Month: August 2018

For a second week in a row 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 may also want to read:
Do Low Carb Diets Shorten Lifespan – a closer look (August 23 2018)
Is Coconut Oil Pure Poison (August 24 2018)

You can follow me on Twitter and Facebook:

 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.

 

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.

 

INTRODUCTION: Headlines warned people this week of the dire risks of a shorter lifespan by eating a low carbohydrate diet, but is it true?  By asking a few simple questions it’s easy to see that this newly published study cannot be used to support this claim.

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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.

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.

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Do you have questions about whether a low-carbohydrate diet would be appropriate for you given your health goals? Or do you wonder medical conditions you may have or medications you may 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/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. 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/8

INTRODUCTION

Diabetes Australia, the national body responsible for making treatment and dietary recommendations for the 1.7 million people living with Diabetes in that country, has just released a new Position Statement titled Low Carbohydrate Eating for People with Diabetes [1], said to be based on the latest evidence on the subject.  The publication is designed to provide practical advice and information for people diagnosed with Diabetes who are considering adopting a low-carbohydrate eating plan and was created in response to numerous inquiries from individuals, healthcare professionals, and the general public. Diabetes Australia. Since I don’t provide dietary support to those with Type 1 Diabetes (but defer instead to someone with CDE credentials), I have limited my discussion to recommendations pertaining only to Type 2 Diabetes.

 

How Diabetes Australia Defines Low Carb

Diabetes Australia defines low-carbohydrate (“low carb”) eating patterns as those that restrict carbohydrate intake — especially processed and packaged foods and beverages, including cakes, candies, chocolate, chips, ice cream, and sugary drinks, as well as breads, cereals, grains, potatoes, fruit, and sugar. They elaborate that when people limit carbohydrates, they eat a higher proportion of protein and fats such as those found in meat, chicken, eggs, oily fish, avocados, nuts, oils, and butter, and eat plenty of low-carb vegetables, such as cauliflower and zucchini.

“When it comes to low carb eating, there is no particular diet or standard approach.”

No One-Sized-Fits-All Approach for People with Diabetes

Diabetes Australia reinforces that the (Australian) “Dietary Guidelines provide general healthy eating advice and are a good starting point for people wanting to improve their eating habits”, but that

“there is no one-size-fits-all approach to living well with Diabetes. Everybody is different.”

The publication makes clear that Diabetes Australia “does not promote or encourage any single diet or eating plan or any particular ‘diabetes diet'” and that “every person with Diabetes needs a personalized approach and support to have the healthiest eating plan and this may change over their lifetime with Diabetes”. They mention that in recent years, low-carb eating has gained popularity with the general population and has also gained interest for people with Diabetes as “an option to help lose weight and to assist in managing blood glucose levels” — because “low-carb diets are relatively easy to follow”.

Diabetes Australia’s Position Statement

In formulating their Position Statement, the organization states that they rely on “strong scientific evidence before making specific health and nutrition recommendations for people with diabetes or those at risk” and that “evidence is usually based on the National Health and Medical Research Council (NHMRC) hierarchy of evidence”[2] whose components are: 1. The evidence base, in terms of the number of studies, level of evidence and quality of studies (risk of bias), 2. The consistency of the study results, 3. The potential clinical impact of the proposed recommendation, 4. The generalisability of the body of evidence to the target population for the guideline, and 5. The applicability of the body of evidence to the Australian healthcare context. This hierarchy of evidence is said to also need to take into account “the quality of the study and the likelihood that the results have been affected by bias during its conduct; the consistency of its findings to those from other studies; the clinical impact of its results; the generalisability of the results to the population for whom the guideline is intended; and the applicability of the results to the Australian (and/or local) health care setting”.

The position statement stresses that Diabetes Australia believes that;

“People with Diabetes should make their own, informed  choices about their Diabetes management (including eating plans) in consultation with their diabetes healthcare team”.

They recognize that “long-term studies can take years to be designed, conducted and published” and underscore that they will continue to review and update their advice in relation to low-carb eating for people with Diabetes based on new evidence as it becomes available.

Key Points

[1] Based on two studies [3,4], the report states that “recent evidence has shown that in the short term (up to 6 months), lower carb eating can help with the management of Type 2 Diabetes but that this benefit is no longer evident after 12 months”.

NOTE:
(a) Both of the studies quoted [3,4] were not low-carb studies but moderate-carb studies of <45% (225g carbohydrate) per day. Low-carbohydrate diets, as defined by this paper, are diets that provide “less than 130 g of carbohydrate daily/ less than 26% of total daily energy intake,” and the paper defines a moderate carbohydrate diet as one that provides “130g—225g of carbohydrate daily/ 26%—45% of total daily energy intake”. The two quoted studies provided dietary intake of carbohydrates that were moderate in carbohydrate intake. Neither was a low-carbohydrate study.
(b) Interestingly, despite neither study being low carb, one of the quoted studies [3] found “greater weight loss at 12 months on moderate carb diets than high carb diets” — which contradicts that there was no benefit after 6 months. Even a moderate-high carb diet had benefits beyond 6 months when compared with a high carb diet!
(c) In addition, the position statement did not consider the recent publication of the 1-year study results from Virta Health [5] outlined in detail in this article.

