Are Low Carbohydrate Diets Linked to Risk of Premature Death?

Once again, dire warnings about the alleged dangers of “low carbohydrate diets” scream out from headlines across the internet;

“Low-Carb Diets Linked to Higher Risk of Premature Death”

~Newsweek August 28, 2018, 12:51 PM

“Low carbohydrate diets are unsafe and should be avoided, study suggests”

~ScienceDaily, August 28, 2018

The general public relies on journalists to thoroughly research their stories before publishing them however in the above two examples and the other incidences of reporting this story it was not indicated that (1) there was no published study (2) the story was based on researcher’s conclusions in provided materials based on an Abstract from a Poster presentation and (3) the provided materials / Abstract didn’t define the term “low carbohydrate” (# of grams of carbohydrate per day) which is central to the claims of the researchers.

The supposed link to “premature death” of a “low carbohydrate diet” were said to be part of a large study that was presented at the European Society of Cardiology (ESC) Congress 2018 in Munich, Germany, but when I went to find the journal in which the study was published so I could read it, I discovered that it’s not even been published yet.  I even checked the lead author’s Publication page on ResearchGate and could not find the published study. Furthermore, the findings were not presented as one of the more than 500 Conference sessions of research studies at the European Society of Cardiology Congress, but was one of the 4,500 Abstract presentations — not even as a talk, but as a Poster Session.

A “Poster Session” at  an academic Conference is where 100s of researchers assemble in a large hall and stand in front of a poster summarizing their research. People walk by, look at the poster and if they wish, ask questions.

Journalists wrote stories based on “materials provided to them by the European Society of Cardiology” (see story source at bottom of ScienceDaily article) which is based on the Abstract available on the website of the European Society of Cardiology’s 2018 Congress from the yet-to-be-published study by M. Mazidi  (Gothenburg, Sweden), N Katsiki (Thessaloniki, Greece), DP Mikhailidis (London, Great Britain) and M Banach (Lodz, Poland) and also published the same day (August 28, 2018) in the European Heart Journal, Volume 39 Supplemental on pages 1112-1113.

The Abstract (viewable below) is downloadable from the journal’s website and the 2018 Congress website and clearly indicates that it was a “Poster Session”.

A glaring omission from the Abstract is that it is not stated anywhere how many grams of carbohydrate per day is defined as a “low carbohydrate diet”.

The Abstract and supplied press materials claim that there is a relationship between “low carbohydrate diets” (not defined!) and death from all-causes, as well as specific death from coronary heart disease, cerebrovascular disease (stroke) and cancer and that the data analyzed was based on a representative sample of 24,825 participants of the US National Health and Nutrition Examination Survey (NHANES) from 1999 to 2010.

The researchers conclude that compared to participants with the highest carbohydrate consumption (also not defined!), those with the lowest carbohydrate intake had a 32% higher risk of all-cause death during the ~6.4-year follow-up. As well, the risk of death from coronary heart disease from “low carbohydrate”diets was 51% higher, from cerebrovascular disease (stroke) was 50% higher and from cancer was 35% higher. They furthermore state that their results were confirmed by a pooled meta-analysis of 7 prospective cohort studies with 447,506 participants and which had an average follow-up of 15.6 years which indicated that risk of death from all causes resulting from “low carbohydrate diets” was 15% higher, from cardiovascular disease was 13% higher and from cancer was 8% higher compared to high carbohydrate diets.

Wait a minute…

The researchers found risk of death from coronary heart disease and cardiovascular disease (heart attack and stroke) as ~50% higher and the pooled data of the studies they compared it to found a 13% higher incidence. Even without defining what a “low carbohydrate diet” is, a 50% increased chance of death is not comparable to a 13% increased chance of death.  Similarly, the researchers found risk of death from cancer from a “low carbohydrate diet” was 35% greater and said their findings were comparable to an 8% higher incidence in the pooled data.

The researchers (1) did not define how many grams of carbohydrate per day was considered a “low carbohydrate diet” and (2) said their data was confirmed by studies that reported very different results.

Yet, they conclude;

Our study highlighted the unfavorable effect of low carbohydrate diets (LCDs) on total- and cause- specific mortality, based on both individual data and by pooling previous cohort studies. Given the fact that LCDs may be unsafe, it would be preferable not to currently recommend these diets. Further studies to clarify the mechanisms involved in these associations and to support our findings are eagerly awaited.

