Lowering LDL and Saturated Fat to Lower Risk of Cardiovascular Disease

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

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

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


Dietary Saturated Fat and LDL

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Which LDL?

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

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

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

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

This is highly significant!

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

In fact, in the paper, the researchers acknowledge;

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

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

The authors conclude;

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

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

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

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

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

More Info?

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

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchfRD/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

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

Share to Flipboard:

High Cholesterol and the Risk of Cardiovascular Disease

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


What is Cholesterol?

Cholesterol is a essential structural component of all the cell membranes in the body and is used in the making of steroid hormones such as cortisol and aldosterone by the adrenal glands, sex hormones such as estrogen, testosterone and progesterone by the gonads, and is also used in the making of bile acid. Approximately 80% of cholesterol made daily by the body occurs in the liver and  intestines, with the remainder being made in the adrenal glands and reproductive organs.

Different Types of Cholesterol

Triglyceride isn’t actually a type of cholesterol, but is measured on lipid panels along with cholesterol.

Triglyceride is made up of three fatty acids (hence “tri-“) attached to a glycerol molecule (also known as glycerine), which is a sugar alcohol. Some triglyceride is taken in through the diet and the rest is manufactured by the body during lipogenesis (literally meaning the ‘making of fat’). Lipogenesis is how the body stores the excess carbohydrate we eat in our diet that isn’t immediately needed for energy.  Yes, excess dietary carbohydrate is stored in the body as glycogen and when glycogen stores are full, it is stored as fat.

As for cholesterol itself, there are several different types found in the blood;

  • high density lipoprotein (HDL)
  • low density lipoprotein (LDL)
  • very low density lipoprotein (VLDL)

Most people think of high density lipoprotein (HDL) as “good cholesterol” and low density lipoprotein (LDL) as “bad cholesterol” but there are actually two sub-fractions of LDL; the small, dense LDL sub-fraction which is associated with atherosclerotic plaque, and the large, fluffy LDL sub-fraction which is considered protective against cardiovascular disease[1].

This is important, because when people are told they have “high cholesterol“, this is usually implies that they have high LDL. This is often presented to them as them having a high level of “bad” cholesterol.

High Cholesterol

A couple of things need to be clarified about “high cholesterol”;

Firstly, “high LDL” cholesterol means high total LDL cholesterol. When blood tests are said to indicate “high LDL” a good question to ask is which LDL cholesterol is high; the small dense ones or the large fluffy ones?”. More on this below.

Secondly, it is important to note that lab tests don’t actually measure total LDL but calculate it from the Friedewald formula; which (in mg/dl) is calculated by total cholesterol (TC) – HDL lipoprotein (HDL)-cholesterol – triglycerides (TGs) / 5. 

When people are told that they have “high LDL” results on a blood test, they are often presented with a recommendation to begin statin medication, but does high total LDL provide sufficient information about cardiovascular risk? More on this below. The use of statin medication will be covered in the subsequent article.

Very low density lipoprotein (VLDL) is produced in the liver and the best way to understand its role is to think of it as a “taxi” which the liver makes and then release into the bloodstream to shuttle triglycerides around to the various tissues.  VLDL cholesterol on blood test results isn’t actually measured either, but estimated as a percentage of the triglyceride value. High VLDL is said to be a risk for cardiovascular disease but as elaborated on below, a more accurate measure is the ratio of Apopoprotein B (the lipoprotein in VLDL) compared to the Apoprotein A (the lipoprotein in HDL). 

Where does LDL come from?

Once a large amount of triglyceride has been unloaded in the tissues by the VLDL “taxi”, it becomes a new, smaller lipoprotein called low density lipoprotein, or LDL which contains mostly cholesterol and some protein.

Some LDLs are removed from the circulation by cells around the body that need the cholesterol contained in them and the rest is taken out of the circulation by the liver.

A key point here is that the only source of LDL is VLDL. This is important.

LDL is what is left once the VLDL which is made by the body has offloaded its triglyceride ‘passenger’ to the tissues.

LDL and Heart Disease

Research has often reported that elevated LDL-cholesterol is a risk factor for cardiovascular disease, including heart disease and stroke and it has been assumed that lowering LDL-cholesterol in the blood would decrease cardiovascular deaths and illness. It is this premise that lead to recommendation of treatment of high LDL with statin drugs.

One major problem is that these studies looked at total LDL which doesn’t distinguish between the small, dense sub-fractions of LDL that are atherosclerotic, and the large, fluffy ones that are not [1].

Total LDL (LDL-C) calculates (not measures!) the total content or concentration of cholesterol within all the LDL particles.

LDL particle number (LDL-P) measures the particle concentration.

Since the amount of cholesterol in each particle varies, measuring LDL-C does not necessarily reflect the actual number of particles  — but an increased number of LDL particles occurs in patients with lots of small, dense particles.

Therefore, LDL-particle number (LDL-P) is a more accurate predictor of cardiovascular events than total LDL (LDL-C).

An NMR lipid profile test directly measures the number of LDL particles (as well as HDL particles). For LDL particles, a value of less  than 1.000 in nmol/L is considered ideal, a value of 1000-1299 is considered moderate,  a value of 1300-1599 is considered borderline high, and a value >1600 is considered high.

Apolipoprotein B:Apolipoprotein A1

Apolipoprotein B (apo B) is the main lipoprotein in VLDL, and subsequently in LDL after the VLDL has offloaded its triglyceride to the tissues. Apolipoprotein B is correlated with the actual number of LDL-particles, which makes it a very good assessor of the risk of cardiovascular disease, 

Apolipoprotein A1 (apo A1) is the main lipoprotein in HDL (commonly called “good” cholesterol).

An Apo B / Apo A1 ratio of > 0.9 is considered at risk for CVD.

Measuring Apo B to Apo A1 requires special blood tests, but a proxy can be calculated by dividing triglycerides (TG) by HDL-cholesterol (HDL-C) from a standard lipid panel. Studies have found this to be a very good assessor of cardiovascular risk.

Triglyceride:HDL Ratio

In Canada (as well as Europe), values are expressed as mmol/L and the ratios are interpreted as follows [2];

TG:HDL-C < 0.87 is ideal

TG:HDL-C > 1.74 is too high

TG:HDL-C > 2.62 is much too high

In the US, values are expressed in mg/dl and the ratios are interpreted as follows [2];

TG:HDL-C < 2 is ideal

TG:HDL-C > 4 is too high

TG:HDL-C > 6 is much too high

Several studies have found that TG:HDL-C ratio also reflects particle size;

One study from 2004 reported that almost 80% of people with a TG:HDL-C ratio of greater than 3.8 (when values are expressed in mg/dl) had mostly small, dense LDL particles, indicating cardiovascular risk. This same study found that more than 80% with a TG:HDL-C ratio of less than 3.8 (when values are expressed in mg/dl) had mostly large, fluffy LDL particles, indicating lower cardiovascular risk[3].