[2] In addition to promoting weight-loss, reducing carbohydrate intake can provide health benefits that include lowered average blood glucose levels and reduced risk of heart disease, such as raised cholesterol and raised blood pressure, and some benefits can be achieved independent of the amount of weight-loss achieved.

[3] All people with Diabetes who wish to follow a low-carb diet should
do so in consultation with their Diabetes healthcare team.

[4] People with Diabetes who begin low-carb eating should monitor their
blood glucose levels and, if necessary, talk to their doctor about the need to
adjust their Diabetes medication to reduce the risk of hypoglycaemia (low
blood glucose).

[5] People with Diabetes, considering low-carb eating, are encouraged to seek
personalized advice from a Dietitian experienced in Diabetes management, as there are some practical considerations that need to be taken into account to ensure the eating plan is safe and enjoyable, provides adequate nutrition for general health, is culturally appropriate, and fits into the person’s lifestyle.

[6] People with Diabetes who are considering low-carb eating should be aware of possible side effects (such as tiredness, headaches, and nausea) and seek
advice from their health care team if concerned.

[NOTE: I’ve never heard or read about people experiencing nausea following low-carb eating, and even at the beginning of following a low-carb style of eating, symptoms such as tiredness and headache are easily addressed with adequate fluid and electrolytes.]

[7] Low-carb eating may not be safe and is not recommended for children,
pregnant or breastfeeding women, people at risk of malnutrition, people
with kidney or liver failure, or those with a history of disordered eating or some rare metabolic conditions.

[8] All people who choose to follow a low-carb eating plan should be encouraged to eat foods proven to be beneficial to good health, including whole fruit and vegetables, whole-grains*, dairy foods, nuts, legumes*, seafood, fresh meat, and eggs.

[*NOTE: Depending on the amount of insulin resistance and hyperinsulinemia that someone with type 2 diabetes has, they may or may not be able to maintain glycemic (blood sugar) control by eating whole-grains and legumes. In their minimally processed forms, these may be able to be reintroduced in small quantities on an individual basis after reversal of Type 2 Diabetes symptoms and lower circulating insulin levels / reduced insulin resistance.]

[9] All people should be encouraged to limit their intake of foods that are high in energy*, carbohydrate or salt*, including processed foods such as sugary drinks, chips, cakes, biscuits, pastries and candies.

[NOTE: Unfortunately, foods that are ‘high in energy’ or ‘high in salt’ are inadequately defined in this publication. “High in energy” would be better framed as “low nutrient density foods,” which are foods high in energy relative to the amount of nutrients they contain.  Cheese, for example, may be energy-dense per 100 g but is also very nutrient-dense. What does “high in salt” mean — high in salt for whom? 

Questions?

Perhaps you have questions as to how I could help you get started on eating low carb to lower your blood sugars, reverse symptoms of Type 2 Diabetes, reduce your risk of heart disease, including raised cholesterol and blood pressure, and lose weight?

Since I provide services both in-person in my Coquitlam (British Columbia) office as well as via Distance Consultation, I am available to help.

Please send me a note using the Contact Me form above, and I will reply as soon as I am able.

To our good health!

Joy

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You can follow me at:

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. Diabetes Australia, Low Carbohydrate Eating for People with Diabetes – Position Statement, August 2018,  https://static.diabetesaustralia.com.au/s/fileassets/diabetes-australia/ee67e929-5ffc-411f-b286-1ca69e181d1a.pdf
2. National Health and Medical Research Council (2009), NHMRC additional levels of evidence and grades for recommendations for developers of guidelines, https://www.nhmrc.gov.au/_files_nhmrc/file/guidelines/developers/nhmrc_levels_grades_evidence_120423.pdf
3. Sainsbury E et al. Effect of dietary carbohydrate restriction
   on glycaemic control in adults with diabetes: a systematic
   review and meta-analysis. Diabetes Research and Clinical
   Practice, 2018; 139: 239-252.
4. Snorgaard O et al. Systematic review and meta-analysis
   of dietary carbohydrate restriction in patients with type 2
   diabetes. BMJ Open Diabetes Research & Care, 2017;
   5(1).
5. Hallberg, S.J., McKenzie, A.L., Williams, P.T. et al. Diabetes Ther (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Diabetes at 1 Year: An Open-Label, Non-Randomized, Controlled Study.  https://doi.org/10.1007/s13300-018-0373-9

