Does cholesterol cause heart disease? Is the “lipid hypothesis” true?

The “Diet Heart” theory:

Very early research in animals suggests the idea that eating fat could raise blood lipids and, therefore, cause health problems. But work in people started with Ancel Keys’ National Diet-Heart study. Keys’ threw out data from 15 of 22 countries to publish the now infamous Seven Countries study. Throwing out data is bad science and a terrible foundation for National health recommendations.

Yet dietary recommendations to improve heart health are based on this premise.

Part of the confusion is that the “diet heart theory” is somewhat interchangeably called the “lipid hypothesis”. Lipid n. a class of substances with a fatty acid group that do not dissolve in water; e.g. natural oils, waxes, and steroids (cholesterol is a steroid).

The “Lipid hypothesis”:

Next up: the Framingham study. To identify common factors or characteristics that contribute to cardiovascular and other diseases, in 1948 this study tracked 5,209 men and women between the ages of 30 and 62 from the town of Framingham, Massachusetts. The idea was: track them, gather objective physical health data along with diet and lifestyle patterns, see who develops cardiovascular disease, see if there are common factors. In 1974 the first report revealed that high blood pressure, high blood cholesterol, smoking, obesity, diabetes, and physical inactivity are all associated with CVD. A huge and applaudable undertaking.

The “lipid hypothesis”, then, is an inference that too much cholesterol in the blood (especially low density lipoprotein (LDL or the so-called “bad” cholesterol) increases the risk of suffering a new event of coronary heart disease and that reducing the level of plasma cholesterol will reduce that risk.

Many of us are prescribed statin or other lipid/cholesterol lowering drugs based on this hypothesis.

Is lower cholesterol better?

Not according to research.

What? Are we talking about the same thing??

Get your last blood test out.

Sadly, most tests still say “cholesterol” or “cholesterol panel” or… but blood cholesterol is not the same other forms of cholesterol.

The cholesterol molecule is a waxy, fat-like substance produced by the liver and found in every cell where it helps those cells perform thousands of functions:

  • cholesterol is made into hormones like testosterone, estrogen, progesterone, and cortisol
  • your body makes vitamin D from cholesterol;
  • bile acid to help us digest certain foods is made from cholesterol;
  • cholesterol is found in the membranes of every cell, it covers and insulates nerve sheaths, and much of our other brain cells.

A better, more accurate term is lipoprotein profile. Your body sends fats, including cholesterol and other nutrients or wastes that do not dissolve in water, from your liver to the cells and from the cells back to the liver assembled inside a lipoprotein.

Lipoproteins are an assembly of different mixture of cholesterol molecules, other fats, and specific proteins. There are different types of lipoproteins: low density, high density, very low density… etc.

The vLDL and LDL lipoproteins tend to carry fat-like nutrients (including cholesterol) from the liver to all your cells. The HDL lipoproteins tend to carry fat-like waste back to the liver.

The heart-diet myth

Eating foods high in cholesterol (the molecule) has no effect on your blood cholesterol (the lipoprotein family).

Studies show this over and over: You can eat 28 eggs per week and not raise your blood cholesterol. In fact, a few studies show that if you add an egg a day your cholesterol profiles *improve*!

If eggs aren’t the villain, what about saturated fat?

It’s less cut and dried because saturated fat from commercial meats (grain-fed, farmed, hormone-laden, antibioticized – is that a word?) also includes accumulated chemicals. That type of fat is more inflammatory than fat from wild or pastured healthy animals. No studies make this distinction.

But the bigger reason is that reductions in saturated fat intake usually increase calories from carbohydrate. The effect of higher-carbohydrate diets, particularly refined carbohydrates but whole grains too, is a metabolic state that elevates liver and cellular production of triglycerides, which are then packaged into LDL cholesterol (so the liver makes more LDL packages) and sent to the body (or at least fat cells). This diet also reduces HDL cholesterol.

But there still must be another factor.

The “good” vs “bad” cholesterol model is dead

Meet the “retention theory”. This is juicy.

Since about the same time as the infamous “Seven Countries study” scientists have held to another idea: the so-called “bad” LDL cholesterol must become modified to become atherogenicin its native form it is not unhealthy.

Specifically, LDL cholesterol must be oxidized or glycated. LDL cholesterol becomes oxidized in the presence of toxicity from chemicals, infection, or any other chronically inflamed state, or in the absence of enough anti-oxidants. LDL cholesterol can become glycated (which means to have a sugar added) any time your blood sugar levels go high.

Under this model, modified lipoproteins are retained in the arterial wall, leading to development of foam cells and ultimately atherosclerotic plaques while native, unmodified LDL cholesterol does not.

But why would oxidized LDL, or LDL with a sugar added to the proteins in its shell, why would modified LDL stick when native doesn’t?

The understood sequence of atherosclerosis:

  • damage to the innermost layer of blood vessel endothelial cells—can be caused by blood borne toxic chemicals, hypertension, or infections.
  • injured blood vessel cells release factors that attract white blood cells to the area.
  • circulating native LDL becomes oxidized by free radicals. These changes may continue to extensive oxidation including protein changes

Forms of oxidized low-density lipoprotein (reproduced from Parthasarathy et al.). (a)Unoxidized native LDL with amino groups of lysine residues of apo B and representative lipids. (b) Lipid peroxides generated elsewhere associated with such LDL. (c) LDL lipids are oxidized resulting in the generation of cholesterol ester and phospholipid peroxides. (d) Such LDL might undergo extensive oxidation leading to protein changes. (e) Extensive protein changes and lipid decomposition might hallmark the end stages of oxidation. PtdCho: phosphatidylcholine; CE: cholesterol esters; Ox-PtdCho: oxidized phosphatidylcholine; Ox-CE: oxidized cholesterol esters; Lyso PtdCho: lysosomal phosphatidylcholine.

