23 Feb 2018 The Cholesterol Nonsense Continues
I really thought we were done with all the anti-cholesterol nonsense, but it just won’t go away.
The anti-cholesterol narrative has been thoroughly discredited over the past couple decades, and even the Dietary Guidelines for Americans has removed their previous dietary limits for cholesterol consumption due to a lack of supporting evidence (although they still suggest consuming as little cholesterol as possible) (1).
But, most people are still avoiding cholesterol-containing foods like eggs and red meat, and the incredibly harmful and dangerous cholesterol-lowering drugs are still the most prescribed drugs in the United States (2).
The anti-cholesterol story began with the notion that high blood cholesterol levels cause plaque formation, which causes heart attacks. This led to the recommendations to reduce dietary cholesterol, which are still pervasive today.
But, not only does cholesterol not cause plaque formation or heart attacks, it actually protects against them and is one of the most protective nutrients available to our bodies.
Cholesterol Does NOT Cause Heart Disease
Efforts to link cholesterol to heart disease have gone on for half a century and have failed miserably.
Well, I guess it depends how you define “failed,” considering the amount of cholesterol-lowering drugs sold and the persistence of the anti-cholesterol dietary advice. But as far as scientific evidence goes, they have certainly failed.
The most influential heart disease study ever done found that the cholesterol levels between those who developed heart disease and those who didn’t were nearly identical (3).
This hardly supports that cholesterol causes heart disease, and many other studies have found that people with higher levels of cholesterol are less likely to die from heart disease and that those with heart disease who have higher cholesterol levels are less likely to die from any cause (4, 5, 6, 7, 8).
This is not to mention that the amount of cholesterol we eat doesn’t affect our blood levels of cholesterol or our risk of heart disease! (9, 10) Our bodies produce their own cholesterol, so the amount of cholesterol we consume has little effect on the amount of cholesterol in our bodies.
In fact, our bodies use between 1,000 and 2,000 mg of cholesterol per day, and if we reduce the amount of cholesterol we consume then our bodies simply make more in response.
So, not only do the cholesterol levels in our blood not cause heart disease, eating high-cholesterol foods doesn’t increase those levels anyway!
But what about the plaques that form in our arteries and cause heart attacks? Aren’t they made up of cholesterol?
Yeah, partially. But, blaming cholesterol for the plaque is kind of like blaming firemen for a fire.
As you’ll read about in a little bit, cholesterol is a vital part of our immune system. So, while it is found in atherosclerotic plaques, it’s there as a protective factor rather than a cause (11). Polyunsaturated fats (PUFA) and their metabolites, on the other hand, are also found in these plaques and play a more causative role by contributing to oxidation and inflammation (12, 13, 14, 15).
But, while cholesterol levels, plaque, and heart disease aren’t affected by the amount of cholesterol we eat, they are directly affected by our metabolism.
Cholesterol and Metabolism
Cholesterol levels are influenced by many different variables, but the factor that has the largest effect is metabolism. This relationship between cholesterol and metabolism has been known for 100 years but is now largely ignored (16, 17, 18).
When our metabolism is high, we produce more cholesterol. But, we also use more cholesterol to produce the protective steroid hormones (and for other uses), which reduces the amount of cholesterol in our blood (18).
The opposite occurs when our metabolism is low. We produce less cholesterol and use less of it to produce the protective hormones, leaving more of it in the blood (18).
So, while the larger amount of cholesterol in the blood isn’t a problem on its own, it’s representative of a low metabolism, which is a problem and is associated with heart disease (19, 20). Plus, it means the body is using less cholesterol, which is also a problem due to cholesterol’s beneficial effects.
The Protective Effects of Cholesterol
Cholesterol is one of the most protective nutrients that exist in our bodies. It’s vital for brain function, immune function, and digestion, and is the precursor to the extremely important steroid hormones.
Our brains contain around 25% of all the cholesterol in our bodies because of its importance in brain function (21). And, a lack of cholesterol is associated with impaired cognitive function as well as depression and impaired mental health (22, 23).
Cholesterol also plays a major role in our immune system and is able to prevent infections and detoxify harmful toxins like endotoxin (11, 24, 25).
And, due to cholesterol’s protective effects, low cholesterol and cholesterol-lowering drugs have been shown to increase the risk of cancer and all-cause mortality (26, 27).
In other words, we can stop with the anti-cholesterol nonsense!
We NEED cholesterol and we don’t need to avoid foods that contain it (like eggs and other animal foods) or that increase our bodies production of it (like sugar and saturated fat). In fact, the cholesterol-producing and metabolism-supporting effects of these foods make them some of the best foods for supporting health.