 

 

The US and Canada and much of the westernized world is in the midst of a Diabetes epidemic but this is just the tip of the iceberg when it comes the underlying metabolic disruption caused by insulin. The part of the iceberg that is visible and that people know about is hyperglycemia (elevated blood sugar) but the part that is invisible and that few are aware of  hyperinsulinemia (elevated blood insulin levels) which often precedes a diagnosis of pre-diabetes or Type 2 Diabetes by decades. It is this high circulating level of insulin that contributes to the significant risk of developing cardiovascular disease including heart attack and stroke, hypertension (high blood pressure), elevated cholesterol and triglycerides, non-alcoholic fatty liver (NAFLD), Poly Cystic Ovarian Syndrome (PCOS), Alzheimer’s disease and other forms of dementia, as well as certain forms of cancer including breast and colon / bowel cancer.

High blood sugar may or may not be a symptom of high levels of insulin levels and in the early stages of metabolic dysfunction almost 75% of people will have normal fasting blood glucose yet have abnormally high levels of circulating insulin.  As a result, these people are at increased risk of the metabolic diseases mentioned above but unlike someone already diagnosed with Type 2 Diabetes they have no idea!

High circulating levels of insulin is entirely missed by most routine lab tests because blood sugar is being monitored as the first indication that someone is becoming insulin resistant.  By the time blood glucose levels are abnormal, the β-cells of the pancreas that produce insulin are already being over-taxed to the point of exhaustion.  Physicians have ”answers” (lab test results) but oftentimes are asking the wrong questions. That is, having normal fasting blood sugar or even HbA1C (3-month blood sugar average) does not necessarily mean everything is ”fine”.  Most sobering is that by the time a person is diagnosed with Type 2 Diabetes they have already lost ~ 40% of their beta-cells mass sometimes more — cell loss which is currently thought to be unrecoverable.

The healthy human body maintains blood sugar in a tightly-regulated range between 60-100 mg/dl (3.3-5.5 mmol/L).  When a healthy person eats food containing carbohydrate — whether as the starch in bread, pasta and rice, the sugar in milk (lactose), fruit (fructose), simple table sugar (sucrose) or high fructose corn syrup in commercially prepared foods, special glucose-sensing cells in the small intestine release signalling hormones called incretin hormones in response to the presence of these carbohydrates. The incretin hormones tell the pancreas to release insulin which in turn tells the body’s cells what to do with the energy from the food we eat; either (1) burn it or (2) send it to the liver to store it, first as glycogen, and the remainder as fat (adipose tissue).  This is called fuel partitioning. When metabolic processes respond appropriately, blood sugar rises modestly after eating carbohydrate-based food but is quickly restored to its normal, tightly-regulated range soon afterwards.

Metabolic problems begin because people eat foods that contain some form of carbohydrate every few hours which results in frequent release of insulin. Glycogen levels in the muscle and liver remain close to full due to the steady supply of refined or processed carbohydrate-based food compounded by the reality that body’s cells are rarely challenged to use stored energy. In the early stages cells simply stop responding appropriately to insulin’s signal. This is called insulin resistance. Insulin resistance is the decreased ability of our cells to partition fuel. It can be compared to someone hearing a noise such as their neighbour playing music, but after a while their brain ”tunes out” the noise.  Even if the neighbour gradually turns up the volume of the music, the person’s brain compensates by further tuning out the increased noise. To compensate for insulin resistance, the β-cells of the pancreas begin producing and releasing more insulin, which results in hyperinsulinemia — too much insulin in the blood.

In the early stages the body is simply trying to keep blood sugar levels within its normally tightly regulated range by making and releasing more insulin to force the cells of the body to take up the excess glucose and burn it, but this just makes the problem worse. It is the increasingly high circulating levels of insulin that contribute to the health risks and metabolic disease listed above.

Just as high blood sugar is not necessarily associated with high circulating levels of insulin, neither is obesity.  Approximately 1/3 of insulin-resistant people are lean. A person who is obese simply makes more fat cells (adipocytes) in order to store the excess energy as sub-cutaneous fat (fat under the skin) which serves as a protective mechanism. Contrary to what most people assume, people don’t become insulin resistant because they are fat; becoming fat may be a protective response to high levels of circulating insulin. Those who are lean but insulin-resistant are thought to have a lower personal fat threshold’ than those that become overweight of obese. That is, they are limited in terms of how many new fat cells their body can make to store excess energy, so they store the excess energy in and around their organs in what’s called visceral fat.  This is where the metabolic disruption occurs.  Whether the person is obese or lean, once they have exceeded their personal fat threshold, the result is the same.

