Author: BBDN

While DEXA scans (Dual Energy X-ray Absorptiometry) are intended to measure bone mineral density, they also provide an accurate estimate of body fat percentage but not everyone wants to- or is able to go for  this kind of testing to determine how much body fat they have. While most gyms and many pharmacies often have handheld impedance body fat analyzers, these can be affected greatly by changes in body water status, as can high tech digital bathroom scales that have body fat analyzers built in.

Determining Body Fat Percentage based on BMI

Body Mass Index (BMI), which is body mass divided by the square of body height is often used to determine whether someone is normal weight, overweight or obese despite the fact that it is limited in its ability to estimate body fat percentage due to misclassification of body fat-defined obesity. For example, a BMI ≥30 which indicates obesity overlooks nearly 50% of women who have a body fat percentage > 35% which the cutoff for obesity. The US Third National Health and Nutrition Examination Survey estimated the diagnostic accuracy of BMI for body fat-defined obesity at 94% for women and 82% for men [1].

The body fat percentage chart below from the American Council on Exercise (ACE) is a commonly used by trainers and gyms to determine body fat percentage but is limited since it is based on BMI.

Determining Body Fat Percentage Based on Anthropometrics

There are a number of equations based on body measurements (anthropometrics) that have been proposed as alternatives to BMI to better estimate whole body fat percentage. Some require more than 10 different measurements, others require up to 4 different skin-fold measurements using calipers and even others are complex equations using multiple measurements. The common problem amongst all of the existing equations is a lack of simplicity, limiting their use in routine Dietetic or medical practice.

Determining Body Fat Percentage Using Relative Fat Mass (RFM)

A recently published study systematically explored more than 350 anthropometric measurements with the aim of identifying a simple linear equation that is more accurate than BMI at estimating whole body fat percentage in both men and women.

The equation is amazingly simple;

Relative Fat Mass (RFM): 64−(20í—(height/waist))+(12í—sex),where sex = 0 for men and 1 for women.

Click here for an article on how to accurately measure your waist circumference for use in this equation.

Compared with BMI, the Relative Fat Mass (RFM) equation was more accurate for body fat-defined obesity among both men and women over 20 years old and RFM was more accurate than BMI for those with a high body fat percentage and this accuracy held for those that were Mexican-Americans, European Americans and Africans-Americans.

Looking at the equations another way, Relative Fat Mass (RFM) in both metric and American measurements is;

Relative Fat Mass (RFM):

Men: 64 — (20 x height/waist circumference)
Women: 76 — (20 x height/waist circumference)

How to Interpret Relative Fat Mass Results

Based on the research of Gallagher et al and data from the World Health Organization, health body fat ranges have been determined as follows;

In the case of Example 1, the 41 year old male with an RFM of 32.2 would be considered at the low end of “obese”.

The 60 year old female of Example 2 with an RFM of 38.9 would be classified at the low end of “overfat”.

The 50 year old female of Example 3 with an RFM of 33.4 would be classified at the higher end of the “healthy” range.

Some Final Thoughts…

Obesity is an significant risk factor for multiple chronic diseases and conditions including Diabetes, coronary artery disease, hypertension (high blood pressure) and certain types of cancer [1].

This new and very simple equation accurately estimates whole body fat percentage enable individuals to easily calculate whether they are have increased weight to lose and will enable clinicians to help their patients achieve optimal weight and waist circumference.

If you want to learn how to eat well and lose weight and inches and achieve a healthy body weight and waist circumference, I can help. I offer a number of services and packages that can be taken in-person in my Coquitlam (British Columbia office) or via Distance Consultation (Skype, long distance telephone). You can click on the Services  to learn more or have a look around the Shop. Please feel free to send me a note using the Contact Me form on the tab above if you have questions and I will reply as soon as possible.

To your good health!

Joy

 https://twitter.com/lchfRD

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

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Copyright ©2018  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

Woolcott OO, Bergman RN. Relative fat mass (RFM) as a new estimator of whole-body fat percentage ─ a cross-sectional study in American adult individuals, Scientific Reports; Volume 8, Article number: 10980 (2018), https://www.nature.com/articles/s41598-018-29362-1

Gallagher, D. et al. Healthy percentage body fat ranges: an approach for developing guidelines based on body mass index. Am J Clin
Nutr 72, 694—701 (2000).

For the second time in the last few days, dire warnings about the dangers of eating certain foods and not eating others dominated the headlines. In a previous post, I addressed the Harvard-based study which claimed that low carb diets shorten lifespan. This post is about a claim made by an adjunct professor from Harvard that ‘coconut oil is pure poison’.