If you have high cholesterol then a low metabolism is to blame, not these foods, and a cholesterol-lowering drug is not the answer.
- “2015-2020 Dietary Guidelines: Answers to Your Questions.” Choose MyPlate, USDA, 7 Jan. 2016, www.choosemyplate.gov/2015-2020-dietary-guidelines-answers-your-questions.
- “The Top 200 of 2018.” com, clincalc.com/DrugStats/Top200Drugs.aspx.
- DuBroff, Robert, and Michel de Lorgeril. “Cholesterol confusion and statin controversy.” World journal of cardiology, 7, no. 7, 2015, pp. 404–09. doi:10.4330/wjc.v7.i7.404.
- Krumholz, Harlan M. “Lack of Association Between Cholesterol and Coronary Heart Disease Mortality and Morbidity and All-Cause Mortality in Persons Older Than 70 Years.” JAMA: The Journal of the American Medical Association, 272, no. 17, 1994, p. 1335. doi:10.1001/jama.1994.03520170045034.
- Ravnskov, Uffe, et al. “Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: A systematic review.” BMJ open, 6, no. 6, 2016, e010401. doi:10.1136/bmjopen-2015-010401.
- Rauchhaus, Mathias, et al. “The relationship between cholesterol and survival in patients with chronic heart failure.” Journal of the American College of Cardiology, 42, no. 11, 2003, pp. 1933–40. doi:10.1016/j.jacc.2003.07.016.
- Horwich, Tamara B., et al. “Low serum total cholesterol is associated with marked increase in mortality in advanced heart failure.” Journal of cardiac failure, 8, no. 4, 2002, pp. 216–24.
- Bae, Jong-Myon, et al. “Low cholesterol is associated with mortality from cardiovascular diseases: A dynamic cohort study in Korean adults.” Journal of Korean medical science, 27, no. 1, 2012, pp. 58–63. doi:10.3346/jkms.2012.27.1.58.
- Fernandez, Maria L. “Rethinking dietary cholesterol.” Current opinion in clinical nutrition and metabolic care, 15, no. 2, 2012, pp. 117–21. doi:10.1097/MCO.0b013e32834d2259.
- P2Namara, D. J. “Cholesterol intake and plasma cholesterol: An update.” Journal of the American College of Nutrition, 16, no. 6, 1997, pp. 530–34.
- Ravnskov, U. “High cholesterol may protect against infections and atherosclerosis.” QJM: An International Journal of Medicine, 96, no. 12, 2003, pp. 927–34. doi:10.1093/qjmed/hcg150.
- Felton, C. V., et al. “Dietary polyunsaturated fatty acids and composition of human aortic plaques.” Lancet (London, England), 344, no. 8931, 1994, pp. 1195–96.
- Gniwotta, C., et al. “Prostaglandin F2-like compounds, F2-isoprostanes, are present in increased amounts in human atherosclerotic lesions.” Arteriosclerosis, thrombosis, and vascular biology, 17, no. 11, 1997, pp. 3236–41.
- Waddington, Emma I., et al. “Fatty acid oxidation products in human atherosclerotic plaque: An analysis of clinical and histopathological correlates.” Atherosclerosis, 167, no. 1, 2003, pp. 111–20.
- Waddington, E., et al. “Identification and quantitation of unique fatty acid oxidation products in human atherosclerotic plaque using high-performance liquid chromatography.” Analytical biochemistry, 292, no. 2, 2001, pp. 234–44. doi:10.1006/abio.2001.5075.
- Mayo Foundation for Medical Education and Research. Collected Papers of the Mayo Clinic and the Mayo Foundation: 1918, Volume 10. By Mayo Clinic, W.B. Saunders Company, 1919.
- Mason, Robert L., et al. “Blood Cholesterol Values in Hyperthyroidism and Hypothyroidism — Their Significance.” New England Journal of Medicine, 203, no. 26, 1930, pp. 1273–78. doi:10.1056/NEJM193012252032601.
- Abrams, J. J., and S. M. Grundy. “Cholesterol metabolism in hypothyroidism and hyperthyroidism in man.” Journal of lipid research, 22, no. 2, 1981, pp. 323–38.
- Asvold, Bjørn O., et al. “Thyrotropin levels and risk of fatal coronary heart disease: The HUNT study.” Archives of internal medicine, 168, no. 8, 2008, pp. 855–60. doi:10.1001/archinte.168.8.855.
- Klein, Irwin, and Sara Danzi. “Thyroid disease and the heart.” Circulation, 116, no. 15, 2007, pp. 1725–35. doi:10.1161/CIRCULATIONAHA.106.678326.
