Most people think of pre-diabetes as a ‘warning sign’ that they are at risk for developing type 2 diabetes, but it is the final stage before diagnosis.

The criteria for diagnosing prediabetes is having a fasting blood glucose between 6.1-6.9 mmol/L (110-12.4 mg/dl) and/or HbA1C between 6.0-6.4% [1], and the criteria for diagnosing Type 2 diabetes is having a fasting blood glucose ≥ 7.0 mmol/L and/or HbA1C ≥ 6.5% [1], see figure 1, below.

By the time a person is prediabetic, their blood glucose results (also called ”blood sugar”) are in the abnormal range on routine tests such as a fasting blood glucose test (FBS) and glycated hemoglobin (HbA1C). They also may already have high blood pressure, abnormal cholesterol, and be at increased risk of cardiovascular disease, including heart attack and stroke, as well as chronic kidney disease.

By assessing a person’s fasting blood glucose and fasting insulin at the same time then using a simple calculation we can accurately estimate the degree of a person’s insulin resistance and beta-cell function before they become pre-diabetic — enabling them to make dietary interventions to prevent that from occurring, lower the likelihood of them progressing to type 2 diabetes.

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

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

Assessing Beta-cell Function – measuring glucose and insulin together

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

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

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

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

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

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

On a graph, it would look like this;

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

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

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

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

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

There are four stages in the progression of Type 2 Diabetes, with Insulin Resistance and Hyperinsulinemia being the stage BEFORE pre-diabetes [3].

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

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

Insulin resistance is where the cells of the body ignore signals from the hormone insulin which tell it to move glucose from broken down from digested food — from the blood and into the cells. When someone is insulin resistant, blood glucose stays higher than it should be, for longer than it should be, which is called hyperglycemia.  When there are insufficient receptors on muscle cells to move glucose out of the blood after eating, this is called insulin resistance. It isn’t known whether insulin resistance comes first or whether hyperinsulinemia (high circulating levels of insulin) does. It is believed that it may be different depending on the person[4].

Assessing Insulin Resistance and Beta-cell Function

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

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

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

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

Cut-off for insulin resistance using the original Matthews values (1985) [5] for HOMA-IR are 2.7

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

Cutoff values for insulin resistance using the HOMA2-IR calculator (1998) [6] is HOMA2-IR of 1.8. Three population-based studies found the same or very close cutoffs applied, including a 2009 Brazilian study [8] which found HOMA2-IR at 1.8, a 2014 Venezuelan study [9] which found HOMA2-IR at 2.0, and a 2014 Iranian study [9] which found HOMA2-IR at 1.8.

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

HOMA-IR has been used to assess Insulin Resistance (IR) and beta-cell function as a one-off measure in >150 epidemiological studies of subjects of various ethnic origins, with varying degrees of glucose tolerance [11].

In the Mexico City Study, which used single glucose-insulin pairs (not the mean of three samples at 5-min intervals) [12], beta-cell function and Insulin Resistance were assessed using HOMA-IR in ~1500 Mexicans with normal or impaired glucose tolerance (IGT). Subjects were followed up for 3.5 years for the incidence of diabetes and to examine any possible relationship with baseline β-cell function and IR. At 3.5 years, ~4.5% of subjects with normal glucose tolerance at baseline and ~23.5% with impaired glucose tolerance at baseline had progressed to type 2 diabetes. That is, the development of diabetes was associated with higher HOMA-IR at baseline.

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

”HOMA-IR can be used to track changes in insulin sensitivity and beta-cell function longitudinally in individuals. The model can also be used in individuals to indicate whether reduced insulin sensitivity or beta-cell failure predominates.[11]

Measuring Hyperinsulemia and beta-cell function

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

Final thoughts…

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

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

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

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

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

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

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

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

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

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

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

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

To your good health!

Joy

 

Copyright ©2019 BetterByDesign Nutrition Ltd.