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While the coconut oil story only broke this week, the lecture given by Dr. Karin Michels where she issued the dire warning about coconut oil took place on July 10, 2018 and is posted on YouTube in German [1].  In a talk titled “Coconut oil and other nutritional errors”, Dr. Michels, adjunct professor of epidemiology at Harvard T.H. Chan School of Public Health and Director of the Institute for Prevention and Tumor Epidemiology at the University of Freiburg in Germany said;

“I can only warn you urgently about coconut oil. This is one of the worst foods you can eat.”

Michels called the health claims about coconut oil “absolute nonsense” and said it’s “pure poison” for its saturated fat content and its threat to cardiovascular health [2].

For purposes of this article, let’s first look at the (1) health claims surrounding coconut oil and then (2) the belief that saturated fat is a threat to cardiovascular health.

(1) Health Claims about Coconut Oil

Most of the health claims surrounding coconut oil relate to the fact that it contains Medium Chain Triglycerides or MCTs which are metabolized differently than long chain fatty acids, going directly to the liver rather than requiring to be broken down through digestion.

Half (44 — 52%) of the saturated fat in coconut oil is a specific Medium Chain Triglyceride called lauric acid [3].

A quarter (~24%) to a third (33%) of the fatty acids in coconut oil contain the long-chain saturated fats, including mysteric (13-19 %) and palmitic acid (8-11%) and ~10-20% of the fatty acids are made up of 2 short chain saturated fatty acids, caproic (decoic) acid (5-9%) and caprylic acid (6-10%) [3].

The remaining 10% of the fatty acids in coconut oil are unsaturated, mostly oleic acid, with a small amount of linoleic acid [3].

Specific Health Benefit Claims of Coconut Oil

There are studies using 100% medium chain triglycerides that have shown modest weight loss with use of MCT oil compared with olive oil over a 4-month period , however a study comparing coconut oil (~50% MCTs) with soy bean oil (almost all long chain triglycerides) did not have a significant impact on weight loss over a 3-month period [4]. While the actual amount of weight loss with MCT oil may not be substantial, studies seem to indicate that it is ”visceral adiposity” or ”belly fat” that decreases, lowering waist circumference[4].

Something that needs to be kept in mind is that only ~ 1/3 of the fat in coconut oil is MCT oil. Most of the fat in coconut oil is saturated fat along with a modest amount of unsaturated fat. People making “fat bombs” and drinking “Bulletproof coffee” with coconut oil while expecting the benefits reported with 100% MCT oil will likely to be disappointed.  For the most part, people who add excess coconut oil to their diet as an elixir are simply adding extra energy to their diet.

Coconut Oil and Cholesterol

When it comes to cholesterol, there are numerous studies that have found that coconut oil raises HDL (the so-called ‘good cholesterol’) to a greater extent than olive oil, however some studies indicated that coconut oil may increase LDL (what used to be assumed to be ‘bad cholesterol’) whereas other studies have found that it doesn’t change LDL cholesterol, or if it did raise it it was in an insignificant amount. The issue is does it matter if LDL cholesterol is raised? Is a rise in total LDL cholesterol associated with an increased risk of heart disease?

(2) Saturated Fat is a Threat to Cardiovascular Health

The basis of the claim by the Harvard adjunct professor that coconut oil is “pure poison” rests with the fact that much of the fat in it is saturated fat and that saturated fat raises total LDL cholesterol, which is associated with heart disease. But is this true?

It is commonly assumed that higher total LDL cholesterol is associated with an increased risk of heart disease, but we now know there are different type of LDL particles – not all of which are associated with atherosclerosis.  While eating foods rich in saturated fat, including coconut oil will raise LDL-cholesterol,  not all LDL-cholesterol is ”bad” [5].

There are two types of LDL cholesterol; the small, dense LDL which are associated with atherosclerosis and the large, fluffy LDL which are protective against cardiovascular disease [5].

While it used to be believed that total LDL-cholesterol (LDL-C) was a good proxy (indirect substitute) measurement for heart disease risk, we now know that a much more accurate measurement is the LDL-cholesterol particle number (LDL-P) which measures the actual number of LDL particles. This is a much stronger predictor of cardiovascular events than LDL-C [6] because the more particles there are, the more small, dense LDL there are.

