinces are required to meet very specific registration requirements, as well as observe other regulatory regulations.

In the US or overseas?

I am a member of the College of Dietitians of British Columbia as well as the College of Dietitians of Alberta and am licensed to provide Registered Dietitian services in most provinces in Canada (except PEI), but if you live in the USA or elsewhere, I can provide you with nutrition education services that would not be considered medical nutrition therapy (MNT) and that would be provided for information purposes only.

More Info

If you would like more information, you can find out more under the Services tab or by looking in the Shop. If you have specific questions, please send me a note using the Contact Me form on the tab above and I’d be glad to reply as I am able.

To your good health!

Joy

You can follow me at:

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Copyright ©2019 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

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

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

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

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

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

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

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

Cardiovascular Disease -a leading cause of death

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

Proposed Mechanism – inflammation

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

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

SIDE-NOTE: This idea that inflammation precedes insulin resistance is something I’ve been coming across recently. Some propose that insulin resistance itself may be a protective mechanism against high levels of circulating glucose (sugar) in the blood [a], in much the same way as the ability to produced more and more subcutanous fat (the fat directly under the skin) may be protective against the accumulation of fat around the organs (called visceral fat) or fat in the organs or even the bone (called ectopic fat). That is, excess energy (calories) seen as high levels of glucose in the blood may be the result of storage problems in fat cells (the body’s inability to make new subcutaneous fat cells), and the subsequent overflow of fat may drive excess high glucose production in the liver. a. Nolan CJ, Prentki M, insulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shift, Diabetes and Vascular Disease Research, Feb 15, 2019

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

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

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

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

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

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

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

Recommended Dietary Changes

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

High Triglycerides(TG)

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

NOTES: * fructose, the sugar in fruit is a simple carbohydrate and can be a major contributor to high TG.  ** there is no distinction between starchy vegetables such as potato and sweet potato (which accounts for a large percentage of overweight children and adult’s ‘vegetable’ servings) and non-starchy vegetables such as leafy greens and cruciferous vegetables, such as broccoli and cauliflower, as well as a whole host of other low carbohydrate non-starchy vegetables. *** it is well established that omega 6 polyunsaturated fats contribute to the inflammation process yet the recommendation doesn’t indicate that there should be a decrease in omega 6 polyunsaturated fats such as from soybean oil, canola oil, etc. and an increase in anti-inflammatory omega 3 fats from fatty fish such as tuna, salmon, sardines, etc even though the paper itself proposes inflammation at the heart of the issue. This makes no sense to me.

Total LDL Cholesterol

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

See Notes above for * , ** and ***.

NOTE: The body of the AHA paper elaborates on the detrimental effect of the small LDL subparticle (LDL-s), yet no such differentiation from total LDL cholesterol (LDL-c) is made in the Dietary Recommendations. Why is that? Particle size of LDL can be established by testing, using Apo B:Apo A ratio (Apo B is a component of lipoproteins involved in atherosclerosis and cardiovascular disease) and by proxy using a TG:HDL ratio. It makes no sense to me that the dietary recommendations focus on total LDL cholesterol when the paper makes it clear that it is the small LDL subparticle that is the risk factor.

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

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

See Notes above for * , ** and ***.

Some final thoughts…

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

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

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

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

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

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

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

To your good health!

Joy

You can follow me at:

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Copyright ©2019 BetterByDesign Nutrition Ltd.

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

References

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

Most people think of pre-diabetes as warning sign’ that they are at risk for developing type 2 diabetes, but it is actually the final stage before diagnosis. By the time a person is prediabetic their blood glucose results (also called ”blood sugar”) are in the abnormal range on routine tests such as a fasting blood glucose test (FBS) and glycated hemoglobin (HbA1C). They also may already have increased high blood pressure, abnormal cholesterol, and be at increased risk of cardiovascular disease, including heart attack and stroke as well as chronic kidney disease. By assessing a person’s fasting blood glucose and fasting insulin at the same time then using a simple calculation we can accurately estimate the degree of a person’s insulin resistance and beta-cell function before they become pre-diabetic — enabling them to make dietary interventions to prevent that from occurring, lower the likelihood of them progressing to type 2 diabetes.

