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7 Myths of Lipids and Health

12 Common Myths of Health and Nutrition

“When my information changes, I alter my conclusions. What do you do, sir?”
Keynes

Lipids are a class of molecules including fatty acids, triglycerides, phospholipids, and cholesterol. Blood lipid levels are one of the most looked-to biomarkers for our health status, and more specifically our mortality risk via heart disease. They can help us generate corrective feedback for modifying our diet and lifestyles towards optimizing our health and longevity.

While science has made great strides in revealing what these biomarkers can tell us, unfortunately many findings have not been incorporated into conventional wisdom. The public practice of nutrition and, sadly, even the advice of public health organizations remains well behind the times. In this post I aim to set straight some common, and in some cases quite damaging, myths about lipids.

  1. Keep blood blood cholesterol levels as low as possible, at least under 200mg/dL (5.2mmol/L). This persistent myth represents a profoundly outdated and never well-supported theory that high blood-cholesterol levels are on the whole detrimental to health/longevity. I won’t bother to reinvent the wheel here, as this has already been thoroughly debunked by many people. Instead, I’ll refer you to an excellent article by Chris Kresser on the topic, which includes many references to large scientific studies on the matter.
    For the history of how this idea got embedded into society, see the three podcasts (1) (2) (3) (with transcripts) featuring Chris Masterjohn. For even more detail, see Gary Taubes’ account of the scientific history in his book “Good Calories, Bad Calories” or his more lay-friendly book Why We Get Fat.
    What’s disturbing to me is the unwillingness of public health authorities to overturn their previous recommendations in light of new findings. For example, a quote from a recent paper displays the mindset:

    “Some have expressed concern that introducing [LDL particle number] into clinical practice will result in confusion to both physicians and patients, and that the public may lose confidence in the healthcare system if cholesterol, which has been emphasized for decades, is challenged as the primary means of risk assessment.” 1 

    I don’t know about you, but it’s this type of paternalistic withholding of evidence that makes me lose confidence in public health and nutritional advice. Not the fact that science causes us to revise our understanding when new evidence emerges.

  2. A good way to influence total blood cholesterol levels is by controlling cholesterol intake. This myth is basically moot in light of myth #1, but in case you didn’t find that convincing, maybe you will find the compound evidence convincing. This one is often used to vilify eggs due to their very high cholesterol content. In truth, most of the cholesterol you eat is in ester form, which can’t be absorbed as such. 2 A small amount of dietary cholesterol is absorbed after being de-esterified, but this amount is typically much smaller than the 1-1.5g/d that the body produces on its own (almost every cell in the body can produce cholesterol; it’s that important). Moreover, there exist negative feedback loops causing the body to reduce its endogenous cholesterol production in response to increased absorption of dietary cholesterol, and vice versa. Kudos to Canada’s health authorities for acknowledging these findings and removing any dietary cholesterol guidelines. 3 What’s the holdup everywhere else in the world?

  3. Blood lipid levels are irrelevant. This view represents an overreaction of those who learn about myths #1 and #2. In fact, blood lipids can indicate quite a bit about risk for cardiovascular disease. For a thorough lay-education in the modern understanding of blood lipids and cardiovascular disease risk, I recommend reading Dr. Peter Attia’s series: The straight dope on cholesterol (it’s a long read, so you might just want to skim the main points). According to Dr. Attia, the best single-measurement predictors are:
    • LDL-P – This is the “particle number” (really a particle concentration).
    • ApoB – This measures apolipoprotein-B densities, and is very highly correlated with LDL-P.
    • non-HDL-C – Another proxy for the above.

    If you are very worried about your numbers and don’t feel confident that your doctor is current with the latest research, then I suggest consulting Chris Kresser’s detailed action plan on the topic. It’s a pay-product, so you may want to educate yourself first using Dr. Attia’s free series.