- Dietschy, John M. “Central nervous system: Cholesterol turnover, brain development and neurodegeneration.” Biological chemistry, 390, no. 4, 2009, pp. 287–93. doi:10.1515/BC.2009.035.
- Elias, Penelope K., et al. “Serum cholesterol and cognitive performance in the Framingham Heart Study.” Psychosomatic medicine, 67, no. 1, 2005, pp. 24–30. doi:10.1097/01.psy.0000151745.67285.c2.
- Wardle, J. “Cholesterol and psychological well-being.” Journal of psychosomatic research, 39, no. 5, 1995, pp. 549–62.
- Han, Runlin. “Plasma lipoproteins are important components of the immune system.” Microbiology and immunology, 54, no. 4, 2010, pp. 246–53. doi:10.1111/j.1348-0421.2010.00203.x.
- Rauchhaus, Mathias, et al. “The endotoxin-lipoprotein hypothesis.” The Lancet, 356, no. 9233, 2000, pp. 930–33. doi:10.1016/S0140-6736(00)02690-8.
- Muldoon, M. F., et al. “Immune system differences in men with hypo- or hypercholesterolemia.” Clinical immunology and immunopathology, 84, no. 2, 1997, pp. 145–49.
- Ravnskov, U., et al. “The statin-low cholesterol-cancer conundrum.” QJM: An International Journal of Medicine, 105, no. 4, 2012, pp. 383–88. doi:10.1093/qjmed/hcr243.
KomelonPosted at 18:46h, 13 September
Jay, I love all your articles. Making Peat (and others) concepts accessible for everybody is a great idea. This one is particularly easy to understand and does a great job of debunking the official propaganda. I have one question though, when doctors and nutritionists talk about “good cholesterol” versus ” bad cholesterol”, how does it play into your explanation?
Jay FeldmanPosted at 10:40h, 14 September
Thanks, I’m glad you’re enjoying them!
The idea that HDL is the “good cholesterol” and LDL is the “bad cholesterol” isn’t really supported.
Cholesterol itself is extremely protective and plays a major role in the immune system. HDL, which is a protein carrier of cholesterol, carries cholesterol to the liver from the periphery, often along with toxins that need to be detoxified and/or excreted by the liver. This is why toxins like alcohol, endotoxin, and PUFA (or more accurately the breakdown products of PUFA) increase HDL levels. So while HDL itself isn’t harmful, high HDL levels may not be a great sign.
LDL is the carrier that transports cholesterol from the liver to the periphery, where it can be used for repair or converted to the protective steroids, among other things. If the arteries are damaged, LDL deposits cholesterol there to aid in repair, which is why it’s blamed for causing plaque buildup (I mentioned why it isn’t actually responsible for the plaque buildup under “cholesterol does not cause heart disease”).
LDL levels often increase with a low metabolism as a protective measure. This causes more cholesterol to be carried to the tissues to drive the production of the protective steroids. So, like HDL, while LDL itself isn’t harmful, very high LDL levels typically aren’t a great sign. However it’s definitely worth emphasizing that the demonization of LDL itself is entirely misplaced. That being said, when LDL is composed of greater amounts of polyunsaturated fatty acids, this allows it to become oxidized/damaged which may contribute to plaque formation and eventually cardiovascular disease.
I hope that’s helpful!
KomelonPosted at 11:59h, 14 September
Super helpful, thanks!
WendyPosted at 12:15h, 26 June
What if we have a low metabolism and too low cholesterol? Does low metab always = low cholesterol?
Jay FeldmanPosted at 17:11h, 29 June
A low metabolism doesn’t always equal low cholesterol, and low cholesterol can be dangerous because of the many important functions of cholesterol. Typically, increasing sugar consumption (fruit sources, honey, table sugar, etc.) and/or increasing saturated fat consumption will help raise cholesterol production.
DannyPosted at 16:34h, 18 August
Hi great article so how do you recommend raising your metabolism
Jay FeldmanPosted at 22:17h, 21 August
Thanks Danny. There are a lot of factors to consider here – I’d recommend signing up for my free Energy Balance Mini Course if you haven’t already (you can sign up for it here: https://jayfeldmanwellness.com/energy/) which will walk you through many of the more important things you can do to raise your metabolism and also taking a look at my podcast where we discuss this all in more detail (https://jayfeldmanwellness.com/podcast/).
TraePosted at 11:07h, 21 July
I have a question about Familial Hypercholesterolemia. I am currently determining my mutation, but my family history is pretty compelling. Is there worry about the upregulation of receptors on macrophages that can contribute to their increased oxidation in the subendothelial space with FH? I am 27 and fit, but every physician on the planet has hounded me on taking a statin because my LDL is 250. Are there merits to lowering LDL concentrations to <200mg/dL?