It is now known that abnormalities with the hormone insulin — including insulin resistance and hyperinsulinemia appear more than 20 years before a diagnosis of Type 2 Diabetes[1], so prevention of type 2 diabetes needs to begin when blood sugar results still appear normal.

Before getting into the technical details of insulin resistance and hyperinsulinemia, I want to explain these concepts in terms that everyone can understand.

Assessing Beta-cell Function – measuring glucose and insulin together

Most people know that a car’s speedometer indicates how fast the car is going. The tachometer indicates how many times per minute the engine is rotating. If a car is doing 180 km / hour (110 miles per hour) on the highway, one would expect the engine to be working hard. But if a car was only doing 70 km / hour (44 miles per hour), one wouldn’t expect the engine to be working that hard, right?

The problem is that blood sugar may be within normal range because the  pancreas is overworking to keep it low! The beta-cells of the pancreas are being overworked but no one notices because they aren’t looking for it.

Even when people have a 2 hour Oral Glucose Test with added insulin assessors (explained below), blood glucose results may appear normal because the pancreas is working way too hard to keep it that way. That is, using the car example, the tachometer is working very hard, but the car is hardly moving!

Let’s look at this scenario in terms of blood test results.

Let’s say a person has fasted overnight and their fasting blood glucose in the morning is normal at 4.9 mmol/L (88 mg/dl), but their fasting insulin is much higher than the ideal 14.0 — 83.3 pmol/L (2-12 uU/ml) — in this case, say it is 220 pmol/L (31.7 uU/ml). This is like having a car running but in ”park” in the driveway, and having the the gas pedal to the floor! The engine turning at 6,000 RPM and we aren’t going anywhere, yet we are burning out the engine. In the case of high fasting insulin and normal fasting blood glucose, the pancreas is working way too hard to maintain blood sugar, and they are burning out their beta-cells and they haven’t even eaten yet!

Say we now give this person 75 g of pure glucose to drink and check what happens to their blood sugar at 30 minutes and/or one hour afterwards. What we expect a healthy person’s blood sugar to do is to go up in response to taking in the glucose, for the pancreas to release the appropriate amount of insulin which results in the blood sugar going back down to at- or slightly below where it started from. This is the normal, healthy response.

On a graph it would look like this;

But in the case of the person whose blood sugar is normal at fasting (i.e. 4.9 mmol/L (88 mg/dl)) but their fasting insulin is much higher than ideal (i.e. 220 pmol/L (31.7 uU/ml) instead of 14.0 — 83.3 pmol/L (2-12 uU/ml), their car is in ”park” but the engine is already turning way too fast! Their beta-cells are working way too hard.

When this person drinks the 75 g of glucose, the beta-cells of their pancreas goes into ”high rev” and releases a huge amount of insulin which may result in their blood sugar at 30 minutes and/or one hour going as high as 15 mmol/l (270 mg/dl), yet dropping back to normal, or below after 2 hours. This is not a healthy response but is characteristic of hyperinsulinemia (too much circulating insulin even when the person is fasting).  

Using the car analogy, their ”tachometer” (pancreas that produces insulin) is working way too hard in order to keep blood sugar low. Burnout of the pancreatic beta-cells is what results in type 2 diabetes (T2D) but without assessing simultaneous glucose AND insulin at fasting, either 30 minutes or 1 hour, and at 2 hours, the fact this person’s pancreas is working way too hard to keep glucose low would be totally missed. 

By the time a person is diagnosed with T2D, they have lost approximately half of their beta-cell mass, so preventing the beta-cells of the pancreas from being overworked is how to delay or prevent becoming type 2 diabetic!

Four Stages of Type 2 Diabetes — why assessing beta-cell function is important

There are four stages in the progression of Type 2 Diabetes, with Insulin Resistance and Hyperinsulinemia being the stage BEFORE pre-diabetes [2].