Another good assessor of cardiovascular risk is the ratio of apolipoprotein B (apoB): apolipoprotein A (apoA) [7]. Lipoproteins are particles that transport cholesterol and triglycerides (TG) in the blood stream and are made up of apolipoproteins, phospholipids, triglycerides and cholesterol. Apolipoprotein B is an important component of many of the lipoprotein particles associated with atherosclerosis such as chylomicrons, VLDL, IDL, LDL — with most found in LDL. Since each lipoprotein particle contains one apoB molecule, measuring apoB enables the determination of the number of lipoprotein particles that contribute to atherosclerosis and for this reason that ApoB is considered a much better predictor of cardiovascular disease risk than LDL-C [7].

Is Higher Saturated Fat in the Diet Associated with Heart Disease?

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

The question is does it?

A 2018 study published in the journal Nutrients looked at health and nutrition data from 158 countries from 1993-2011 and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease and that high carbohydrate consumption,  particularly as cereals and wheat was most associated with the risk of cardiovascular disease [9]. Significantly, both of these relationships held up regardless of a nation’s average national income.

These findings support those of the 2017 PURE (Prospective Urban and Rural Epidemiological) study, the largest-ever epidemiological study which recorded dietary intake of 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations. The PURE study found an association between raised cholesterol and lower  cardiovascular risk and that ”higher carbohydrate intake was associated with higher risk of total mortality”. It also reported that ”total fat and individual types of fat were related to lower total mortality (death)” [10].

A recent study published in the American Journal of Clinical Nutrition reports that long-term consumption of the saturated fat found in full-fat dairy products is not associated with an increased risk of cardiovascular disease (atherosclerosis, coronary artery disease, etc.) or other causes of death, and may actually be protective against heart attack and stroke [11].

This recent large-scale epidemiological data provides strong evidence that eating a diet containing saturated fat is not associated with heart disease. While eating saturated fat raises blood levels of LDL cholesterol, we now know that there is more than one type of LDL cholesterol and only the small, dense LDL cholesterol is linked to atherosclerosis. The large, fluffy LDL is protective [12].

Some final thoughts…

For the last forty years, Americans and Canadians have diligently reduced their consumption of eggs, full fat cheese, butter and red meat all because they had been told that the saturated fat in these foods would raise their total LDL cholesterol (which it does) and which will predisposed them to heart disease (not necessarily). While we know that eating foods high in saturated fat will raise total LDL levels, total LDL as mentioned above is not a good measure of cardiovascular risk. LDL particle size and ApoB: ApoA are much better predictors.

Another very good estimator of heart disease risk comes from assessing triglyceride (TG):HDL ratio [8]. It is widely accepted from both sides of the saturated fat debate that high levels of TG predispose people to heart disease, especially when associated with low levels of HDL (‘good cholesterol’).

Since (1) excess carbohydrate in the diet contributes to a rise in TG level and (2) the higher the ratio of HDL is to TG, the more protective it is against heart disease, it would logically follow that including some coconut oil in the diet (which contributes to raising HDL) and minimizing excess carbohydrate (especially as refined carbs) in the diet would together have no negative impact on the risk of heart disease and likely have benefit (based on the evidence presented in previous articles).

Adding excess saturated fat – whether as coconut oil or butter in the diet achieves no special benefit but avoiding it does nothing to lower the risk of heart disease risk and may even increase it.

Coconut is not “pure poison” but it isn’t a magic elixir either.  It is a healthy, natural fat rich in saturated fat with a good supply of MCT oils that can be used in moderate portions for cooking and for raising the ‘smoke point’ of butter when used in cooking (keeping butter from burning when heated). It’s time to stop vilifying saturated fat which is based on proxy measurements of total LDL cholesterol and on the assumption that increased total LDL is a predictor of heart disease.  We have much more accurate proxy measures and need to use them.

If you would like some help known which fats you can and should eat and in what amounts based on your existing health conditions and weight management goals, I can help. I provide services via Distance Consultation (Skype, long distance telephone) as well as in-person in my Coquitlam (British Columbia) office.

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

To our good health!