A 2005 study [4] reported that a TG:HDL-C ratio of 3.5 or greater was highly correlated with atherosclerosis in men, as well as insulin resistance and metabolic syndrome.

A recent 2014 [5] study found that a high TG:HDL-C ratio was a strong independent predictor of cardiovascular disease, coronary heart disease and all-cause mortality both before- and after adjustment for age, smoking, BMI and blood pressure.

Based on this metric, lower cardiovascular risk would be associated with lower triglycerides, raising HDL or both.

But how?

Lowering TG:HDL-C ratio

Losing weight will lower triglycerides, however low-fat diets are not usually helpful in this regard because they are often also high in carbohydrate[2].

Decreasing intake of carbohydrates especially fructose which is found in fruit, as well as processed products made with high fructose corn syrup has been anecdotally reported to decrease hunger, making weight loss easier. Most importantly, clinical studies using well-designed low carbohydrate diets (already covered in several previous articles) are associated with both a lowering of triglycerides and a increase in HDL.

Lowering the risk of cardiovascular disease through weight loss, along with a lowering of triglycerides and an increase in HDL is where I can help.

UPDATE (June 23, 2019): Part 2 of this article titled Lowering LDL and Saturated Fat to Lower the Risk of Cardiovascular Disease is available by clicking here.

More Info?

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

To your good health!

Joy

You can follow me on:

Twitter: https://twitter.com/lchfRD
Facebook: https://www.facebook.com/lchf-rd/
Instagram: https://www.instagram.com/lchf_rd
Fipboard: http://flip.it/ynX-aq

Copyright ©2019 The Low Carb Healthy Fat 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. Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
  2. Sigurdsson AF, The Triglyceride/HDL Cholesterol Ratio, updated January 12, 2019, https://www.docsopinion.com/2014/07/17/triglyceride-hdl-ratio/
  3. Hanak V, Munoz J, Teague J, et al, Accuracy of the triglyceride to high-density lipoprotein cholesterol ratio for prediction of the low-density lipoprotein phenotype B, The American Journal of Cardiology, Volume 94, Issue 2, 2004, Pages 219-222, https://doi.org/10.1016/j.amjcard.2004.03.069
  4. McLaughlin T, Reaven G, Abbasi F, et al. Is there a simple way to
    identify insulin-resistant individuals at increased risk of cardiovascular
    disease? Am J Cardiol. 2005;96(3):399Y404.
  5. Vega GL, Barlow CE, Grundy SM et al, Triglyceride to High Density Lipoprotein Cholesterol Ratio is an Index of Heart Disease Mortality and of Incidence of Type 2 Diabetes Melletus in Men, Journal of Investigative Medicine & Volume 62, Number 2, February 2014

Share to Flipboard:

Consumption of Dairy Fat Doesn’t Increase the Risk of CVD — may protect

A new study published this week 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[1].

The study which took place over almost a quarter of a century measured three specific fatty acids found in dairy products in 2,900 older adults, aged 65 years and above— first in 1992, again in 1998 and finally in 2015. The three fatty acids they measured were pentadecanoic, heptadecanoic, and palmitoleic acids.

During the 22 year period, 2,428 of the participants died of which 833 were due to heart disease.  When the data was analyzed, none of the three fats was associated with the risk of total mortality (death) or heart disease — in fact, high levels of heptadecanoic acid was associated with a lower risk of death from heart disease and stroke.

This is significant because while higher amounts of saturated-fat consumption, including the saturated fats in this study increase blood LDL cholesterol, they also increase HDL cholesterol and decrease triglycerides[2], both of which are protective. Since it was unknown what the ‘net effect’ on total mortality (death) and cause-specific death, this study was done to determine what effect, if any increased dairy fats had on these outcomes.

The results were clear.

Not only did long-term consumption of these three dairy fats have no effect on either total death or heart disease, high levels of one of the fats found in full-fat dairy was actually found to be associated with a lower risk of heart disease and stroke!

The authors of the study conclude;

“For decades dairy fat consumption has been hypothesized to be a risk factor for CVD, as well as potentially diabetes, weight gain, and cancer, little empirical evidence for these effects existed from studies of clinical events. In current years, a growing number of prospective studies have shown generally neutral or protective associations between self-reported dairy foods and dairy fat consumption with the risk of CVD, diabetes, weight gain and cancers, raising questions about this conventional wisdom.”

The results of this long-term study with almost 3,000 older adults demonstrates that the saturated fat found in full-fat dairy is not associated with cardiovascular disease (CVD), diabetes or cancer and may even be protective against both heart attack and stroke.

Final Thoughts…

With both the American and Canadian Dietary Guidelines currently being revised— and “front of label labeling” in Canada to advise against foods high in saturated fat, it is time for both the US Office of Disease Prevention as well as Health Canada to review their respective recommendations with regards to consumption of low-fat dairy, in light of current research.

Dairy protects play an important role in health and nutrition and are rich sources of calcium, potassium, and phosphorus and are a ready supply protein and essential fat not only to growing children, but to older adults who risk osteoporosis and sarcopenia (muscle wasting). Given the results of this study on the saturated fat in dairy, as well as the results of a recent 158-country study which found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease, it is time to  re-evaluate the long-held belief that animal fat (whether in meat or dairy), is somehow ‘dangerous’.

A Few Words “Fat Phobia”

I regularly come across people in my practice who grew up in the last 40 years and who have spent their entire lives avoiding any form of animal fat.  The very idea of eating the yolk in egg is a source of anxiety — and it need not be so.

I am not suggesting that these folks suddenly start eating copious amounts eggs, meat, cheese, cream and butter but often suggest they start with things such as avocado, olives, nuts and seeds that are rich in monounsaturated fats that have been less villainized than saturated fat. I encourage them to use a little cream on top of fresh berries or use a bit of butter to cook with. In time, I may show them delightful egg recipes that have other foods they are used to eating and enjoy, such as a spinach-ricotta pie, which makes a lovely summer-time dinner when it’s too hot too cook.

Overcoming “fat phobia” takes time — especially when it has been ingrained in you since you’re young. I understand. When we work together, you set the pace.

People are sometimes concerned than they can’t follow a low-carbohydrate lifestyle because they “can’t eat all that fat”, but the truth is, not all low-carb diets have large amounts of fat. It’s only because fat has 2  1/2 times the calories as protein and carbs that some types of low-carb diet are still considered “high fat”. There is a whole range of low-carb diets which you can read about here as well as different types of ketogenic (“keto”) diets that you can read about here.

Have questions about which type of low carbohydrate diet may be best for you? Or perhaps you have questions about my services and their costs.  Maybe you’d just like to meet me for a one-hour consultation (in-person or via Skype) to ask questions and see if this may be an option for you. 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.

To our good health!