Stage 1: Insulin Resistance (including hyperinsulinemia)
Stage 2: Pre-diabetes
Stage 3: Type 2 Diabetes
Stage 4: Metabolic and Vascular Complications

Insulin resistance and  hyperinsulinemia together are essentially ”pre-pre-diabetes”, therefore stopping progression of the disease at this point reduces the risk associated with high blood pressure, abnormal cholesterol, heart attack and stroke, as well as chronic kidney disease.

Insulin resistance is where the cells of the body ignore signals from the hormone insulin which tell it to move glucose from broken down from digested food — from the blood and into the cells. When someone is insulin resistant, blood glucose stays higher than it should be, for longer than it should be, which is called  hyperglycemia.  When there are insufficient receptors on muscle cells to move glucose out of the blood after eating, this is called insulin resistance. It isn’t known whether insulin resistance comes first or hyperinsulinemia (high circulating levels of insulin) does. It is believed that it may be different depending on the person[3].

Assessing Insulin Resistance and Beta-cell Function

Homeostatic Model Assessment (HOMA-IR) estimates the degree of insulin resistance (IR), beta-cell function (the cells of the pancreas that produce insulin) and insulin sensitivity (%S) and is determined from the results simultaneous fasting blood glucose test and a fasting insulin test.

Alternatively, HOMA-IR can be determined from a fasting blood glucose test and a fasting C-peptide test [3]. C-peptide is released in proportion to insulin, so it can be used to estimate insulin. Individual results are best compared to local population cut off values for HOMA1-IR [4] (1985) or the updated HOMA2-IR [5] (1998) .

HOMA1-IR  is defined as [fasting insulin (µU/mL)í— fasting glucose (mmol/L)]/22.5 [4] and HOMA2-IR is calculated using an online HOMA2 calculator released by the Diabetes Trials Unit, University of Oxford available at http://www.dtu.ox.ac.uk/homacalculator/index.php (updated January 8, 2013).

The original HOMA1-IR equation proposed by Matthews in 1985 [4] was widely used due to its simplicity, however it was not always reliable because it did not consider the variations in the glucose resistance of peripheral tissue and liver, or increases in the insulin secretion curve for blood glucose concentrations above 10 mmol/L (180 mg/dL) or the effect of circulating levels of pro-insulin. [6]. The updated HOMA2-IR computer model [5] has been used since 1998 and corrects for these.

Cut-off for insulin resistance using the original Matthews values (1985) [4] for HOMA-IR are 2.7

Insulin sensitive is considered less than 1.0
Healthy is considered 0.5-1.4
Above 1.8 is early insulin resistance
Above 2.7 is considered significant insulin resistance

Cuffoff values for insulin resistance using the HOMA2-IR calculator (1998) [5] is HOMA2-IR of 1.8. Three population based studies found the same or very close cutoffs applied, including a 2009 Brazilian study [7] which found HOMA2-IR at 1.8, a 2014 Venezuelan study [8] which found HOMA2-IR at 2.0 and a 2014 Iranian study [9] which found HOMA2-IR at 1.8.

Use of HOMA-IR to Assess Insulin Resistance and Beta-cell Function in the Individual

HOMA-IR has been used to assess Insulin Resistance (IR) and beta-cell function as a one-off measures in >150 epidemiological studies of subjects of various ethnic origins, with varying degrees of glucose tolerance [10].

In the Mexico City Study which used single glucose-insulin pairs (not the mean of three samples at 5-min intervals) [11], beta-cell function and Insulin Resistance were assessed using HOMA-IR in ~1500 Mexicans with normal or impaired glucose tolerance (IGT) (27). Subjects were followed up for 3.5 years for the incidence of diabetes and to examine any possible relationship with baseline β-cell function and IR. At 3.5 years, ~4.5% of subjects with normal glucose tolerance at baseline and ~23.5% with impaired glucose tolerance at baseline had progressed to type 2 diabetes. That is, the development of diabetes was associated with higher HOMA-IR at baseline.