Assessing whether my clients have higher than ideal levels of insulin is as important as assessing whether they already have higher than ideal levels of blood sugar, in fact it is even more important. When people already have pre-diabetes or Type 2 Diabetes, they’ve likely been told by their doctors that they are increased cardiovascular risk and that this is a risk factor for other metabolically related conditions, including high blood pressure, fatty liver disease, Alzheimer’s and other forms of dementia and certain types of cancer. Having normal blood sugar many are told “everything is fine” when very often it is not.  These people are at risk and don’t even know it.

It is important that my clients know whether they have symptoms of hyperinsulinemia and to help them understand the factors that contribute to it. This helps people to have the motivation to make necessary dietary and lifestyle changes to reduce their disease risk and totally avoid the progression to Type 2 Diabetes, long before blood sugar levels begin to rise.

For those that already are pre-diabetic or been diagnosed as having Type 2 Diabetes, it is not too late. A carbohydrate-modified diet as well implementing very specific lifestyle changes makes the reversal of symptoms entirely possible and does not require dietary or exercise extremes.

I think that for too long we as clinicians have tackled this as an insulin problem caused by overweight and created by “eating too much and moving too little” rather than as the exact opposite; that people get overweight because of an underlying insulin problem. When we address hyperinsulinemia, weight, blood sugar, blood pressure and high cholesterol and triglycerides are corrected. There are studies documenting this (covered in previous articles) and my “A Dietitian’s Journey” tells my own sample-set-of-one story reversing Type 2 Diabetes that I had for 10 years, as well as the related conditions of high blood pressure and abnormal cholesterol and triglycerides. It can be done.

Have questions as to how I can help you either in-person in my office or via Distance Consultation? Please send me a note using the Contact Me form above and I will reply as soon as I am able.

To our good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

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

References

Reaven, G., Insulin resistance, type 2 diabetes mellitus, and cardiovascular disease: the end of the beginning. Circulation, 2005. 112(20): p. 3030-2.

Reaven, G.M., Pathophysiology of insulin resistance in human disease. Physiol Rev, 1995. 75(3): p. 473-86.

Taylor, R. and R.R. Holman, Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Clin Sci (Lond), 2015. 128(7): p. 405-10.

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.

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.

Ludwig, D.S. and M.I. Friedman, Increasing adiposity: consequence or cause of overeating? JAMA, 2014. 311(21): p. 2167-8.

Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.

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.

I’d heard of Alzheimer’s disease (AD) being referred to by some clinicians as ”Type 3 Diabetes” but until yesterday the link between AD and abnormalities in glucose metabolism in the brain was an academic interest. Now it’s personal. You see, yesterday I found out that my dad (90 years old) was diagnosed with Alzheimer’s disease. His once-sharp mind is no longer capable of recalling what happened yesterday or in fact what just happened. It is as though he has ”partial amnesia”.

The majority of those that are diagnosed with AD (95%) have the same form of the disease that my dad has called sporadic Alzheimer’s disease. Only 5% are diagnosed with a genetically-linked form inherited from the maternal side of the family [2].

In sporadic Alzheimer’s disease the first part of memory that is affected is the person’s unique memory of specific events (called episodic memory).

I remember three or four years ago asking my dad to recount the details of our family history from his side of the family that he often told yearly at holiday dinners — yet he couldn’t even remember their existence! I tried prompting him with parts of the story to try and trigger the memory but was met with ”I’m sorry dear, I don’t recall“.  I was dumbfounded because he told this same exact story over and over again for years, and then suddenly it was gone. From his perspective, it didn’t exist. His behaviour and other forms of memory were completely normal, so I discounted his forgetfulness to ”aging” but I now know this was the first noticeable indication that something was not working as it should.

As Healthy People Age

As healthy people age, brain cells waste away (atrophy) and are not replaced such that brain volume decreases at a rate of about 1.6% / decade after the age of 30 years old [1]. So, at 40 years old, a person is expected to have a 1.6% decrease in brain volume, at 50 years old a 3.2% decrease, and so on. At 90 years old, a healthy person would be expected to have lost a little less than 10% of their brain volume.

My maternal grandmother was healthy and lived until well over 100 years old and I can see in retrospect that the kinds of memory changes my dad was showing a few years ago (at age ~85) were not simply part of normal aging.

Changes in Alzheimer’s Disease

Over the last 30 years, there has been a lot of progress in terms of understanding changes in brain energy metabolism during AD as compared with what occurs in normal, healthy aging. Until recently, many thought that lower brain function of those developing AD led to less use of glucose by the brain, but now it is thought that it is actually the other way around; that decreased glucose uptake into the cells of the brain leads to decrease metabolism in the brain. This decrease glucose uptake into the cells of the brain are believed to be a critical part of the early development of AD and that significantly lower brain glucose metabolism may be present long before the onset of any clinically measurable mental decline in AD [2].