Joy

You can follow me at:

 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. Otto MC , Lemaitre, RN, Song, X et al; Serial measures of circulating biomarkers of dairy fat and total and cause-specific mortality in older adults: the Cardiovascular Health Study,The American Journal of Clinical Nutrition, https://doi.org/10.1093/ajcn/nqy117
  2. Mensink RP, Zock PL, Kester AD, Katan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr 2003;77(5):1146–55

 

CVD Risk Improves By Use of Ketogenic Diet in Type 2 Diabetes at 1 year

One of the concerns raised by opponents of a very low carb or ketogenic diet is that it increases risk of cardiovascular disease such as heart attack and stroke, but does it?

Results of a peer-reviewed study of cardiovascular outcomes of people with Type 2 Diabetes (T2D) that was published at the beginning of May in the Journal of Cardiovascular Diabetology[1] found that those that followed a ketogenic diet significantly improved in 22 of 26 cardiovascular disease risk factors, including biomarkers of cholesterol / lipoproteins, blood pressure, inflammation, and carotid intima media thickness (cIMT).

Previous published results from the same researchers and published in February of 2018 demonstrated that reversal of T2D symptoms was able to be achieved and sustained long term using a ketogenic diet[2,3].

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was not only a significant decrease in blood sugar and weight, but a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

The results of this most recent study do much to dispel the myth that a therapeutic ketogenic diet puts individuals at increased risk for heart attack and stroke. In fact, it reduces their risk.

Methods

Continuous Care Intervention (CCI) Group Participants

At the beginning of the study, there were 238 participants enrolled in the continuous care intervention (CCI) group and all had a diagnosis of Type 2 Diabetes (T2D) with an average HbA1c of  7.6%  ±1.5%.  They ranged in age from 46 – 62 years of age, 67% were women and 33% were men. Weight of the subjects ranged from 200 pounds to 314 pounds (117±26 kg) with an average weight of 257 pounds (117 kg) and Average Body Mass Index (BMI) was 41 kg·m-2 (class III obesity) ±9 kg·m-2, with 82% categorized as obese.  The majority of participants (87%) were taking at least 1 medication for glycemic control medication.

At the end of a year, 218 participants (83%) remained enrolled in the  continuous care intervention (CCI) group.

Intervention and Monitoring of CCI Group

Each participant in the CCI group received an Individualized Meal Plan which enabled them to attain and maintain nutritional ketosis. They also received behavioral and social support, biomarker tracking tools, and ongoing care from a health coach with medication management by a physician.

Subjects typically required <30 g·day−1 total dietary carbohydrates.

Daily protein intake was targeted to a level of 1.5 g·kg−1 based on ideal body weight and participants were coached to incorporate dietary fats until they were no longer hungry.

Other aspects of the diet were individually tailored to ensure safety, effectiveness and satisfaction, including consumption of 3-5 servings of non-starchy vegetables and sufficient mineral and fluid intake.

Participants ability to achieve and maintain nutritional ketosis was determined by subjects monitoring their blood ketone level of β-hydroxybutyrate (BHB) using a portable, handheld device. Blood glucose and β-hydroxybutyrate (BHB) levels were initially tracked daily using a combination blood glucose and ketone meter and frequency of tracking was modified by the care team based based on each individual’s needs and preferences.

Participants with high blood pressure (hypertension) were provided with an automatic home blood pressure machine (sphygmomanometer) and they were instructed to record their readings daily to weekly in the supplied app, depending on recent blood pressure control. Antihypertensive medication prescriptions were adjusted based on home blood pressure readings and reported symptoms.

Downward Adjustment and/or Discontinuation of Medications

As blood pressure came down, diuretic medication was the first antihypertensive medication to be discontinued. This was followed by beta blockers (unless the participant had a history of coronary artery disease).

Angiotensin-converting-enzyme inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) were generally continued due to their known protective effect on the kidneys in those with Type 2 Diabetes.

Statin medications were adjusted to maintain a goal of LDL-P under 1000 nmol L−1 (or based on participant preference after full risk/benefit discussion with the physician).

The Usual Care (UC) Group

For comparison purposes, an independent group of patients with Type 2 Diabetes were also recruited for the study and were referred to Registered Dietitians that provided dietary advice according to the American Diabetes Association Guidelines [4].

Laboratory Assessors

Since an abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) is a known risk factor for CVD [5] and is very common in people with Type 2 Diabetes, a number of laboratory tests were conducted at the beginning of the study and the end to determine if they improved, stayed the same or got worse.

Most common in people with Type 2 Diabetes is where there are increased triglycerides (TG), decreased high-density lipoprotein cholesterol concentration (HDL-C) and increased small low-density lipoprotein particle number (small LDL-P).

The authors of this study state that evidence suggests that increased very low-density lipoprotein particle number (VLDL-P) and a large VLDL-P in particular may be one of the key underlying abnormalities in this abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) associated with T2D.

The authors also outline how higher concentrations of small LDL are often associated with increased total LDL particle number (LDL-P) and increased ApoB which is the main protein constituent of  very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL). The authors provide previous study evidence that demonstrates that in people with insulin resistance and T2D, increased total LDL particle number (LDL-P) and increased ApoB may exist even with normal to low LDL-C concentrations values. For this reason, LDL-C alone was not relied on as a measure of abnormal lipid / cholesterol profile (“atherogenic dyslipidemia”) in this study as it could miss the impact of increased total LDL particle number (LDL-P) and/or ApoB.

The authors mentioned that in previous studies with carbohydrate restriction of up to 1 year, while triglycerides (TG) usually decrease and HDL-C often increase, LDL-C sometimes increased and other times decreases. The authors note that although higher LDL-C is a known risk factor for CVD, low LDL-C may also reflect higher small, dense LDL, total LDL particle number (LDL-P) or ApoB and thus be a risk factor, as well.

Since inflammation is involved at all stages of the atherosclerotic process, higher high-sensitivity C-reactive protein (CRP) and/or higher white blood cell count (WBC) were assessed as risk factors for CVD.

Finally, since high blood pressure (hypertension) is also an added risk factor for CVD in people with T2D, tighter blood pressure control was deemed to reduce the risk of DVD, stroke and other microvascular events.

Continuous Care Intervention (CCI) Group

Standard laboratory fasting blood draws of the CCI group were obtained at the start of the study (baseline), at 70 days (3 months) and at ~ 1 year follow-up.

Lipid/cholesterol-related tests included ApoB, ApoA1, total cholesterol, triglycerides, direct HDL-C concentrations and LDL was calculated using the Friedewald equation.

The LipoProfile3 algorithm was used to determine relationship of lipid subfractions to cardiovascular (CVD) risk – specifically the number of HDL particles (HDL-P) previously reported  to be associated with death, Myocardial Infarction (MI), stroke and hospitalization, HDL-C (HDL cholesterol) which is the amount of cholesterol those particles are carying, which is not associated with these negative outcomes and HDL-P subclasses [6].

Risk was also determined using the lipoprotein insulin resistance score (LP-IR) which was proposed to be associated with the homeostasis model assessment of insulin resistance (HOMA-IR) and glucose disposal rate (GDR) [7].