  • oxidized LDL and VLDL can damage neighboring cells increasing local inflammation and recruiting additional white blood cells.
  • normally, cholesterol acts as a bit of a “band-aid” it forms white streaks on the injured blood vessel to prevent leaks. Normally, white blood cells and others repair the injured area and then vacuum up the LDL cholesterol streaks. If this is native LDL, at some point the white blood cells become full—they won’t suck up any more LDL.
  • but if the streaks are oxidized LDL or VLDL which their degraded oxidized lipid and modified proteins—while both can stimulate white blood cell uptake, there is no “off”. These cells become enlarged and transform into what are called “foam cells”. This is what brings about enlarged plagues.
  • next: both oxidized lipids and oxidized proteins can generate antibodies. The presence of antibodies indicates the progression of atherosclerosis.

Noting the publication dates on this work, below, it is honestly hard to believe that “the lipid hypothesis” is still being used to set targets for total and/or LDL cholesterol.

If cholesterol is needed for health, at some point there will be too little of it and health will suffer. In fact, this is true. People with cholesterol levels below 175 mg per dL were twice as likely to die than those with cholesterol levels greater than 226 mg per dL. In this very large study of nearly 2300 people, additional adjustment for illness factors, such as diabetes or smoking status, did not alter these findings.

Controlling free radical stress due to chemical and/or metal toxicity and/or infection seems to prove more useful—solve the problem at the root cause rather than massively medicate people to lower cholesterol. Cholesterol becomes a problem when it is heavily oxidized due to chronic inflammation.

Find and Fix What’s Really Wrong.

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Regardless of the source of inflammation (or even unhealthy blood lipid profiles) there is hope and we can help.

References

Chisolm, G.M., Ma, G., Irwin, K.C., Martin, L.L., Gunderson, K.G., Linberg, L.F., … DiCorleto, P.E. (1994). 7 beta-hydroperoxycholest-5-en-3 beta-ol, a component of human atherosclerotic lesions, is the primary cytotoxin of oxidized human low density lipoprotein. Proceedings of the National Academy of Sciences of the United States of America, 91(24), 11452–11456.

Frostegard, J., Wu, R., Lemne, C., Thulin, T., Witztum, J.L., de Faire, U. (2003)Circulating oxidized low-density lipoprotein is increased in hypertension. Clinical Science (London). 105:615–620.

Goldberg, S., Gardener, H., Tiozzo, E., Kuen, C. Y., Elkind, M. S., Sacco, R. L., & Rundek, T. (2014). Egg Consumption and Carotid Atherosclerosis in the Northern Manhattan Study. Atherosclerosis, 235(2), 273–280.

Hoff, H.F., O’Neil, J., Chisolm, G.D., Cole, T.B., Quehenberger, O. … Jurgens, G. Modification of low density lipoprotein with 4-hydroxynonenal induces uptake by macrophages. Arteriosclerosis. 1989;9:538–549.

Parthasarathy, S., Raghavamenon, A., Garelnabi, M.O., & Santanam, N. (2010). Oxidized Low-Density Lipoprotein. Methods in Molecular Biology (Clifton, N.j.), 610, 403–417.

Ross, R. (1999) Atherosclerosis – An inflammatory disease. New England Journal of Medicine. 340:115–126.

Salonen, J.T., Yla-Herttuala, S., Yamamoto, R., Butler, S., Korpela, H., … Witztum, J.L. (1992) Autoantibody against oxidised LDL and progression of carotid atherosclerosis. Lancet. 339:883–887.

Schupf, N., et al. (2005) Relationship between plasma lipids and all-cause mortality in nondemented elderly. Journal of the American Geriatric Society. 53:219–26.

Siri-Tarino, P. W., Sun, Q., Hu, F. B., & Krauss, R. M. (2010). Saturated fat, carbohydrate, and cardiovascular disease. The American Journal of Clinical Nutrition, 91(3), 502–509.

Virella, G., Virella, I., Leman, R.B., Pryor, M.B., Lopes-Virella, M.F. (1993) Anti-oxidized low-density lipoprotein antibodies in patients with coronary heart disease and normal healthy volunteers. International Journal of Clinical and Laboratory Research. 23:95–101.

Wang, J., Qiang, H., Zhang, C., Liu, X., Chen, D., Wang, S. (2003) Detection of IgG-bound lipoprotein(a) immune complexes in patients with coronary heart disease. Clinica Chimica Acta. 327:115–122.

Marie Sternquist

Marie Sternquist, MS CHHC is a graduate of the University of Colorado, with 30 years of health-related clinical research published peer-reviewed medical journals, Marie's interests lie in how chemical and metal toxicities affect our health, hormones and immune function—and how to heal these problems with whole foods. In 2014, Marie completed the Health Coach program at the Institute for Integrative Nutrition where she studied 100’s of dietary theories with an emphasis on developing step-by-step nutritional programs and is currently working on her Nutritionist certification through the Masters in Functional Nutrition program and the University of Western States. Marie’s signature nutrition programs have helped thousands of people just like you regain health and quality of life. In 2016, Marie Sternquist completed her Advanced Level in Nutrition Response Testing®, joining her husband Dr. Greg Sternquist as an advanced clinician. Marie is also a wilderness explorer, skier, photographer and mom. Visit her at www.SuccessHealthCoach.com and www.OurNutritionKitchen.com

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