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

References

1. Diabetes Canada Clinical Practice Guidelines Expert Committee; Punthakee Z, Goldenberg R, Katz P. Definition, Classification and Diagnosis of Diabetes, Prediabetes and Metabolic Syndrome. Can J Diabetes. 2018 Apr;42 Suppl 1:S10-S15. doi: 10.1016/j.jcjd.2017.10.003. PMID: 29650080.
2. Sagesaka H, S.Y., Someya Y, et al, Type 2 Diabetes: When Does It Start? Journal of the Endocrine Society, 2018. 2(5): p. 476-484.
3. Mechanick JI, G.A., Grunberger G, et al, Dysglycemia-Based Chronic Disease: an American Association of Clinical Endocrinologists Position Paper. Endocrine Practice, 2018. 24(11): p. 995-1011.
4. Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.
5. Matthews, D. R; Hosker, J. P; Rudenski, A. S; Naylor, B. A; Treacher, D. F; Turner, R. C; “•Homeostasis model assessment: insulin resistance and β-cell function from fasting plasma glucose and insulin concentrations in man”–; Diabetologia; July, 1985; Volume 28, Number 7: Pp 412-419
6. Levy JC, Matthews DR, Hermans MP. Correct homeostasis model assessment (HOMA) evaluation uses the computer program. Diabetes Care. 1998;21:2191—2192
7. Song YS, Hwang Y-C, Ahn H-Y, Comparison of the Usefulness of the Updated Homeostasis Model Assessment (HOMA2) with the Original HOMA1 in the Prediction of Type 2 Diabetes Mellitus in Koreans, Diabetes Metab J. 2016 Aug; 40(4): 318—325
8. Geloneze B, Vasques AC, Stabe CF et al, HOMA1-IR and HOMA2-IR indexes in identifying insulin resistance and metabolic syndrome: Brazilian Metabolic Syndrome Study (BRAMS), Arq Bras Endocrinol Metabol. 2009 Mar;53(2):281-7
9. Bermíºdez V, Rojas J, Martí­nez MS et al, Epidemiologic Behavior and Estimation of an Optimal Cut-Off Point for Homeostasis Model Assessment-2 Insulin Resistance: A Report from a Venezuelan Population, Int Sch Res Notices. 2014 Oct 29;2014:616271
10. Tohidi M, Ghasemi A, Hadaegh F, Age- and sex-specific reference values for fasting serum insulin levels and insulin resistance/sensitivity indices in healthy Iranian adults: Tehran Lipid and Glucose Study, Clin Biochem. 2014 Apr;47(6):432-8
11. Wallace TM, Levy JC, Matthews DR, Use and Abuse of HOMA Modeling, Diabetes Care 2004 Jun; 27(6): 1487-1495. https://doi.org/10.2337/diacare.27.6.1487
12. Haffner SM, Kennedy E, Gonzalez C, Stern MP, Miettinen H: A prospective analysis of the HOMA model: the Mexico City Diabetes Study. Diabetes Care 19:1138—1141, 1996

 

INTRODUCTION: Last Friday, February 8, 2019, the Montreal Gazette published a special article with accompanying video by Dr. Joe Schwarcz, Professor of Chemistry from McGill University titled “Keto Diets Work, but is There a Catch?” and this morning the follow-up was published titled “The Known Benefits of Low-Carb Keto Diets”. This post contains a summary of both.

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

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

This article began;

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

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

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

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

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

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

Some therapeutic ketogenic diets are used in the treatment of epilepsy and seizure disorder and are extremely high in fat. Other types of therapeutic ketogenic diets are used in the treatment of various forms of cancer (those that feed on glucose), such as brain cancer. There are ketogenic diets that are used in the treatment of Polycystic Ovarian Syndrome  (PCOS), as well as for weight loss and for increasing insulin sensitivity in those with Type 2 Diabetes and insulin resistance.

Even among those using a nutritional ketogenic diet for weight loss and to increase insulin sensitivity, there is no one ”keto diet”.

There are ketogenic diets with a higher percentage of fat than protein, with a higher percentage of protein than fat and mixed approaches which may have different ratios of protein to fat — depending on whether the individual is in a weight loss phase or a weight maintenance phase.

There are as many permutations and combinations as there are people following a keto diet for these reasons.

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

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

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

The article states that;

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

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

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

Great explanation!

The article raises a few excellent points;

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

“No long-term studies of keto diets”

The article correctly states that;

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

…but incorrectly adds;

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

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

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

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

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

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

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

High Fat Keto Diet and Cardiovascular Risk Factors

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

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

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

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

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

What about over the long term?

Unfortunately, the article concludes with;

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

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

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

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

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

Final Thoughts…

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

Reference

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

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

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

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

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

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

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

Schwarcz reiterates;

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

Low-Carb “Keto” Diets and Diabetes

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

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

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

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

Schwarcz continues;

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

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

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

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

Schwarcz reiterates;

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

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

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

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

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

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

Bon appetit, Dr. Schwarcz!

If you would like to know more about the services I offer (including low carbohydrate and ketogenic diets) please click on the Services tab, and if you have questions about those please feel free to send me a note using the Contact Me form located on the tab above.

To your good health!

Joy

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Reference

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

Copyright ©2019 BetterByDesign Nutrition Ltd.

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