Finally, risk was also determined using the 10-year atherosclerotic  cardiovascular disease (ACSVD) risk score of the American College of Cardiology [8].

Carotid ultrasonography (cIMT) measure was performed at baseline and 1 year to characterize atherosclerotic risk.

The Usual Care (UC) Group

Body measurements, vital signs and fasting blood draws for the Usual Care (UC) group were obtained at the start of the study (baseline) and at 1 year using the same clinical facilities and laboratory and data collection methods. Carotid ultrasonography (cIMT) measure was also performed at baseline and 1 year to characterize atherosclerotic risk.

Results

There were no significant difference in the baseline characteristics of the two sub groups of CCI participants (web-based on onsite-based) and no significant difference at 1 year, so for the purpose of analysis, data from both groups were combined.

As well, there were no significant difference in the baseline characteristics of the Usual Care (UC) group (which served as an observational comparison group) and the Continuous Care Intervention Group (CCI) except mean body weight and BMI were higher in the CCI versus the UC group.

The within-Continuous Care Intervention group changes in the following lipids and lipoproteins were all statistically significant and were as follows; ApoA1  [a component of high-density lipoprotein (HDL)] increase by + 9.8%) ApoB / ApoA1 ratio decreased by − 9.5% Triglycerides (TG) decreased by − 24.4% LDL-C increased by + 9.9% but LDL-particle size also increased by + 1.1% (that is, large fluffy LDL increased compared with small, dense LDL) HDL-C increased by + 18.1% total HDL-P increased by + 4.9% large HDL-P increased by 23.5% Triglyceride/ HDL-C ratio decreased by − 29.1% large VLDL-P decreased by − 38.9% small LDL-P decreased by − 20.8% There were no significant changes in total LDL-P or ApoB.

These results are impressive!

Simply by decreasing the amount of carbohydrate in the diet over the course of a year there was a dramatic improvement in lipid and lipoprotein markers associated with markers of cardiovascular risk.

In addition, the Continuous Care Intervention group had a significant reduction in;

systolic blood pressure decreased − 4.8%

diastolic blood pressure decreased − 4.3%

C-Reactive Protein (CRP) decreased almost 40% (i.e. − 39.3%) 

white blood cell (WBC) count decreased − 9.1%

Below are graphs of the changes in biomarkers for the Continuous Care Intervention (CCI) group (figure 1) and the Usual Care (UC) Group;

FIGURE 1: changes in biomarkers for the Continuous Care Intervention (CCI) group

 

FIGURE 2: changes in biomarkers for the Usual Care (UC) group

Below is a comparative graph of the two groups, the Continuous Care Intervention (CCI) Group and the Usual Care (UG) Group

FIGURE 3: changes in biomarkers for the Continuous Care Intervention (CCI) group compared to the Usual Care (UC) group

Some Final Thoughts…

This study demonstrates that a therapeutic ketogenic diet followed over the course of 1 year significantly improved 22 of 26 cardiovascular disease risk markers in those with Type 2 Diabetes. This is huge!

The size of the study group was large and had an 83% retention rate over the course of the year – which in and by itself demonstrates that the intervention diet was one that people had no difficulty staying with in their day-to-day lives, without the use of meal replacements (shakes or bars).

While not a randomized control trial between CCI and UG groups, this study supports that a ketogenic diet is both safe and effective for periods of up to a year (and in other studies has been documented to be safe and effective for up to two-years). Not only can a well-designed ketogenic diet reverse many of the symptoms of Diabetes (documented in this earlier article) it can also significantly improve risk markers for cardiovascular disease.

Do you have questions about how a carefully-designed low carbohydrate or ketogenic diet can help you improve symptoms of Type 2 Diabetes and lower markers of risk factors for cardiovascular disease?

Please send me a note using the “Contact Me” form above to find out more about how I can provide you with in-person or Distance Consultation services (via Skype or long distance telephone).

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Bhanpuri NH, Hallberg SJ, Williams PT et al, Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study, Cardiovascular Diabetology, 2018, 17(56)
  2. McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD, A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes, JMIR Diabetes 2017;2(1):e5, URL: http://diabetes.jmir.org/2017/1/e5, DOI: 10.2196/diabetes.6981
  3. Hallberg SJ, McKenzie AL, Williams, PT 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.
  4. America Diabetes Association, Lifestyle management. Diabetes Care. 2017;40 (Suppl 1):S33–S43
  5. Fruchart J-C, Sacks F, Hermans MP, Assmann G, Brown WV, Ceska R, et al. The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in patients with dyslipidemia. Am J Cardiol. 2008;102:1K–34K.
  6. May HT,  Anderson JL, Winegar DA, Utility of high density lipoprotein particle concentration in predicting future major adverse cardiovascular events among patients undergoing angiography, Clinical Biochemistry, 2016;49(15): 1122-1126
  7. Shalaurova I, Connelly MA, Garvey WT, Otvos JD. Lipoprotein insulin resistance index: a lipoprotein particle-derived measure of insulin resistance. Metabol Syndr Relat Disord. 2014;12:422–9.
  8. Goff DC, Lloyd-Jones DM, Bennett G, Coady S, D’Agostino RB, Gibbons R, et al. ACC/AHA guideline on the assessment of cardiovascular risk: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;2014:S49–73 (tool: http://tools.acc.org/ASCVD-Risk-Estimator-Plus/#!/calculate/estimate/)

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.

Two More Good Indicators of Cardiovascular Risk

In a recent article about why Waist Circumference and Waist-to-Height Ratio is so important, I explained that a meta-analysis from 2012 which pooled data from 300,000 adults of different races and ages found that the lowest risk of cardiovascular disease and shorter lifespan was associated with a Waist to Height Ratio (WHtR) of 0.5. That is, we are at lowest risk when our waist circumference is less than half our height (even if our BMI is in the normal range). I also explained exactly how to take waist circumference, so that the results are accurate.

There are other measures of cardiovascular risk that I think are worth considering.

  1. A 2015 study of 3200 adults found that Waist-to-Hip Ratio (WHR) is more accurate in predicting 10-year cardiovascular risk than Waist to Height Ratio (WHtR), however whether this relationship would hold up in a sample as large as the meta-analysis above is unknown. I feel it is worth mentioning Waist-to-Hip Ratio (WHR) as an indicator of cardiovascular risk, as it is easy to do.
  2. Another index this 2015 study found to accurately predict 10-year  cardiovascular risk was something called Conicity Index which I will touch on even though it is not as easily determined as Waist-to-Hip Ratio (WHR) or Waist to Height Ratio (WHtR).

Determining Waist to Hip Ratio

As mentioned in the previous article, to use these indices requires waist measurements and hip measurements to be done accurately and at a specific place on the body.  To make it easier, I will repeat how to measure waist circumference here and below, how to measure hip circumference.

Measuring Waist Circumference

For the purposes of calculating risk associated with increase abdominal girth, waist circumference needs to be measured at the location that is at the midpoint (i.e. half way) between the lowest rib and the top of the hip bone (called the “iliac crest”). Below is a picture that should help.