  4. Replacing saturated fats with carbohydrates improves blood lipid profiles. This is too general of a statement to be absolutely true or false. My purpose in mentioning it is not to argue that its opposite is true, but to note that the evidence does not overwhelmingly support this idea. First of all, the “saturated fatty acids” comprise a large group of molecules with different biochemical properties. Most of these molecules do present strong evidence for raising total cholesterol and LDL cholesterol. However, most also tend to raise HDL (so-called “good cholesterol”), and when consumed in lieu of carbohydrates (possibly depending on the glycemic index of the carbs), a drop in triglycerides occurs. High levels of triglycerides are a much stronger risk factor for heart disease than total cholesterol, and are in the same ballpark as LDL-C. 4 So these competing effects must be evaluated. One large meta-analysis of 60 randomized controlled trials concluded: 

    “The efficacy of replacing SFAs [saturated fatty acids] with carbohydrates depends on the effects on body weight in the long term, and that effect is uncertain.” 5

  5. If you want to live a long time, then it’s better to cook with vegetable oils high in polyunsaturated fatty acids (PUFAs) than with traditional cooking fats like butter, ghee, lard, tallow, and coconut, all high in saturated fatty acids (SAFAs). 6 There are 8 known human intervention trials where high-PUFA oils were compared directly with SAFAs: in 3 trials vegetable oils clearly increased mortality, in 2 there was moderate evidence for an increase (not meeting statistical significance), and in the other 3 there was no substantial evidence either way. 7 What’s more, the evidence from these trials is actually more strongly against vegetable oils when it’s taken into account that some of the null findings were trials with omega-3 fats added as well. This myth may turn out to be one of the worst mistakes in the history of public health.

  6. Saturated fats kill: This idea is still put forth by most public health authorities in the world. It’s largely surmised from the above myths. The logic is: saturated fats cause higher cholesterol (total and LDL), which causes heart disease, which is the leading cause of death in the developed world, hence should be minimized. Therefore, we should minimize saturated fats. This line of reasoning relies on several layers of surrogate objectives (see my post on objectives). While this reductionist, divide-and-conquer approach is intuitively appealing, in practice it often fails to optimize the primary objective, which in this case would be the minimization of all-cause mortality.
    We have already shown that saturated fats fare well when compared to PUFAs in randomized controlled trials. To further address the validity of the proposition at hand, meta-analyses have looked at the direct relationships between dietary saturated fat and the primary objective of all-cause mortality and secondary objective of heart disease, removing the middle man of blood lipids:

    “A meta-analysis [including >300k people] of prospective epidemiologic studies [the highest-quality type of observational study] showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD [coronary heart disease] or CVD [cardiovascular disease].” 8 9

    An ‘Expert Consultation’ held jointly by the World Health Organization (WHO) and Food and Agriculture Organization (FAO) of the US had this to say regarding the epidemiological evidence: 10

    “Intake of SFA [saturated fatty acid] was not significantly associated with CHD [coronary heart disease] mortality… SFA intake was not significantly associated CHD events…” 11

    and this to say regarding the evidence from randomized controlled trials that purposefully lowered saturated fat intake:

    “…fatal CHD was not reduced by…the low-fat diets…” 12

    However, I don’t consider this case totally closed [what nutritional issue ever is?]. There are claims that some of the studies included in the above meta-analyses adjusted for variables innapropriately, such as adjusting for lipid profile risk factors that are in fact influenced by saturated fat consumption. 13

  7. Regarding the specific omega-3 fats EPA and DHA (found nearly exclusively in animal life, best sources in marine life): Omega-3 fats have been all the rage over the past 15 years or so. Recently we even learned that they may help to keep our telomeres long. But there are some common misconceptions regarding best practices of their consumption:

    1. The more the better. There’s very good reason to make sure you get some omega-3s. However, omega-3 fats are very fragile, and very susceptible to peroxidation, even more so than the much-maligned omega-6s. Peroxidation has been implicated as a contributor to early death, mitochondrial damage, liver disease, DNA mutations, excessive bleeding, stroke, and the atherosclerotic properties (oxidation) of LDL cholesterol. 14 There is direct evidence from experiments in rats that too much omega-3 can shorten their lifespan. 15 16 In humans, overconsumption of omega-3s have also been linked to endocannabinoid imbalances, producing symptoms of anxiety and chronic fatigue. 17

      How much is too much? That depends heavily on your omega-6 consumption, as omega-3s can reduce the toxic effects of excess omega-6s. The best thing to do is probably to strive for very low levels of omega-6 consumption (deficiencies are technically possible, but would be very difficult for otherwise healthy people to achieve in our modern food environment) and hence low levels of omega-3. In The Perfect Health Diet, the Jaminets recommend keeping omega-6 consumption under 4% of total calories, preferably around 2%, and if that is accomplished, then an omega-6:3 ratio of 3:1 is a good target. 18 

    2. The source doesn’t matter. Most of the beneficial effects of omega-3s in the body are from the long-chain forms, primarily EPA and DHA. These are most plentifully found in marine life, but ruminants eating their natural diets of grass also contain some in their meat. Omega-3s found in plants are almost exclusively alpha linolenic acid (ALA). This may be converted to the longer chain EPA/DHA, but the process is very inefficient (5-10%), so a much higher consumption would be required of it, risking increased peroxidation of these fats in the body. Hence it seems safer to get your omega-3s from marine life.