Which “low carbohydrate diet” did they study? How many grams of carbohydrate per day? We don’t know because the Abstract doesn’t say and the study hasn’t yet been published.

Some Final Thoughts…

It is not responsible journalism for the media to scream headlines warning of higher risk of premature death from “low carbohydrate diets” based on supplied press materials and an Abstract of a Poster Session of an unpublished study that doesn’t even define “low carb”.

There are many studies and meta-analyses using a low-carbohydrate or ketogenic dietary intervention that span 18 years and that are outlined in detail in 76 publications involving  6,786  subjects and that include 32 studies of 6 months or longer and 6 studies of 2 years or longer that demonstrate that low carb diets of a specified number of grams of carbohydrate per day are both safe and effective. You can read more about that here.

Perhaps you have questions such as is a low-carbohydrate diet appropriate for you given your health goals, medical conditions or medications you are taking? Please feel free to send me a note using the “Contact Me” form and I will reply as soon as possible.

I provide both in-person services in my Coquitlam (British Columbia) office as well as Distance Consultation services (via Skype / long distance phone) and I’d be happy to help you achieve your health and nutrition goals.

To our good health,

Joy

You can follow me on Twitter and Facebook:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

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

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

Low carbohydrate diets and all cause and cause-specific mortality – page 1

 

Low Carb diets and all cause mortality – European Society of Cardiology_Page_2

 

Reference

Mazidi M, Katsiki N, Mikhailidis DP et al, Abstract (P5409): Low carbohydrate diets and all-cause and cause-specific mortality: a population based cohort study and pooling prospective studies, European Heart Journal, Volume 39 (Supplemental), pages 1112-1113.

 

Is Coconut Oil “Pure Poison”?

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’.


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/lchfRD/

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

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

References

  1. 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.

Do Low Carb Diets Shorten Lifespan?

Headlines are designed to attract readers to a story, to have people talking about it on social media and sharing it, so the way a study is framed is critical. Readers need to be discerning to ask questions about the story so they can tease apart truth from significance. What do I mean by this?

A fact can be true but really be quite meaningless, having little significance, which is often the case in these types of sensationalized reports. Let me give you an example to help explain what I mean. Let’s say there are 3 blond-haired 6 year old children and 2 red-haired 6 year old children in a room and one of the red-headed children slips on some water on the floor, falls and injures themselves, I could truthfully claim that injury rate of 6 year olds is 20% (1 in 5) but that the injury rate among red-headed children is much higher, at 50%. This is true, but is it significant? First of all the study groups were too small to make a comparison meaningful and that the child’s injury had nothing to do with them having red-hair and everything to do with the fact that there was water on the floor.

Looking at the recently published study which claimed that low carb diets could shorten lifespan[1], there are several questions we need to ask ourselves to begin to determine if the findings were meaningful such as “how was the information collected”, “how many people were in each comparison group” and “were there confounding factors” (factors that could confuse understanding the data).

How was the Information Collected

Subjects were asked to complete a 66-item semi-quantitative food frequency questionnaire (FFQ) indicating how many times in the last year they ate specific foods. The FFQ it was based on was the 61-item Harvard Food Frequency Questionnaire, a page of which appears below.

That’s right, people needed to estimate how many times in the last year they ate 1 oz of chocolate, or 1 cup of breakfast cereal or an ounce of nuts. Seriously?? How accurate would you be at adding up in your head all the 1 oz servings of chocolate that you estimated that you ate in a year. If you ate breakfast cereal in a serving size other than a cup, how would you even begin to accurately estimate how many 1 cup servings you had in an entire YEAR including for breakfast and night time snacks? Thinking about this, one can see why FFQ data is considered very inaccurate and certainly can’t be used to estimate the percentage of carbohydrate a person has in their diet!

The first part of the study took place between 1987 and 1989 and asked ~15,000 people between the ages of 45 and 64 years living in 4 communities in the US to complete the FFQ.  The data from the second part of the study was a meta-analysis which combined the data from the first part of the study with data from 7 multi-national population studies using the same FFQ and the third part of the study took place between 1993–95.

Page 3 from the 61-question Harvard Food Frequency Questionnaire

One huge problem with this paper was that it assumed that even if people changed their diet between the first visit in 1987-1989 and the third visit in 1992-1993, that people didn’t change their diets from the third visit until the data was analyzed in 2013; a period of ~ 20 years. There are all sorts of reasons people change the way they eat over time including health reasons (wanting to lose weight, for example), becoming parents, changes in economic situation, getting married and having someone else doing the cooking, or taking cooking classes! Assuming people ate the same way from 1993 until 2013 makes no sense.