The use of HOMA-IR on an individual basis enables clinicians to quantify both the degree of insulin sensitivity and β-cell function on assessment — before the person makes any dietary changes. Once the individual understands the significance of their HOMA-IR results, it can provide significant motivation for them to make dietary changes to slow— or prevent the progression toward abnormal glucose tolerance, or type 2 diabetes. When HOMA-IR is repeated 6 months into dietary changes, it provides significant feedback to the individual regarding the effectiveness of of dietary changes, and the motivation to continue.

”HOMA-IR can be used to track changes in insulin sensitivity and beta-cell function longitudinally in individuals. The model can also be used in individuals to indicate whether reduced insulin sensitivity or beta-cell failure predominates.[10]

Measuring Hyperinsulemia and beta-cell function

Detection of hyperinsulinemia (high circulating levels of insulin) can occur using an Oral Glucose Sensitivity Index (OGIS) where available, or with a 2-hr Oral Glucose Tolerance Test (2-hr OGTT) with simultaneous assessors of insulin.  These are tests where a fasting person drinks a known amount of glucose (usually 75 g or 100 g of glucose) and their blood sugar and insulin values are measured before the test starts (baseline, while fasting) and at 2 hours. An additional assessor of blood glucose and insulin can be requested at 1 hour which is very helpful for detecting abnormalities that would missed if only assessing at fasting and at 2 hours. In the OGIS, both blood glucose and blood insulin levels are measured at baseline (fasting), at 120 minutes and at 180 minutes[3].

Final thoughts…

As mentioned at the start of this article, abnormalities in insulin, including insulin resistance and/or hyperinsulinemia begin to occur as much as 20 years before a diagnosis of type 2 diabetes — while blood sugar results are still normal. That is when we need to diagnose abnormalities!

If we simply monitor fasting blood glucose, we will miss that someone’s pancreas may be overworking.

Even if we monitor fasting blood glucose and glycated hemoglobin (HbA1C), we can miss that someone’s pancreas is overworking by constantly producing too much insulin.

Furthermore, even if a standard 2 hour Glucose Tolerance Test is run and the person’s fasting blood glucose and 2 hour glucose level after a load is measured, we still can miss that someone’s pancreas is being pushed way too hard if those values appear normal at baseline and at the end of the test.

By running a 2 hour Glucose Tolerance Test with simultaneous glucose and insulin at baseline (fasting), 30 minutes or 1 hour, and at 2 hours we can observe the pancreas being pushed way too hard and implement dietary changes to avoid further beta-cell damage or beta-cell death.

In British Columbia, the cost of a standard 2 hour Oral Glucose Tolerance Test is $11.82 before tax and $13.36 with HST.

Each additional glucose assessment is $3.48 before tax and $3.93 after tax.

Each insulin assessment costs $32.82 before tax and $37.09 after tax, so a 2 hour Oral Glucose Tolerance Test with additional glucose assessor at 1 hour and 3 insulin assessors at fasting, 1 hour and 2 hour costs as follows;

2 hour Oral Glucose Tolerance (fasting, 2 hours)           = $  13.36  with HST
additional glucose at 1 hour                                                       = $   3.93   with HST
3 insulin assessors at fasting, 1 hour, 2 hours                   = $111.27  with HST
TOTAL                                                                                                   = $128.56 with HST

When there are clinical reasons to suspect that a person may be insulin resistant and/or hyperinsulinemic and assessment of simultaneous glucose and insulin function can provide sufficient motivation for individuals to implement dietary changes that can prevent progression to type 2 diabetes, is this testing not worth <$130?

NOTE (March 9, 2021): Some family medicine doctors won’t order tests to assess insulin along with glucose in order to “save healthcare system dollars” — but instead will send their patient to an endocrinologist which costs the system ~$300 before any tests are run. Why? In parts of Canada, if audited, family medicine physicians have to re-pay for preventative tests (which are deemed “unnecessary”) . Self-paying for these tests is an option to consider.