      Even given that you are getting EPA and DHA, we still have evidence that the source matters. For example, in the DART-2 trial of >3k men with angina, one group was told to either eat 2 servings of fish per week or to take 3 capsules of fish oil per day. Those who opted to take fish oil had significantly higher cardiac death. 19 While this is limited evidence, I prefer to err on the side of caution here. Moreover, we also know of two mechanisms whereby getting omega-3 from fish consumption is likely superior to fish oil pills:

      • Oxidation: Whether or not the omega-3s that you ingest are (per)oxidized is a concern, as it may unnecessarily promote heart disease, as mentioned above. But many, if not most, generic fish oils will not remain fresh when stored on warehouse shelves for months. Not all brands are created equal, and packaging with antioxidants like vitamin E can help. If you choose to use fish oil, at least break open a pill from your bottle and give it the smell test. It should have maybe a slight hint of the sea or slight smell of fresh fish, not an overpowering fishy smell or any hint of rot. While there’s some reason to believe that oxidized fish oil is still better than not consuming enough omega-3s, 20 why take the risk? At the least, keep fish oil refrigerated as a precaution.

      • Phospholipds vs Triglycerides: Most fish oils have no phospholipid EPA/DHA, which is present instead in triglyceride form. While fatty fish such as salmon have no more than 10% in phospholipid form, this may still be enough to make a difference. Preliminary evidence in rodents suggests that the phospholipid form is far more potent at reducing body fat, plasma insulin, hepatic steatosis (beginning non-alcoholic fatty liver disease) and low-grade adipose tissue inflammation, even on a diet of caloric excess. 21 22 23 Another good option for getting phospholipid omega-3s is krill oil.

 

Wrap up

If you are surprised that so much common wisdom about health and lipids could be on such shaky footing, then join the club. The lack of rapid diffusion of scientific findings to common practice was one of the main motivators for me to start this site. If you simply don’t believe that the [albeit limited] evidence I have posted tells the whole story, then I encourage you to investigate more deeply, and post contrary findings in the comments.

An education in the modern scientific understanding of nutrition can be obtained cheaply by reading “The Perfect Health Diet,” by Paul and Shou-Ching Jaminet. It’s not a light read, but if you invest a bit of time into learning how to make yourself thrive via nutrition, then you will reap the benefits for a lifetime. Not a bad deal.

Disclaimer: The information presented on this site is not medical advice, and should not be construed as a substitute for medical care or clinical testing. Any content or services offered by Biohack Yourself and it’s authors is not intended to constitute, or substitute for, the practice of medicine, or a clinical or healthcare diagnosis.

Note: Some of the links on this page are affiliate links. By purchasing through them, you get the same or lower price, and help support Biohack Yourself. These links are only to products that I have thoroughly evaluated and believe to be useful.

 

Further Reading

The Jaminets’ blog: The Perfect Health Diet, and book: The Perfect Health Diet.

Stephan Guyenet: The Diet-Heart Hypothesis: Stuck at the Starting Gate.

 

Acknowledgements

Many of the studies uncovered for this post were found on the excellent blog Suppversity. Thanks to Adel Moussa for his work on that blog.