How Many People Were in Each Comparison Group

As with the risk of injury amongst red-headed 6 year olds in the example above, the way the groups are divided and how many people are in each group matters.

Carbohydrate ranges were broken down into 5 groups;
<30% of calories as carbohydrate
30-40% of calories as carbohydrate
40-50% of calories as carbohydrate
50-55% of calories as carbohydrate
55-65% of calories as carbohydrate
>65% of calories as carbohydrate

A major problem with how the groups were broken up was that there were only 315 people that fell in the <30% of calories as carbohydrate group compared with more than 6,000 in the 40-50% of calories as carbohydrate  group and the more than 3,000 in both the 50-55%  and 55-65% of calories as carbohydrate groups.

As with the risk of injury of being red-headed example above, the way the groups were divided and how few people were in the lowest group of carbohydrate consumption makes the higher relative risk of being in the lower carbohydrate group truthful, but meaningless.

Were There Confounding Factors?

There’s an even bigger problem with this study.

Researchers did not update the carbohydrate intake of subjects that developed heart disease, Diabetes, or stroke before the third visit. Let’s say that some people in the lowest carb intake group developed Type 2 Diabetes and went to see their public health Dietitian who recommended that they increase their carb intake to be around the recommended ~50% (45-65%)  of their dietary caloric intake, or more. If they followed that advice and developed complications and died, their death would have been attributed to them eating a “low carb diet” rather than eating 50% or more of calories as carbohydrate over the subsequent 20 years.  The same holds true with dietary changes that subjects made based on their doctor’s or Dietitian’s recommendation when they got heart disease or had a stroke.  Because the groups were so lopsided in terms of size, being diagnosed with one of these serious conditions had the most impact on the lowest carb intake group because it was comparatively much smaller.

There were other confounding factors including, as someone pointed out on Twitter, that there was no mention of analysis done on alcohol consumption in the paper, so there’s no way of knowing if higher death rates were associated with higher alcohol consumption. As well, there was a higher rate of smoking in the lower carbohydrate intake group, so were the deaths smoking-related or diet-related?

Some final thoughts…

There are many more problems with this study, outlined in depth by people such as Dr. Zoe Harbcombe but there is one glaring fact. Epidemiological studies (population studies) do not establish causation.  When properly done, the results of epidemiological studies indicate that there may be a relationship between factors that needs to be tested in a randomized control trial.

Nevertheless, researchers concluded that there was a ‘negative long-term association between life expectancy and a low carbohydrate diet’ (which they defined as a diet of <40% of calories as carbohydrate, which is not a low carbohydrate diet, but a moderate-carbohydrate intake.

How the dietary information was collected, how the comparison groups were set out and the how the subjects were distributed amongst those groups and the multiple significant confounding factors make it impossible to conclude that a low carbohydrate diet shortens lifespan.

Evidence that Low Carbohydrate Diets are Both Safe and Effective

There are many studies and meta-analyses using a low-carb intervention that span 18 years that are outlined in 76 publications involving  6,786  subjects and that include 32 studies of 6 months or longer and 6 studies of 2 years or longer that demonstrate that low carb diets are both safe and effective. You can read more about that here.


Do you have questions about whether a low-carbohydrate diet would be appropriate for you given your health goals? Or do you wonder how medical conditions you have or medications you take factor in? Please send me a note using the “Contact Me” form and I’ll be happy to reply. I provide both in-person services in my Coquitlam (British Columbia) office as well as Distance Consultation services (via Skype or long distance phone) and would be happy to help.

To our good health,

Joy

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

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

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

References

  1. Seidelmann SB, Claggett B, Cheng S, et al. Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis. The Lancet Public Health 2018. https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(18)30135-X/fulltext
  2. Harvard Food Frequency Questionnaire  https://regepi.bwh.harvard.edu/health/FFQ/files/80out.pdf

Unreliability of Many Blood Glucose Monitors – cause for concern

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

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

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

 

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

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

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

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

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

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

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

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

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

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

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

The full testing protocol and results can be found here.

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

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

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

Type 2 Diabetes?

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

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

Have questions?

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

To our good health!

Joy

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

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