If you would like to know about the services that I offer, please click on the Services tab to learn more and if you have questions related to these, please send me a note using the Contact Me form located on the tab above and I will reply as I am able.

To your good health!

Joy

https://twitter.com/lchfRD

 https://www.facebook.com/BetterByDesignNutrition/

Copyright ©2019 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. Sagesaka H, S.Y., Someya Y, et al, Type 2 Diabetes: When Does It Start? Journal of the Endocrine Society, 2018. 2(5): p. 476-484.
2. Mechanick JI, G.A., Grunberger G, et al, Dysglycemia-Based Chronic Disease: an American Association of Clinical Endocrinologists Position Paper. Endocrine Practice, 2018. 24(11): p. 995-1011.
3. Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.
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INTRODUCTION: Last Friday, February 8, 2019, the Montreal Gazette published a special article with accompanying video by Dr. Joe Schwarcz, Professor of Chemistry from McGill University titled “Keto Diets Work, but is There a Catch?” and this morning the follow-up was published titled “The Known Benefits of Low-Carb Keto Diets”. This post contains a summary of both.

PART I – “Keto Diets Work, but is There a Catch?”

Dr. Joe Schwarcz, The Montreal Gazette, February 8, 2019 (reference below)

This article began;

“There is little doubt that cutting way back on carbs results in weight loss. But how does all that fat impact cardiovascular risk factors?”

This is a very good question, however it is incorrectly based on the assumption that a “keto diet” is necessarily very high in fat, especially saturated fat, something which is not necessarily the case.

Dr. Schwarcz stated in the article in the Montreal Gazette that on a “keto diet” there is no bread, pasta, cereal, potatoes, carrots, rice, fruit or beer but that one can;

“gorge on fish, butter, eggs, high-fat cheese, whipped cream, coconut oil and meat to your heart’s delight.”

As mentioned in an earlier article that I wrote on a site dedicated to low carbohydrate diets;

“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. “

Assuming that the specific type of “keto diet” that Dr. Schwarcz is referring to is one where one that (1) avoids bread, pasta, cereal, potatoes, carrots, rice, fruit* or beer and (2) indulges in foods high in fat, such as fish, butter, eggs, high-fat cheese, whipped cream, coconut oil and meat, it is a very appropriate question to ask as to what effect does this type of keto diet have on cardiovascular risk factors.

Note: Most keto diets used for weight loss allow fruit as berries, such as raspberries, strawberries, blueberries, blackberries as well as those fruit that we often think of as vegetables, including tomato, avocado, cucumbers, lemon and lime.  Dr. Schwarcz raised a concern in the video that not eating fruit limits one’s access to the important antioxidants in fruit, which for the most part is incorrect.

The article states that;

“There is little doubt that cutting way back on carbs results in weight loss. The question is, why?

The body’s main source of energy is glucose, generally supplied by starches and sugars [i.e. carbs] in the diet. If consumption of these carbohydrates is drastically reduced, below about 50 grams a day, energy has to be derived from an alternate source. At first, the 65 or so grams of glucose the body needs per day are produced from amino acids, sourced from proteins. But this process itself has a high energy requirement, and furthermore, the body is not keen on using up proteins that are needed to maintain muscle integrity. Fortunately, there is a backup system that can swing into action.

The liver begins to convert fats into ”ketone bodies,” namely beta-hydroxybutyrate, acetoacetate and acetone. These are then shuttled into the mitochondria, the cells’ little energy factories, where they are used as fuel. At this point the body is said to be in ”ketosis,” with excess ketones being excreted in the urine.”

Great explanation!

The article raises a few excellent points;

The article states that the “usual argument” for the more efficient weight loss associated with extremely low carb diets as compared to low fat diets is that (1) low carb diets produce a metabolic advantage because a lot of calories are needed to convert proteins to glucose.  The article adds that not everyone agrees with this premise and states that others suggest that (2) ketone bodies have either a direct appetite suppressant effect or that they (3) alter levels of the respective appetite stimulating and inhibiting hormones, ghrelin and leptin. Lastly, the article states that some argue that (4) ketogenic diets lead to a lower calorie intake which the article’s author believes is “due to the greater satiety effect of protein”.