It is now widely believed that there is decreased glucose metabolism in the brain in those with AD. When compared with healthy aged-matched people, those with AD have ~25% more brain atrophy than would be expected for their age. This is, after correction for age-associated brain atrophy, the majority of PET scan studies conducted from 1981- until the present, show that glucose utilization by the brain is decreased by as much as ~25% in AD [2].

While healthy, normal aging is associated with some slow brain atrophy, it is not thought to be associated with decreased glucose metabolism.

Normal Brain Glucose Use

The brain, heart, liver and kidneys together use ~ 60% of the body’s resting metabolic energy needs and while the heart and kidneys are metabolically more active than the brain, the brain is larger. As a result, the brain uses about ¼ of the body’s total energy needs [2]. This energy is used for blood flow in the brain, use of oxygen by the brain and for glucose metabolism — but most of the glucose used by the brain is used to maintain a glucose gradient (difference) between glutamate neurons which enable communication along this neurotransmitter system.

Glucose transporters (GLUTs) bring glucose into the brain in a three-step process: (i) Transport across the blood-brain barrier (ii) transport into the brain cells (astrocytes) and (iii) transfer of the glucose into the neurons of the glutamate neurotransmitters.

When the brain is active, the Adenosine Triphosphate molecule (ATP) which is the ”currency” of energy transfer inside cells decreases, and the brain needs more glucose, so glucose uptake is stimulated by the cell. It is unknow at what point partial reduction in glucose transport begins to limit brain function in AD.

Brain Glucose Use in Alzheimer’s Disease

Alzheimer’s Disease is a neurodegenerative disease that results in progressive worsening of memory and cognitive function, as well as behavior changes and disorientation.

Even though normal healthy aging is not associated with AD. Aging itself is the main risk factor for sporadic AD, with rates ~doubling every five years after 65 years of age [3] and affecting more than 60% of people over the age of 95 years of age [4].

The brain of those with AD is marked by an accumulation of βeta-amyloid plaques between brain cells and by neurological ”tangles” within brain cells.  As mentioned earlier, there are two types of AD — familial / early onset AD and sporadic / late onset AD. The early onset type is much rarer (~5% of all AD) and is inherited from the maternal (mother’s) side of the family. Except for a different age of onset, what is seen clinically, and the progression of decreased cognitive function is not significantly different between the two types of AD. The βeta —amyloid plaques occur slowly before any change in memory or understanding become apparent. The progressive brain atrophy speeds up later in the disease process, bringing the cognitive decline frequently associated with AD.

There are also other forms of dementia besides Alzheimer’s disease, including fronto-temporal dementia and vascular dementia but these are very different from either of the two sub types of AD.

PET scan studies point to lower brain glucose metabolism in AD, with difference between normal aging subjects and those with AD being as much as ~20—25% lower in AD with most of the atrophy occurring in the region of the brain called the hippocampus, which is involved in memory processing.

Mild Cognitive Impairment (MCI)

There is intermediate stage between normal healthy aging and AD, called Mild Cognitive Impairment (MCI) which includes some decreased thinking ability (cognitive decline). When these thought process changes and memory loss are present in the elderly, but don’t significantly affect daily life or interactions it is considered to be MCI. There are a few studies of glucose metabolism in MCI which show that it is lower than in healthy aged-match controls but less than in moderate to severe AD.

As MCI progresses to AD, glucose usage decreases in additional regions of the brain (cingulate, inferior parietal lobes, temporal lobes) [2].

Nutritional Factor that Affects Glucose Metabolism

The omega-3 fatty acid found mainly in fatty fish known as Docosahexaenoic acid (DHA; 22:6ρ‰3) is known to have an important role in normal brain development. In animal studies,  supplementation with DHA was found to increase expression of the glucose transporters (GLUTs) that bring glucose into the brain and in primate studies, brain DHA concentration was found to be directly proportional to brain glucose uptake in the same region of the brain [2]. Insufficient intake of DHA and/or low levels in the hippocampus (the region of the brain initially impacted by AD) may play a role in cognitive decline in older adults.

Metabolic Factors that Affect Glucose Metabolism

While the glucose transporters (GLUTs) involved in getting glucose across the blood-brain barrier and into the brain cells (GLUT1) and across glutamate neurons (GLUT3) are not sensitive to insulin, GLUT4 which is another glucose transporter involved in memory and cognition in areas of the brain including the hippocampus are insulin-sensitive [5]. It is thought that brain insulin signaling may be defective in AD [5].

Older adults and the elderly often develop glucose intolerance which often progresses to Type 2 Diabetes then to Metabolic Syndrome which is a combination of Type 2 Diabetes, high blood pressure (hypertension), increased waist circumference (visceral obesity) and abnormal cholesterol tests (dyslipidemia).

Insulin resistance, which often comes before glucose intolerance / high blood sugar tops the list of known risk factors to cognitive decline [5, 6] and younger adults that are obese are predisposed to Metabolic Syndrome which is associated with increased risk of degenerative changes in the brain [6].