Where to measure waist circumference

This measurement should be taken with a flexible seamstress-type tape measure, being sure that the tape measure is at the same height in the front and the back, when looking in front of a mirror. That is, the tape measure should be perpendicular to the floor (not higher in the back or the front).

It’s also important that the person’s abdomen (belly) is completely relaxed when taking the measurement, not sucked in.  One way to do that is to taking a deep breath and let it out fully just as the measurement is taken.

If your Waist to Height ratio is greater than 0.5, then you are at increased risk for cardiovascular events and a shortened lifespan. Looking at the graph above, one can see that for every little bit over 0.5, the risk rises steeply.

Measuring Hip Circumference

Hip circumference needs to be measured at the widest portion of the buttocks (butt) and as with waist circumference, the tape measure needs to be parallel to the flood (same height in the front and the back, when looking in front of a mirror).

For both the waist and hip measurement, the tape measure should be snug around the body, but not pulled so tight that it is constricting and it is best if a stretch‐resistant but flexible seamstress-type tape measure is used.

Assessing Waist-to-Hip Ratio

If the waist circumference is measured in inches, then the hip circumference needs to be as well – same if the measurement is in centimeters; both need to be in the same units.

To calculate the Waist-to-Hip Ratio take the waist circumference and divide it by the hip circumference.

Waist-to-Hip Ratio and Risk of Cardiovascular Disease

The following ratios are associated with low, moderate and high risk of cardiovascular risk;

Low Risk: For men, if the ratio is 0.95 or less, for women if the ratio is 0.80 or less

Moderate Risk: For men, if the ratio is 0.96 – 1.0, for women if the ratio is 0.81 – 0.85

High Risk: For men, if the ratio is 1.0 or more, for women if the ratio is 0.85 or more.


The Waist-to-Hip Ratio can also be thought of as people being shaped like “apples” or “pears”.

People who carry most of their excess weight around their middle (“apples”) have more visceral fat and this type of fat is much more dangerous than the fat under our skin (called “sub-cutaneous fat”) because it is found around the heart, liver, pancreas and other organs and increases the risk not only of cardiovascular disease, but also Type 2 Diabetes and hypertension.

People who’s hips are much wider than their waist (so-called “pears”) have less visceral fat and therefore lower risk of these weight-related health problems.

Conicity Index

Conicity Index(CI) is a little more cumbersome a calculation than either Waist-to-Hip (WHR) Ratio or Waist-to-Height (WHtR), but was found in the 2015 study mentioned above with 3200 subjects to be a strong predictor of cardiovascular risk.

Conicity literally means “cone-shaped” and determines how much our  body fat distribution like two end-to-end cones.

In the first figure below, body weight is distributed evenly, however when someone has a conical distribution, their weight is more heavily distributed around the abdomen. As a result, it has increased conicity and is more highly correlated to increased cardiovascular disease (as well as Type 2 Diabetes and hypertension).

For those who are interested in calculating Conicity Index (CI), the formula is below along with the formula for Waist-to-Hip (WHR) Ratio, Waist-to-Height (WHtR).

Indices of central adiposity [1]

Final Thoughts…

Given the sample size of the data on which Waist-to-Height (WHtR) is based (300,000 adults) and that it is an easy to determine and robust measure of cardiovascular risk, this is the one I tend to favour.  That said, Waist-to-Hip (WHR) Ratio was previously used for years and found to be a simple and accurate predictor of risk. From that point of view, either could be used, but why not both?

In my clinical experience, I have encountered many people with much wider hips than waist (so-called “pears”) but whose Waist-to-Height (WHtR) is considerably greater than 0.5, and for this reason I tend to put more credence on Waist-to-Height (WHtR) than Waist-to-Hip (WHR) Ratio as a measure of visceral fat and increased cardiovascular risk.

Since both Waist-to-Height (WHtR) and Waist-to-Hip (WHR) Ratio are very easy to determine, for those with a family risk of cardiovascular disease, Type 2 Diabetes or hypertension, I think it makes sense to aim for a waist measurement that is within both of these easily obtained measures.

Do you have questions about how I can help you lower your risk of cardiovascular disease, Type 2 Diabetes or hypertension? I provide both in-person and Distance Consultation services via Skype or telephone (and remember, many extended benefits plans will reimburse for visits with a Registered Dietitian).

Please feel free to send me a note using the “Contact Me” form on the tab above to find out more.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Rabiee B,  Motamed N, & Perumal D, et al. Conicity index and waist-hip ratio are superior obesity indices in predicting 10-year cardiovascular risk among men and women. Clin. Cardiol. 38, 9, 527–534 (2015)

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.

New Study – More Animal Fat Consumption less cardiovascular disease

INTRODUCTION: A brand new study published last week in Nutrients looked at health and nutrition data from 158 countries worldwide and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease. As well, the study found that high carbohydrate consumption, particularly as cereals and wheat was most associated with the risk of cardiovascular disease. Significantly, both of these relationships held up regardless of a nation’s average national income.

Data from this study adds to the mounting evidence from 8 recent meta-analyses and systemic reviews of randomized control trials (RCT) summarized in this article that did not find an association between  saturated fat intake and the risk of heart disease[1-8]. It also supports evidence from the recent global PURE (Prospective Urban and Rural Epidemiological) study published in The Lancet this past December which found that those who ate the largest amounts of saturated fats had significantly reduced death rates, and that those that ate the lowest amounts of saturated fat (6-7% of calories) had increased risk of stroke [9].

Global Correlates of Cardiovascular Risk: a comparison of 158 Countries

This new study compared the average intake of 60 food items with obesity rates and life expectancy in 158 countries and found that a relationship existed between eating specific foods and raised blood pressure, death from cardiovascular disease and raised blood glucose (high blood sugar) — all of which are associated with cardiovascular disease.  The study examined nutritional data from  1993-2011 and found that total fat consumption and animal fat consumption were the dietary factors least associated with the risk of cardiovascular disease and that high carbohydrate consumption, especially as cereals and wheat was the dietary factor most associated with the risk of cardiovascular disease [10].

These findings add to the mounting evidence which calls into question whether dietary saturated fat is related to heart disease.

Total Cholesterol and Cardiovascular Risk

The present study found that eating animal fat and animal protein raised total cholesterol, however total fat and animal protein consumption were found to have a very impressive negative relationship with cardiovascular death in the European data, and a moderately negative relationship to cardiovascular death, worldwide. That is, the more total fat and animal protein eaten, the lower cardiovascular death rates were.

Often in studies,  the assumption is that high LDL is linked to risk of cardiovascular disease – not that there is a direct relationship between animal / saturated fat and cardiovascular disease.  That is, high LDL is a surrogate marker of cardiovascular disease. But does that assumption hold weight?