Notes:

  1. http://chriskresser.com/thoughts-on-paleofantasy-bpa-toxicity-research-and-book-updates
  2. Djoussé, Luc, and J. Michael Gaziano. “Dietary cholesterol and coronary artery disease: a systematic review.” Current atherosclerosis reports 11.6 (2009): 418-422.
  3. Djoussé, Luc, and J. Michael Gaziano. “Dietary cholesterol and coronary artery disease: a systematic review.” Current atherosclerosis reports 11.6 (2009): 418-422.
  4. Thijssen, M.A. and R.P. Mensink. (2005). Fatty Acids and Atherosclerotic Risk. In Arnold von Eckardstein (Ed.) Atherosclerosis: Diet and Drugs. Springer. pp. 171–172. ISBN 978-3-540-22569-0.
  5. Mensink, Ronald P., et al. “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 77.5 (2003): 1146-1155.
  6. Note that this does not pertain to olive oil, which, although a vegetable oil, is not high in PUFA.
  7. Jaminet, Paul, and Shou-Ching Jaminet. Perfect Health Diet: regain health and lose weight by eating the way you were meant to eat. Scribner, 2012.
  8. Siri-Tarino, Patty W., et al. “Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.” The American journal of clinical nutrition 91.3 (2010): 535-546.
  9. The aforementioned meta-analysis unfortunately received partial funding from the dairy industry, so may be biased.
  10. I found this on the blog of Dr Briffa
  11. Fats and Fatty Acids in Human Nutrition. Annals of Nutrition and Metabolism, 2009; 55 (1-3).
  12. Fats and Fatty Acids in Human Nutrition. Annals of Nutrition and Metabolism, 2009; 55 (1-3).
  13. http://blog.cholesterol-and-health.com/2010/01/saturated-fat-is-not-associated-with.html?showComment=1283604601107#c5584064523416042242
  14. Jaminet, Paul, and Shou-Ching Jaminet. Perfect Health Diet: regain health and lose weight by eating the way you were meant to eat. Chapter 11: The Dangerous Fats: PUFA. Scribner, 2012.
  15. Church, M. W., et al. “Excess n-3 fatty acid consumption by mothers during pregnancy and lactation caused shorter life span and abnormal ABRs in old adult offspring.” Neurotoxicology and teratology 32.2 (2010): 171-181.
  16. Tsuduki, Tsuyoshi, et al. “Long-term intake of fish oil increases oxidative stress and decreases lifespan in senescence-accelerated mice.” Nutrition 27.3 (2011): 334-337.
  17. http://suppversity.blogspot.com/2012/06/phospholipid-or-triglyceride-whats-in.html
  18. Jaminet, Paul, and Shou-Ching Jaminet. Perfect Health Diet: regain health and lose weight by eating the way you were meant to eat. Chapter 11: The Dangerous Fats: PUFA. Scribner, 2012.
  19. Burr, M. L., et al. “Lack of benefit of dietary advice to men with angina: results of a controlled trial.” European journal of clinical nutrition 57.2 (2003): 193-200.
  20. Ottestad I, Vogt G, Retterstøl K, Myhrstad MC, Haugen JE, Nilsson A, Ravn-Haren G, Nordvi B, Brønner KW, Andersen LF, Holven KB, Ulven SM. Oxidised fish oil does not influence established markers of oxidative stress in healthy human subjects: a randomised controlled trial. Br J Nutr. 2011 Dec 5:1-12. Analysis
  21. http://suppversity.blogspot.com/2013/02/leaning-out-on-bulk-approx-6g-of.html
  22. http://suppversity.blogspot.com/2012/06/phospholipid-or-triglyceride-whats-in.html
  23. Rossmeisl M, Macek Jilkova Z, Kuda O, Jelenik T, Medrikova D, Stankova B, Kristinsson B, Haraldsson GG, Svensen H, Stoknes I, Sjövall P, Magnusson Y, Balvers MG, Verhoeckx KC, Tvrzicka E, Bryhn M, Kopecky J. Metabolic Effects of n-3 PUFA as Phospholipids Are Superior to Triglycerides in Mice Fed a High-Fat Diet: Possible Role of Endocannabinoids. PLoS One. 2012;7(6):e38834. Epub 2012 Jun 11.

{ 3 comments… add one }

  • dylan 2013/04/10, 21:42

    Really enjoy your Blog Winslow… look fwd to following you on twitter and sharing your info and the like with my clients and followers on there and FB.
    cheers

    • Winslow Strong 2013/04/13, 17:47

      Hi Dylan,

      Thanks for the kind words. From the looks of your site, it seems that you are into biohacking also? Keep spreading the knowledge!

  • Surthrival Colostrum 2016/07/05, 13:08

    Just curious as to your personal connection with investigating lipids. Did you have issues with blood sugar levels yourself or someone close to you?

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