Decreased skeletal muscle mass (sarcopenia) in older adults and the elderly may contribute to the increased risk of insulin resistance associated with aging, as muscle is the main site of insulin-mediated glucose utilization in the body. In older adults, adequate dietary protein intake as well as incorporating some form of resistance training of large muscle groups may play a role in decreasing cognitive decline by increasing glucose update from the blood to the muscle where it can then be transported to areas of the brain.

Ketones: the body’s preferred alternative fuel

In healthy people that haven’t eaten in while (such as after an overnight fast or a during relatively long period of time between meals) ketone bodies (ketones) are the body’s key replacement fuel which maintains brain function. The brain even has a separate transport system for ketones which is independent of glucose transport [2].

When blood sugar levels drop over a period of several hours or even days during fasting the energy requirements of the body are dependent on the availability of two ketones — acetoacetate and β-hyydroxybutyrate for normal function.  During prolonged fasting over a period of days and in starvation up to ~60% of the human brain’s energy requirements can be met by a combination of acetoacetate and β-hydroxybutyrate [7].

The brain can convert ketones to ATP, the energy ”currency” of the cell by oxidizing ketones (converting β-hydroxybutyrate to acetoacetate, acetoacetate to acetoacetyl CoA, and acetoacetyl CoA to acetyl CoA which then is used to generate ATP).  While brain cells (astrocytes) can beta-oxidize fatty acids [8] to produce ketones, transport of fatty acids across the blood-brain barrier is too slow to make fatty acids as useful alternative as fuel for the brain.

Ketones cannot fully replace glucose as a brain fuel as a small quantity of glucose is essential for the brain, however this does not need to be supplied in the diet but can be manufactured by the liver (as well as to a lesser degree by the kidneys and the intestines) from fat or protein in a process known as gluconeogenesis (literally ”making new glucose”).

The body can make ketones from fat stores in a process called ketogenesis but first there needs to be a lowering of blood glucose, which will result in decreased blood insulin levels. This can occur during fasting, as well as by following a low-carbohydrate diet. When insulin level decreases, free fatty acids from fat cells (adipose tissue) can be freed into the blood. These long chain fatty acids are then brought to the liver where they are broken down (β-oxidized) to acetyl CoA, which are then condensed into ketones.

Use of a Therapeutic Ketogenic Diet in Alzheimer’s Disease

It is thought that in Alzheimer’s disease the combination of brain glucose insufficiency and the inadequate supply of naturally-produced ketones (which normally would naturally be produced by the body in response to low blood glucose) puts the high energy consuming areas of the brain in mild, but constant shortage of energy.

Since the brain can’t get its main fuel source which is glucose nor its preferred back- up fuel source which are ketones (because blood glucose doesn’t drop) this forces the brain to rely on a third, but inadequate source of energy — which is making glucose from fat stores or protein (gluconeogenesis).

Over time, specific regions of the brain such as the hippocampus are thought to be put in a situation of long-term chronic fuel shortage and gradually these brain cells burn out’, which leads to the brain changes seen in Alzheimer’s Disease [2].

It is thought that if brain ketone metabolism is unaffected in AD — or at least is affected less than glucose, a ketogenic diet may provide the brain with ketones it can use as an alternative fuel to glucose, enabling it to function more normally, reducing cognitive decline resulting from brain glucose insufficiency.

If you have questions about how eating a low carbohydrate diet can significantly reduce insulin resistance, a major risk factor for Alzheimer’s disease, as well as reverse symptoms of Metabolic Syndrome, please send me a note using the “Contact Me” form on this web page and I’ll be glad to reply as soon as I’m able. Remember, I provide services via Distance Consultation (via secured Skype) as well as in-person in my Coquitlam office.

To our good health!

Joy

you can follow me at:

 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. Svennerholm, L., K. Bostrí¶m, and B. Jungbjer, Changes in weight and compositions of major membrane components of human brain during the span of adult human life of Swedes. Acta Neuropathol, 1997. 94(4): p. 345-52.
2. Cunnane, S., et al., Brain fuel metabolism, aging, and Alzheimer’s disease. Nutrition, 2011. 27(1): p. 3-20.
3. Canadian study of health and aging: study methods and prevalence of dementia. CMAJ, 1994. 150(6): p. 899-913.
4. Brayne, C., et al., Dementia before death in ageing societies–the promise of prevention and the reality. PLoS Med, 2006. 3(10): p. e397.
5. Watson, G.S. and S. Craft, Modulation of memory by insulin and glucose: neuropsychological observations in Alzheimer’s disease. Eur J Pharmacol, 2004. 490(1-3): p. 97-113.
6. Raffaitin, C., et al., Metabolic syndrome and risk for incident Alzheimer’s disease or vascular dementia: the Three-City Study. Diabetes Care, 2009. 32(1): p. 169-74.
7. Cahill, G.F., Fuel metabolism in starvation. Annu Rev Nutr, 2006. 26: p. 1-22.
8. Guzmán, M. and C. Blázquez, Is there an astrocyte-neuron ketone body shuttle? Trends Endocrinol Metab, 2001. 12(4): p. 169-73.