Perhaps a better question is “which LDL”? Small, dense LDL cholesterol  which easily penetrates the artery wall is associated with heart disease [11,12,13,14], but the large, fluffy LDL cholesterol is not [15,16], so studies seeking to impute LDL as the cause of cardiovascular diseasee need to differentiate between these LDL particles.

As well, total cholesterol is made up of the different sub-particles of LDL cholesterol, HDL cholesterol, VLDL cholesterol and triglycerides (TG), so lumping them all in together as ‘total cholesterol’ doesn’t tell us anything about risk of cardiovascular disease. We know that dietary saturated fat consistently raises the “good” HDL-cholesterol — which moves cholesterol away from the arteries and back to the liver where it can either be re-used or eliminated [17,18], so higher saturated fat intake will raise “good” HDL cholesterol, which in turn will raise total cholesterol. Total cholesterol going up is not a ‘bad’ thing.

What is important is not that total cholesterol went up but that along with increased total cholesterol, cardiovascular disease went down.

Higher Blood Sugar Associated with Higher Consumption of Cereals and Wheat

One finding of this study was that higher blood sugar (a known risk factor for cardiovascular disease) was most strongly associated with indicators of obesity such as high body mass index (BMI). What was new however is that higher consumption of cereals, especially cereals and wheat was associated with higher cardiovascular disease.

Researchers remarked that such results were not surprising “because the links between raised blood glucose, obesity, type 2 diabetes and cardiovascular disease are well established [19]”.

“…regardless of the statistical method used, the results always show very similar trends and identify high carbohydrate consumption (mainly in the form of cereals and wheat, in particular) as the dietary factor most consistently associated with the risk of CVDs.

High carbohydrate consumption, particularly as cereals and wheat was the dietary factor most consistently associated with the risk of cardiovascular disease.

Researchers looked at a maximum number of potentially significant variables and compared them to results across different regions and time periods and while they acknowledged that the accuracy of the data from developing countries may be lower, the global results that they found confirmed their earlier 2016 study data from European data only which found a significant link between cardiovascular disease and high carbohydrate consumption [20].

Of significance, the above associations held up regardless of a nation’s average national income.

Given these finding support those of the PURE epidemiological study [9] would lend support the notion that one can compare data between countries of substantially different level of income (as the PURE study did) and that high-carbohydrate and low-fat diets are not necessarily associated with poverty, as claimed [21].

The PURE study findings and those of this present study challenge the very basis of the long-standing ‘diet-heart hypothesis’ and it certainly results in some uncertainty as to what constitutes a healthy diet.

In my view, what is needed are some well-designed randomized controlled trials to determine if saturated fat intake is directly associated with cardiovascular disease – and not associated with a surrogate marker, such as LDL cholesterol.

Purported Weakness of the Data

Self-reported food-frequency questionnaires on which this study is based have long been criticized as being unreliable, however it is important to note that in the United States the NHANES Dietary Data and the Continuing Survey of Food Intakes by Individuals (USA) has also collected data using food-frequency questionnaires and such data is used as the “cornerstone to inform nutrition and health policy” [22].

In Canada, the Canadian Community Health Survey (CCHS) relies on a 24-hour recall data which is known to researchers to result in under-reporting of food intake, especially among those with a high BMI and with adolescents [23].  Given that the 2017 Obesity Update found Canada among its most overweight countries — with 25.8% of the population aged 15 and over considered obese [24], the CCHS data becomes less and less reliable, as obesity rates continue to climb.

Enduring Belief – despite recent evidence

The results of this most recently published study embody the same findings as the recent global PURE (Prospective Urban and Rural Epidemiological) study [9] publish this past December in The Lancet which found a link between raised cholesterol and lower cardiovascular risk.

This study also confirms the findings of the eight recent meta-analysis and systemic reviews of randomized control trials (RCT) summarized in the previous article which did not find an association between saturated fat intake and the risk of heart disease [1-8].

Yet, in spite of recent robust evidence there is an enduring belief that ‘saturated fat causes heart disease’ — a belief which has influenced nutrition guidelines in both the US and Canada for 40 years (since 1977).

As elaborated on in a recent article, it is now known that the ‘diet-heart hypothesis’ originated by Ancel Keys and supposedly confirmed in his ‘Seven Countries Study’ omitted known data from 22 available countries  and that when all countries were factored in there was a great deal more scatter showing a much weaker relationship between dietary fat and death by coronary heart disease than was suggested by Keys’s data.

Also as covered previously, it has been known since December 2016 that the three Harvard researchers who vindicated sugar as the cause of heart disease and blamed dietary fat — were funded by the sugar industry and that one one of those 3 researchers, Dr. DM Hegsted contributed to and edited the 1977 US Dietary Guidelines which embodied his findings of 10 years earlier, advising Americans to reduce their intake of saturated fat and cholesterol in order to reduce their risk of heart disease.

Also covered in a previous article, Canadian Dietary Recommendations regarding dietary intake of saturated fat were based on ‘health claim assessments’ conducted by Health Canada in 2000 (18 years ago) titled Dietary Fat, Saturated Fat, Cholesterol, Trans Fats and Coronary Heart Disease which was based on the US literature available from 1993-2000 and which concluded that a health risk exists between saturated fat and heart disease.

Given all of the factors mentioned above, it is my conviction that before the American and Canadian governments revise their respective national Dietary Guidelines what is needed is for them to conduct a long-overdue external, independent scientific review of the current evidence for the enduring belief that saturated fat contributes to heart disease.

If you have questions as to how I can help you live a low carb lifestyle, please send me a note using the “Contact Me” form located on the tab above.

To our good health,

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

  1. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
  2. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
  3. Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406
  4. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
  5. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
  6. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
  7. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
  8. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
  9. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  10. Grasgruber P, Cacek J, Hrazdira E, et al, Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries, Nutrients 201810(4), 411.
  11. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189–99
  12. Gardner CD, Fortmann SP, Krauss RM, Association of Small Low-Density Lipoprotein Particles With the Incidence of Coronary Artery Disease in Men and Women, JAMA. 1996;276(11):875-881
  13. Lamarche B, Tchernof A, Moorjani S, et al, Small, Dense Low-Density Lipoprotein Particles as a Predictor of the Risk of Ischemic Heart Disease in Men, 
  14. Packard C, Caslake M, Shepherd J. The role of small, dense low density lipoprotein (LDL): a new look, Int J of Cardiology,  Volume 74, Supplement 1, 30 June 2000, Pages S17-S22
  15. Genest JJ, Blijlevens E, McNamara JR, Low density lipoprotein particle size and coronary artery disease, Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:187-195
  16. Siri-Tarino PW, Sun Q, Hu FB, Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, The American Journal of Clinical Nutrition, Volume 91, Issue 3, 1 March 2010, Pages 502–509
  17. Mensink RP, Zock PL, Kester A, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, The American Journal of Clinical Nutrition, Volume 77, Issue 5, 1 May 2003, Pages 1146–1155
  18. Toth PP, The “Good Cholesterol” – High Density Lipoprotein, Circulation 2005;111:e89-e91
  19. Després, J.P.; Lemieux, I.; Alméras, N. Abdominal obesity and the metabolic syndrome. In Overweight and the Metabolic Syndrome; Springer: New York, NY, USA, 2006; pp. 137–152
  20. Grasgruber, P.; Sebera, M.; Hrazdira, E.; Hrebickova, S.; Cacek, J. Food consumption and the actual statistics of cardiovascular diseases: An epidemiological comparison of 42 European countries. Food Nutr. Res. 201660, 31694.
  21. Sigurdsson, AF, The Fate of the PURE Study – Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/
  22. Ahluwalia N, Dwyer J, Terry A, et al; Update on NHANES Dietary Data: Focus on Collection, Release, Analytical Considerations and Uses to Inform Public Policy, Advances in Nutrition, Volume 7, Issue 1, 1 January 2016, Pages 121–134
  23. Health Canada, Reference Guide to Understanding and Using the Data – 2015 Canadian Community Health Survey – Nutrition, June 2017
  24. OECD Health Statistics 2017, June 2017, http://www.oecd.org/els/health-systems/Obesity-Update-2017.pdf