“No long-term studies of keto diets”

The article correctly states that;

“There are numerous studies published over the last 20 years that have compared low-fat diets to low-carb diets with the overall conclusion that the low-carb diets are more effective in terms of weight loss, at least in the short term.

…but incorrectly adds;

“Unfortunately, there are no long-term studies of keto diets.”

While there have been 3 long-term clinical trials (2 years) published over the past 10 years involving low carb diets, unfortunately as documented in and earlier article none of these involved research groups that actually ate a low carbohydrate diet. There is, however the recent two-year data from the Virta Health’s study that was published this past December 2018 which demonstrated the long term safety of a ketogenic diet and that participants on average;

(1) lost 12.4 kg (28 pounds) in two years; most of which was achieved in the first year maintained with only a slight increase of 2.3 kg (5 pounds) in the second year.

In addition to the weight loss, participants in the Virta Health study;

(2) significantly lowered medication use for Type 2 Diabetes (read more here)

(3) lowered glycated hemoglobin (HbA1C) by a full percentage point at two years (7.7% to 6.7%)

(4) lowered fasting blood glucose from 9.1 mmol/L (164 mg/dl) at the start of the study to 7.4 mmol/l (134 mg/dl ) at two years.

High Fat Keto Diet and Cardiovascular Risk Factors

The article concludes with the initial question as to how a diet “high in fat, such as fish, butter, eggs, high-fat cheese, whipped cream, coconut oil and meat” impacts markers of cardiovascular risk.

“As one would expect, LDL, the ”bad cholesterol,” does go up, although the increase is mostly in the ”large particle” sub fraction that is deemed to be less risky.

Triglycerides, a significant risk factor, actually decrease on a very-low-carbohydrate diet, as does the body’s own production of cholesterol.

Levels of HDL, the ”good cholesterol,” increase.

That is, over the short term, markers of cardiovascular risk doesn’t change to any degree.

What about over the long term?

Unfortunately, the article concludes with;

“the problem is that there are no studies of people who have followed a keto diet long enough to note whatever effect such a diet may have on heart disease.”

…but as mentioned above, we do have the two-year data from the Virta Health’s study that was published this past December 2018 and which demonstrates that;

(1)  LDL cholesterol of the intervention group at the start of the study averaged 2.68 mmol/L (103.5 mg/dl) and at two years was slightly higher as expected, to 2.96 mmol/L (114.5 mg/dl), however this level after 2 years was almost identical to what it was at 1 year; 2.95 mmol/L(114 mg/dl). That is, LDL (mostly the large particle sub-fraction) increased as expected the first year but didn’t continue to rise.

(2) At baseline, HDL cholesterol (“good cholesterol”) of the intervention group averaged 1.11 mmol/L (41.8 mg/dl) and after two years was stable at the same level it had risen to at 1 year, namely 1.28 mmol/L (49.5 mg/dl).

(3) At baseline, triglycerides of the intervention group averaged 2.23 mmol/L (197.2 mg/dl) and at two years was down to 1.73 mmol/L (153.3 mg/dl ), only up slightly for the one year average of 1.68 mmol/L (148.9 mg/dl).

Final Thoughts…

While Dr. Schwarcz seemed to be unaware of the publication of the two-year Virta Health study data in December 2018 that demonstrates both long-term safety and efficacy of a ketogenic diet for weight loss and improvement in metabolic health (including markers of cardiovascular risk), the Montreal Gazette article and accompanying video does indicate that a very high fat ketogenic diet does not adversely impact markers of cardiovascular risk.

Reference

1. Dr. Joe Schwarcz, “The Right Chemistry: Keto diets work, but is there a catch?” Montreal Gazette, February 8, 2019, https://montrealgazette.com/opinion/columnists/the-right-chemistry-keto-diets-work-but-is-there-a-catch

PART II – “The Known Benefits of Low-Carb Keto Diets”

Dr. Joe Schwarcz, The Montreal Gazette, February 15, 2019 (reference below)

This morning, Dr. Joe Schwarcz, Professor of Chemistry from McGill University and popular radio show host released a follow-up to last week’s opinion article and video that was published in the Montreal Gazette on the cardiovascular risks of a keto diet; this one on the known benefits of low-carb keto diets.