 

Those who are younger than 40 years old probably grew up hearing that saturated fat is ”bad” and polyunsaturated fat is ”good”, but where did we get this idea and is it true?

The process of what I call the ”vilification of fat” began when researcher Ancel Keys presented a graph at a talk at Mount Sinai Hospital in New York in January 1953 and later published it in a research paper titled Atherosclerosis: a problem in newer public health [1]. It was said to show the relationship between fat calories as a percentage of total fat” and the number of deaths from degenerative heart disease per 100,000 people’ for men between the ages of 45-49 and 55-59. The linear relationship of these data points from the Six Country Study (Japan, Italy, England & Wales, Australia, Canada and the USA) suggested that there was a strong relationship between the amount of fat calories as a percentage of dietary intake and deaths from degenerative heart disease for men aged 55-59. At the time of publication of the Six Country Study, Keys said that it was possible to only get complete data from those 6 countries [1] at the time. He concluded;

”Whether or not cholesterol etc. are involved, it must be concluded that dietary fat somehow is associated with cardiac diseases mortality, at least in middle age [1].

In Key’s mind, the total amount of dietary fat was ”somehow associated” with cardiac death in middle aged men, but he expressed doubt whether or not cholesterol was involved.

In 1957, Yerushalamy and Hilleboe [2] published data from 22 countries which showed there was no linear relationship between fat calories as a percentage of total fat” and the number of deaths from degenerative heart disease per 100,000 people’.

Keys went onto conduct what became known as the Seven Country Study which collected data on almost 13,000 men aged 40-59 from the USA, Finland, the Netherlands, Yugoslavia, Greece and Japan. Findings were only published in 1970 in the journal Circulation in several papers from separate countries [3]. Keys no longer believed that total fat was associated with heart disease but that saturated fat was the villain. Keys concluded that the average consumption of animal foods (with the exception of fish) was positively associated with 25-year heart disease death rates and that the average intake of saturated fat was strongly related to 10 and 25-year coronary heart disease death rates.

What solidified this association was that the 1970 publication on the Seven Country Study contained Keys’ 1953 graph from the Six Country Study (above) [4]. Even though it indicated a linear relationship between total fat intake and degenerative heart disease it became tied in the minds of many that this graph ”proved” that saturated fat was linked to heart disease—even though that is not what the graph shows at all.  It isn’t even about saturated fat. Keys also neglected to mention Yerushalamy and Hilleboe’s data from 22 countries showed no relationship between total fat consumption and heart disease.

The Diet Heart Hypothesis

The diet-heart hypothesis originated with Ancel Keys and is the belief that eating foods high in saturated fat contributes to heart disease. Keys believed that replacing fat from meat, butter and eggs with newly-created polyunsaturated vegetable oils such as soybean oil would reduce heart disease and deaths by lowering blood cholesterol levels.

The Sugar Industry Funding of Research Vilifying Fat

In the mid-1960’s, the Sugar Research Foundation (predecessor of the Sugar Association) wanted to offset research that had been published and that suggested that sugar was a more important a cause of heart disease and stroke from atherosclerosis than dietary fat. The Sugar Research Foundation invited Dr. Fredrick Stare and the late Dr. D. Mark Hegsted of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board and then approved $6,500 in funds ($50,000 in 2016 dollars) to support a review article that would respond to the research showing the danger of sucrose [5]. Letters exchanged between the parties came to light a November 2016 article published by Kearns et al [6] which said that the Sugar Research Foundation had tasked the Harvard researchers with preparing ”a review article of the several papers which find some special metabolic peril in sucrose and, in particular, fructose [7]”.

The Sugar Industry paying researchers to blame dietary fat and vindicate sugar for heart disease seems a little like the tobacco industry having secretly funded articles demonstrating that something other than smoking was responsible for lung cancer.

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

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

The report concluded;

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

The Harvard researchers went on to say;

”there can be no doubt that levels of serum cholesterol can be substantially modified by manipulation of the fat and cholesterol of the diet” and that “on the basis of epidemiological, experimental and clinical evidence, that a lowering of the proportion of dietary saturated fatty acids, increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit.”

At no point did Stare, Hegsted and McGandy disclose that they were paid by the Sugar Research Foundation for the two-part review.

