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.

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To your good health!

Joy

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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
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