Joy

 https://twitter.com/lchfRD

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

Copyright ©2018  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. May, A. USA Today “Coconut oil is ‘pure poison,’ Harvard professor says in talk on nutrition”, August 22, 2018,  https://www.usatoday.com/story/news/nation-now/2018/08/22/harvard-professor-coconut-oil-pure-poison/1060269002/?utm_source=dlvr.it&utm_medium=twitter
2. Drayer L, Nedelman M. CNN, The facts behind coconut oil is ‘pure poison’ claim, August 22, 2018
3. Chempro — Edible Oil Analysis Retrieved from http://www.chempro.in/fattyacid.htm
4. Liau KM, Lee YY, Chen CK, Rasool AHG. An Open-Label Pilot Study to Assess the Efficacy and Safety of Virgin Coconut Oil in Reducing Visceral Adiposity. ISRN Pharmacology. 2011;2011:949686. doi:10.5402/2011/949686.
5. 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.
6. Cromwell, W.C., et al., LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study — Implications for LDL Management. J Clin Lipidol, 2007. 1(6): p. 583-92.
7. Lamarche, B., et al., Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Québec cardiovascular study. Circulation, 1996. 94(3): p. 273-8.
8. Manninen, V., et al., Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. Circulation, 1992. 85(1): p. 37-45.
9. Grasgruber, P., et al., Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries. Nutrients, 2018. 10(4).
10. Dehghan, M., et al., Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet, 2017. 390(10107): p. 2050-2062.
11. de Oliveira Otto, M.C., et al., Serial measures of circulating biomarkers of dairy fat and total and cause-specific mortality in older adults: the Cardiovascular Health Study. Am J Clin Nutr, 2018.
12. 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.

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

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

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

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

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

Dysfunctional Insulin Release & Insulin Resistance

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

To your good health,

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/BetterByNutrition/

Copyright ©2018  BetterByDesign Nutrition Ltd.

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

References

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

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

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

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

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

I am in complete agreement.

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

Uelmen explains,

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

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

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

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

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

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

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

This is true and I agree with her recommendation;

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

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

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

Uelmen makes other excellent points;

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

She offers this terrific advice;

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

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

Uelmen advises;

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

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

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

Uelman says;

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

…and this is excellent advice!

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

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

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

Final thoughts…

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

Why is this?

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

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

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

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

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

To our good health,

Joy

 https://twitter.com/lchfRD

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Copyright ©2018  BetterByDesign Nutrition Ltd. 

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

References

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

 

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

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

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

So what was its specially prepared formula?

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

Here are the words of the ad, above;

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

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

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

The obesity crisis should have come as no surprise.

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

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

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

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

…and promote them they did!

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

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

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

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

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

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Final Thoughts…

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

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

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

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

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

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

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

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

To our good health,

Joy

Copyright ©2018 a division of BetterByDesign Nutrition Ltd.

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

References

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

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

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

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

Why the difference when both had 25 g of carbs?

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

What about Insulin Response in response to these two foods?

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

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

What is the Insulin Index?

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

Below is a graph from that paper:

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

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

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

This was huge!

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

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

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

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

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

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

(1) insulin

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

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

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

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

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

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

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

To your good health!

Joy

References

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

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

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Copyright ©2018  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.

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

Part 1 can be read here.

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

Response of Incretin Hormones to Meal with Fat and Carbohydrate

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Meal Size and Meal Frequency

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

[study on right hand side of slide]

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

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

Eating Speed

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

Glycemic Load as a Proxy for the Amount of Carbohydrate Processing

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

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

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

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

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

What happened?

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

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

Structure and Speed of Absorption

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The Effect of Combining Refined Carbohydrates with Fat

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

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

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

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

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

How Does Bariatric Surgery / Gastric Bypass Work

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

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

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

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

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

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

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

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

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

Practical ”Takeaways”

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

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

I can help.

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

To your good health!

Joy

 

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The full lecture can be watched here:

References

(continued from Part 1)

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I keep coming across the same misconceptions about a “low carb diet” in online articles and on social media, so I decided to write an article dispelling the 10 most common myths.

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

A recent study[1] published at the end of March 2018 in Nutrients looked at health and nutrition data from 158 countries worldwide and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease, so even if someone following a low carb diet chose to eat foods high in saturated fat, it does not mean they are necessarily at higher risk of heart attacks or strokes.

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

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

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

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

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

How much protein is “too much”?

The RDA for Protein is set at 56 gm per day (based on 0.8 g protein per kg of body weight) is the minimum amount to prevent deficiency.  This is not the optimal amount, but the absolute minimum amount. So, whether a given person is eating 1200 calories a day or 2500 calories per day they have an absolute requirement for 56 gm of protein per day[2].

The maximum amount of protein per day is set at ~200 g / day and is calculated based on >2.5 g protein per kg of body weight, and the range from 56 g to 200 g of protein per day is referred to as the range of safe intake[2].

According to Dr. Donald Layman, Professor Emeritus of Human Nutrition from the University of Illinois, a high protein diet doesn’t start “until well above 170 g / day”[2].