A commentary in the Journal of Accountability in Research [8] summarized the significance of those articles as follows;

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

The same Dr. Hegsted that was funded by the Sugar Industry to write the above articles vindicating sugar and vilifying dietary fat went on to work on editing the 1977 US Dietary Guidelines [9], which entrenched the vilification of fat into the US Food Pyramid for the next 40+ years. The rest, they say, is history.

The same year (1977), Canada’s Food Guide recommended that Canadians limit fat to <30% of daily calories with no more than 1/3 from saturated fat but did not specify an upper limit for dietary cholesterol. This was based on the belief that total dietary fat and saturated fat were responsible blood levels of LDL cholesterol levels and total serum cholesterol [10]. Cholesterol in general (total cholesterol) and LDL cholesterol was assumed to be tied to heart disease, so the focus was on lowering the proxy measurements of LDL cholesterol and total cholesterol.

Recommendations for the continued restriction of dietary fat continued in both the US and Canada in the 2015 revision of the Dietary Guidelines 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 [11]. 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)” [12].

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 [13].

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 [14].

We now know that fat was made out to be the villain in scientific reviews paid for by the sugar industry and this combined with Ancel Key’s Diet-Heart Hypothesis ended up being the impetus for the creation of an entire food industry designed to extract fat from industrial seed oils, such as soybean oil and rapeseed (Canola). These industrial seed oils are the so-called ”healthy polyunsaturated fats” that we are encouraged to eat instead of so-called ”dangerous” saturated fat, yet these industrial seed oils are only able to be produced using solvent-based chemical extraction under very high temperature. Should we be confident in industrial fats brought to us by the same industry that brought us ”trans fats”? With a lack of evidence that natural fats such as butter or cream are dangerous, perhaps eating a bit of real animal fat and plenty of natural plant-based monounsaturated fats such as olive oil is the better way to go?

For more than forty years, generations of Americans and Canadians have avoided eggs, full fat cheese and creamery butter — and done so because they have believed that saturated fat raising LDL cholesterol predisposed them to heart disease. We know much more than we did in the 1970s when the first Dietary Guidelines were created in the US (under the watchful editorial oversight of one of the researchers that had been paid by the sugar industry to vilify fat).  We now know that eating foods with saturated fat will raise LDL-cholesterol, but not all LDL-cholesterol is ”bad”[14]. Before we knew this high total LDL-cholesterol (LDL-C) was seen as a good proxy (indirect substitute) measurement for heart disease risk, but no longer.

It has been known since the early 1990s that a high TG:HDL ratio is very good estimator of coronary heart disease risk [15].

The measurement of the LDL-cholesterol particle number (LDL-P) which measures the actual number of LDL particles is a much stronger predictor of cardiovascular events than LDL-C [16] because the more particles there are, the more small, dense LDL there are.

The ratio of apolipoprotein B (apoB): apolipoprotein A (apoA) is another good estimator of cardiovascular risk. 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 [17].

In light of the recently published epidemiological evidence and much stronger proxy measurement of cardiovascular risk we must update our thinking that fat in general, or saturated fat in particular is the ”villain”. It’s not.

Perhaps you could use some help as to which fats you should eat more of and in what amounts, or on deciding on what ratio of protein to fat in your diet will best help you reach your health and weight goals? I can help.

I provide services via Distance Consultation (Skype, long distance telephone) as well as in-person in my Coquitlam 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 will 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. Keys, A., Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp N Y, 1953. 20(2): p. 118-39.
2. Yerushalamy, J. and Hilleboe HE, Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med, 1957. 57(14): p. 2343-54.
3. Coronary heart disease in seven countries. Summary. Circulation, 1970. 41(4 Suppl): p. I186-95.
4. Harcombe, Z., An examination of the randomised controlled trial and epidemiological evidence for the introduction of dietary fat recommendations in 1977 and 1983:  A systematic review and meta-analysis. 2015, University of the West of Scotland.
5. Husten, L., How Sweet: Sugar Industry Made Fat the Villain. 2016.
6. Kearns, C.E., L.A. Schmidt, and S.A. Glantz, Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med, 2016. 176(11): p. 1680-1685.
7. McGandy, R.B., D.M. Hegsted, and F.J. Stare, Dietary fats, carbohydrates and atherosclerotic vascular disease. N Engl J Med, 1967. 277(4): p. 186-92 contd.
8. Krimsky, S., Sugar Industry Science and Heart Disease. Account Res, 2017. 24(2): p. 124-125.
9. Hegsted D.M. Introduction to the Dietary Goals for the United States. p. 17 of 130.
10. McDonald, B.E., The Canadian experience: why Canada decided against an upper limit for cholesterol. J Am Coll Nutr, 2004. 23(6 Suppl): p. 616S-620S.
11. Grasgruber, P., et al., Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries. Nutrients, 2018. 10(4).
12. 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.
13. 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.
14. 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.
15. 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.
16. 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.
17. 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.