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.

Saturated Fat and Heart Disease – Bad Fat Enduring Beliefs Part 2

This is Part 2 in the series which examines the enduring belief that dietary saturated fat causes heart disease.

INTRODUCTION: The “diet-heart hypothesis” is the belief that saturated fat and dietary cholesterol cause heart disease was first proposed by Ancel Keys in the 1950s. He encouraged Americans to reduce their fat intake by a third, while at the same time openly admitted as late as 1967 that there was little direct evidence that a change in diet would reduce the risks of arteriosclerosis [1]. As covered in the first part of this article, three Harvard researchers, Stare, Hegsted and McGrady were paid generously by the sugar industry to publish their review in the New England Journal of Medicine vindicating sugar as a cause of heart disease and laying the blame squarely on dietary fat; and in particular on saturated fatThese researchers concluded that there was “only one avenue” by which diet contributed to the development and progression of “hardening of the arteries” (atherosclerosis), resulting heart disease and that was due to how much dietary cholesterol people ate and its effect on blood lipids [2].  This sounds like a very certain claim, however it is known that they lacked evidence because a year later (1968) a report from the Diet-Heart Review Panel of the National Heart Institute made the recommendation that a major study be conducted to determine whether changes in dietary fat intake prevented heart disease – because such a study had not yet been done (see Part 1) [3].

Fast forward ten years and in 1977, one of the three researchers who was paid by the sugar industry, Dr. DM Hegsted contributed to and edited the 1977 US Dietary Guidelines [4], which embodied his findings 10 years earlier. Americans were told they should reduce their intake of saturated fat and cholesterol to reduce their risk of heart disease.

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, not dietary cholesterol [5].

Recommendations for the continued restriction of dietary fat continued in both the US and Canada in 2015 are based on the enduring belief that lowering saturated fat in the diet will lower blood cholesterol levels and reduce heart disease.

The question is does it?

NOTE TO CANADIANS: Canadian Dietary Recommendations regarding dietary intake of saturated fat are based on ‘health claim assessments’ conducted by Health Canada which are directly tied to American research and recommendations.  Eighteen years ago, Health Canada reviewed the ‘health claim’ regarding Dietary Fat, Saturated Fat, Cholesterol, Trans Fats and Coronary Heart Disease and based on the US literature available from 1993-2000 and concluded that a health risk exists between saturated fat and heart disease, as stated here; “The effectiveness of lowering dietary saturated fat in reducing plasma cholesterol, especially low-density lipoprotein (LDL)- cholesterol, the major risk factor for CHD, is well established.” Since Health Canada’s review in 2000 (18 years ago), the link between dietary saturated fat and heart disease remains public health policy.

While it has been shown that saturated fats can raise LDL-cholesterol such a finding is meaningless unless it is specified which type of LDL-cholesterol  goes up. There is more than one type of LDL-cholesterol, small, dense LDL cholesterol which easily penetrates the artery wall is associated with heart disease [6,7,8,9], whereas the large, fluffy LDL cholesterol is not [10, 11].

Another factor that needs to be considered is that dietary saturated fat also consistently raises the “good” HDL-cholesterol which moves cholesterol away from the arteries and back to the liver, where it can either be re-used or eliminated [12,13].

What are the findings of current scientific literature?

Eight recent meta-analysis and systemic reviews which reviewed evidence from randomized control trials (RCT) that had been conducted between 2009-2017 did not find an association between saturated fat intake and the risk of heart disease [14-21].

Furthermore, recently published results of the largest and most global epidemiological study published in December 2017 in The Lancet [23] found that those who ate the largest amount of saturated fats had significantly reduced rates of mortality and that low consumption (6-7% of calories) of saturated fat was associated with increased risk of stroke.

Here is a synopsis of the findings of the eight meta-analysis and systemic reviews;

“Intake of saturated fatty acids was not significantly associated with coronary heart disease mortality” and “saturated fatty acid intake was not significantly associated coronary heart disease events”

Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled

“There were no clear effects of dietary fat changes on total mortality or cardiovascular mortality”.

Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)

“Current evidence does not clearly support cardiovascular guidelines that encourage high consumption of polyunsaturated fatty acids and low consumption of total saturated fats.”

Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406

“The present systematic review provides no moderate quality evidence for the beneficial effects of reduced/modified fat diets in the secondary prevention of coronary heart disease. Recommending higher intakes of polyunsaturated fatty acids in replacement of saturated fatty acids was not associated with risk reduction.”

Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4

“The study found no statistically significant effects of reducing saturated fat on the following outcomes: all-cause mortality, cardiovascular mortality, fatal MIs (myocardial infarctions), non-fatal MIs, stroke, coronary heart disease mortality, coronary heart disease events.”

Note: The one significant finding was an effect for saturated fats on cardiovascular events however this finding lost significance when subjected to a sensitivity analysis (Table 8, page 137).

Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)

“Epidemiological evidence to date found no significant difference in CHD mortality and total fat or saturated fat intake and thus does not support the present dietary fat guidelines. The evidence per se lacks generalizability for population-wide guidelines.”

Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749

“Available evidence from randomized controlled trials (1968-1973) provides no indication of benefit on coronary heart disease or all-cause mortality from replacing saturated fat with linoleic acid rich vegetable oils (such as corn oil, sunflower oil, safflower oil, cottonseed oil, or soybean oil).”

Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353

“Available evidence from adequately controlled randomised controlled trials suggest replacing saturated fatty acids with mostly n-6 PUFA is unlikely to reduce coronary heart disease events, coronary heart disease  mortality or total mortality. These findings have implications for current dietary recommendations.”

Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30

Only one recent meta analysis conducted by the American Heart Association (by the authors of the Diet-Heart Policy for Americans, mentioned above) found a relationship between saturated fat intake and coronary heart disease, yet failed to examine cardiovascular mortality (death) or total mortality [22].