Schwarcz begins by fondly reminiscing about going to the circus with his mother when he was about 7 or 8 years old and the memories of the snack that she packed for him of crusty Hungarian bread, slathered with butter and topped with green bell pepper. He said that he’s loved it ever since, but “now we question such snacks. Why? Because of the carbohydrate content of the bread”.

“I’ve been looking into this for quite a while. There is really a plethora of papers and information that floods us about the keto diets; the very low carbohydrate diets”.

To his credit, Dr. Schwarcz acknowledged (possibly as a result of my written response to his article of last week in the Montreal Gazette) that there isn’t just one “keto diet” (singular) but several very low carbohydrate diets (plural) .

Schwarcz reiterates;

“I would have thought that by having all of that fat in the diet that risk levels for certain cardiovascular factors would go up, but really there isn’t really that much alteration in these factors”.

Low-Carb “Keto” Diets and Diabetes

Transitioning from the lack of cardiovascular risks associated with low-carb keto diets, Schwarcz adds;

“When it comes to Diabetes the information is really overwhelming to the benefit of these low carb diets. There are people — Type 2 Diabetes sufferers, who have been able to give up their medication by following a stringent, low carbohydrate diet.”

Schwarcz dismisses anecdotal reports of people’s “brain fog” resolving and possible benefits for cancer, Parkinson’s disease and Alzheimer’s disease as not being scientifically based but is unequivocal about the known benefits;

“What we do know is that weight loss can be very significant on a low carbohydrate diet and as I said — surprisingly, without any significant risk factors.”

Schwarcz continues;

“On the other hand, the longest terms studies that I’ve seen which were really properly controlled have only been about six months, and that really isn’t long enough.”

NOTE: In this case, Dr. Schwarcz is referring only to randomized, controlled double blind studies — excluding the data from long term studies of other types.

“We also know from dietary studies that after about a year, it doesn’t much matter what diet you’re on when it comes to weight loss — whether it’s low fat, whether it’s low carb, the results tend to be the same as long as you’re cutting out some calories.”

NOTE: While this may be true, what Schwarcz neglects to mention is that the major difference is that in a calorie-restricted low-fat diet, people are deliberately restricting food intake, often feeling hungry — whereas in a low carbohydrate diet, people naturally feel less hungry due to the satiety (hunger-reducing effect of protein and fat) which results in them eating less. In one case people are purposely restricting calories in the the other case, they don’t feel as hungry so they naturally eat less.

Schwarcz reiterates;

“However, for people who are afflicted with Diabetes, I think there is no question that the very low carb diets are worth trying.”

Towards the end of the video Dr. Schwarcz reflects on his childhood snack of crusty Hungarian bread, slathered with butter and topped with a quarter of a green bell pepper and admits that he looks askew at this snack.

“I admit that I’ve been eating less bread — I haven’t cut it out because I don’t think I need to do that, but I’m eating less.”

Schwarcz adds that for those who are gravitating towards a low carbohydrate diet, they can opt instead to eat bell pepper with a dollop of hummus with tahini (ground sesame seeds) or raw broccoli dipped in a bit of hummus.

“It tastes good! I think it is possible to cut down on the bread!”

Since Dr. Schwarcz is presumably not Diabetic and has all the nostalgia of memories of the circus as a child, he concludes the video by happily biting into a slice of crusty Hungarian bread that’s been slathered with butter and topped with a quarter of a green bell pepper…for nostalgia reasons, of course!

Bon appetit, Dr. Schwarcz!

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To your good health!

Joy

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Reference

Montreal Gazette, February 15, 2019, Dr. Joe Schwarcz, Known Benefits of Low Carb “Keto” Diets” https://montrealgazette.com/category/opinion

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