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

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

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

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

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

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

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

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

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

In fact, the human body doesn’t require any dietary carbohydrate provided the amount of protein and fat in the diet is sufficient (to be used as substrates, as mentioned above); from page 275 of Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005)[3];

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

This does not mean that low carb diets contain no carbohydrate!

As mentioned above, some liberal low carb diets have enough carbohydrate such that the person does not go into ketosis, while therapeutic ketogenic diets (done under medical supervision) such as those used for the management of epilepsy or as an adjunct to cancer treatment may have < 30 g of carbohydrate.

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

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

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

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

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

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

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

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

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

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

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

There is almost no recipe that can’t be easily adapted for those that choose to eat low carb because food should not only be healthy, but enjoyable.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Final Thoughts…

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

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

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

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

(1) insulin

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

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

or

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

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

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

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

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

To your good health!

Joy

References

1. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
2.  Layman, Donald, The Evolving Role of Dietary Protein in Adult Health, Nutrition Forum, British Columbia, Canada, June 23, 2013 https://youtu.be/4KlLmxPDTuQ
3. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein and Amino Acids (2005), pg 275

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Copyright ©2018  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.

 

 

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

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

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

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

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

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

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

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

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

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

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

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

1. Overview of Gastrointestinal Physiology

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

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

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

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

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

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

Nutrient-Sensing

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

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

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

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

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

The Incretin Effect

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

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

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

The Physiological Effects of the Incretin Hormones

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

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

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

1. Hunger-Satiety Signalling in the Gut

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

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

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

3 a. The Effect of Cooking Foods on Body Weight

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

3b. The Effect of Cooking Foods on Nutrient Availability

Carbohydrate-rich Foods

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

Lipid and Protein-rich Foods

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

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

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

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

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

The conclusion of this study was worth noting;

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

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

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

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

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

Grinding / Juicing Fruit

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

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

Note: It’s not relevant to the outcome, but on this graph, slow and quick puree and juice as just differences in the amount of time it took for the liquid to be drunk.

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

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

Grinding Grains

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Perhaps you wonder what all this information means for you.

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

I can help.

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

To your good health!

Joy

The conclusion of this lecture is available here.

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References

1. Gribble, Fiona M., and Frank Reimann. ”Enteroendocrine Cells: Chemosensors in the Intestinal Epithelium.” Annual Review of Physiology 78, no. 1 (2016): 277—99. https://doi.org/10.1146/annurevphysiol-
   021115-105439.
2. Reimann, Frank, and Fiona M Gribble. ”Mechanisms Underlying Glucose-Dependent Insulinotropic Polypeptide and Glucagon-like Peptide-1 Secretion.” Journal of Diabetes Investigation 7 (2016): 13—19. https://doi.org/10.1111/jdi.12478.
3. Nauck, Michael A., and Juris J. Meier. ”Incretin Hormones: Their Role in Health and Disease.” Diabetes, Obesity and Metabolism 20 (2018): 5—21. https://doi.org/10.1111/dom.13129.
4. Perry, B., and Y. Wang. ”Appetite Regulation and Weight Control: The Role of Gut Hormones.” Nutrition & Diabetes 2, no. 1 (January 2012): e26. https://doi.org/10.1038/nutd.2011.21.
5. Groopman, Emily E., Rachel N. Carmody, and Richard W. Wrangham. ”Cooking Increases Net Energy Gain from a Lipid-Rich Food.” American Journal of Physical Anthropology 156, no. 1 (2015): 11—18.
   https://doi.org/10.1002/ajpa.22622.
6. Evenepoel, Pieter, Dirk Claus, Benny Geypens, Martin Hiele, Karen Geboes, Paul Rutgeerts, and Yvo Ghoos. ”Amount and Fate of Egg Protein Escaping Assimilation in the Small Intestine of Humans.”
7. American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 5 (November 1999): G935—43. https://doi.org/10.1152/ajpgi.1999.277.5.G935.
8. Carmody, R. N., G. S. Weintraub, and R. W. Wrangham. ”Energetic Consequences of Thermal and Nonthermal Food Processing.” Proceedings of the National Academy of Sciences 108, no. 48 (2011):
   19199—203. https://doi.org/10.1073/pnas.1112128108.
9. Morifuji, Masashi, Mihoko Ishizaka, Seigo Baba, Kumiko Fukuda, Hitoshi Matsumoto, Jinichiro Koga, Minoru Kanegae, and Mitsuru Higuchi. ”Comparison of Different Sources and Degrees of Hydrolysis of
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