NOTE: In 1961, the American Heart Association was the author of the original policy paper recommending to limit saturated fats to protect against heart disease and therefore has a significant interest in defending its longtime institutional position.

With the exception of the American Heart Association review, the conclusion of 9 different meta-analysis and review papers of randomized control trials conducted by independent teams of scientists worldwide do not support the belief that dietary intake of saturated fat causes heart disease.


The PURE (Prospective Urban Rural Epidemiology) was the largest-ever epidemiological study and was published in The Lancet in December 2017 [23]. It recorded dietary intake in 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations.  It found;

“High carbohydrate intake was associated with higher risk of total mortality, whereas total fat and individual types of fat were related to lower total mortality. Total fat and types of fat were not associated with cardiovascular disease, myocardial infarction, or cardiovascular disease mortality, whereas saturated fat had an inverse association with stroke. Global dietary guidelines should be reconsidered in light of these findings.”

Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062

Those critical of the study say that it has methodological problems, including problems related to the authors dividing consumption of macronutrients (protein, fat and carbohydrate) into 4 groups (quintiles).  Some say that this is reason the data showed an inverse relationship between saturated fat and cardiovascular disease [24]. Criticisms also include that one cannot compare data between countries of substantially different level of income because “low fat consumption is very uncommon in high income countries” and that ‘the ability to afford certain foods may change the dietary pattern (e.g. high-carbohydrate and low-fat diets may be associated with poverty) [24].

Final thoughts…

Both the American and Canadian governments are currently in the process of revising their Dietary Guidelines and I feel that what is needed now is an external, independent scientific review of the current evidence-base for the belief that saturated fat contributes to heart disease.

Have questions or need support following a low carb lifestyle in a way that makes sense for you?

Please send me a note using the “Contact Me” tab above and I will reply shortly.

To our good health!

Joy

You can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

 

References

  1. Keys A, Aravanis C, Blackburn HW et al. Epidemiological studies related to coronary heart disease: characteristics of men aged 40–59 in seven countries Acta Med Scand 1967 460: 1–392.
  2. McGandy, RB, Hegsted DM, Stare,FJ. Dietary fats, carbohydrates and atherosclerotic vascular disease. New England Journal of Medicine. 1967 Aug 03;  277(5):242–47
  3. The National Diet-Heart Study Final Report.” Circulation, 1968; 37(3 suppl): I1-I26. Report of the Diet-Heart Review Panel of the National Heart Institute. Mass Field Trials and the Diet-Heart Question: Their Significance, Timeliness, Feasibility and Applicability. Dallas, Tex: American Heart Association; 1969, AHA Monograph no. 28.
  4. Introduction to the Dietary Goals for the United States – by Dr D.M. Hegsted. Professor of Nutrition, Harvard School of Public Health, Boston, MASS., page 17 of 130, https://naldc.nal.usda.gov/naldc/download.xhtml?id=1759572&content=PDF
  5. McDonald BE, The Canadian experience: why Canada decided against an upper limit for cholesterol, J Am Coll Nutr. 2004 Dec;23(6 Suppl):616S-620S.
  6. Tribble DL, Holl LG, Wood PD, et al. Variations in oxidative susceptibility among six low density lipoprotein subfractions of differing density and particle size. Atherosclerosis 1992;93:189–99
  7. Gardner CD, Fortmann SP, Krauss RM, Association of Small Low-Density Lipoprotein Particles With the Incidence of Coronary Artery Disease in Men and Women, JAMA. 1996;276(11):875-881
  8. Lamarche B, Tchernof A, Moorjani S, et al, Small, Dense Low-Density Lipoprotein Particles as a Predictor of the Risk of Ischemic Heart Disease in Men, 
  9. Packard C, Caslake M, Shepherd J. The role of small, dense low density lipoprotein (LDL): a new look, Int J of Cardiology,  Volume 74, Supplement 1, 30 June 2000, Pages S17-S22
  10. Genest JJ, Blijlevens E, McNamara JR, Low density lipoprotein particle size and coronary artery disease, Arteriosclerosis, Thrombosis, and Vascular Biology. 1992;12:187-195
  11. Siri-Tarino PW, Sun Q, Hu FB, Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease, The American Journal of Clinical Nutrition, Volume 91, Issue 3, 1 March 2010, Pages 502–509
  12. Mensink RP, Zock PL, Kester A, Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials, The American Journal of Clinical Nutrition, Volume 77, Issue 5, 1 May 2003, Pages 1146–1155
  13. Toth PP, The “Good Cholesterol” – High Density Lipoprotein, Circulation 2005;111:e89-e91
  14. Skeaff CM, PhD, Professor, Dept. of Human Nutrition, the University of Otago, Miller J. Dietary Fat and Coronary Heart Disease: Summary of Evidence From Prospective Cohort and Randomised Controlled Trials, Annals of Nutrition and Metabolism, 2009;55(1-3):173-201
  15. Hooper L, Summerbell CD, Thompson R, Reduced or modified dietary fat for preventing cardiovascular disease, 2012 Cochrane Database Syst Rev. 2012 May 16;(5)
  16. Chowdhury R, Warnakula S, Kunutsor S et al, Association of Dietary, Circulating, and Supplement Fatty Acids with Coronary Risk: A Systematic Review and Meta-analysis, Ann Intern Med. 2014 Mar 18;160(6):398-406
  17. Schwingshackl L, Hoffmann G Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression BMJ Open 2014;4
  18. Hooper L, Martin N, Abdelhamid A et al, Reduction in saturated fat intake for cardiovascular disease, Cochrane Database Syst Rev. 2015 Jun 10;(6)
  19. Harcombe Z, Baker JS, Davies B, Evidence from prospective cohort studies does not support current dietary fat guidelines: a systematic review and meta-analysis, Br J Sports Med. 2017 Dec;51(24):1743-1749
  20. Ramsden CE, Zamora D, Majchrzak-Hong S, et al, Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968-73), BMJ 2016; 353
  21. Hamley S, The effect of replacing saturated fat with mostly n-6 polyunsaturated fat on coronary heart disease: a meta-analysis of randomised controlled trials, Nutrition Journal 2017 16:30
  22. Sachs FM, Lichtenstein AH, Wu JHW et al, Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association,  Circulation. 2017 Jul 18;136(3)
  23. Dehghan M, Mente A, Zhang X et al, The PURE Study – Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet. 2017 Nov 4;390(10107):2050-2062
  24. Sigurdsson, AF, The Fate of the PURE Study – Fat and Carbohydrate Intake Revisited, Doc’s Opinion, October 16 2017,  www.docsopinion.com/2017/10/16/pure-study-fats-carbohydrates/

Note: References 11-23 were from a document prepared by the Nutrition Coalition

Special thanks to Dr. Carol Loffelmann and Dr. Barbra Allen Bradshaw of The Canadian Clinicians for Therapeutic Nutrition for their tireless research.


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.