Positive Health Online

The Myth of the Cholesterol Theory

Over the past few decades we have been fed with the hypothesis that states that dietary saturated fat, total fat and cholesterol are associated with cardiovascular disease and atherosclerosis. Despite decades of health advice to eat low fat, low cholesterol diets and take cholesterol lowering medication, heart disease continues to be a leading cause of mortality. How can this be? The cynical might say because of commercial and political interests.

The hypothesis originated in the early 1950s from a study which correlated higher fat consumption with increased mortality rates from cardiovascular disease in just six out of a total of 22 countries.[1] Yet, since then there have been many studies disproving the link. As far back as 1964, a study[2] led by a world renowned heart surgeon found no link between the incidence or extent of atherosclerosis and cholesterol levels in 1,700 patients.

The truth is that 60% of people who die from heart attacks have normal or low blood cholesterol levels. People with normal cholesterol levels are just as likely to die of a heart attack than those with high cholesterol; blood levels of cholesterol are not a predictor of a heart attack.[3, 4, 5]
 

Statins

Lowering cholesterol with statins is being heavily promoted as a primary treatment target by the medical profession. A highly critical paper on statins,[6] questioned their effectiveness, exposed their side effects and attacked the science behind the cholesterol heart disease hypothesis.

A US study in 2008[7] involved a group of 74 patients with raised cholesterol who were randomly divided into two groups. One group received treatment with a statin drug, together with printed materials about diet and exercise recommendations. The other group received fish oil and red yeast rice supplements and received face to face lifestyle advice from a variety of professionals, both orthodox and alternative. The results after three months were that the alternative treatment group showed a 42.4% reduction in cholesterol levels compared to a 39.6% reduction in the statin group.

Another study, a meta-analysis, the gold standard in evidence based medicine, showed that statins were ineffective.[8]

Statins have side effects, amongst which are liver damage, nerve damage,[9] cognitive decline (memory loss[10] and depression has been reported), violent behaviour, mood alteration[11] and muscle damage. Statins are known to block the production of CO Q10,[12] which is needed for cellular energy production. It is particularly important for the heart muscle function; anyone taking statins should supplement 60-100mg CO Q10.

A New Theory of Cardiovascular Disease

Natasha Campbell-McBride has intensively studied atherosclerosis and heart disease.[13] She discusses the theory of cholesterol as a damage control agent, like an ambulance being sent to an accident. It is already a well known fact that scar tissue contains good amounts of cholesterol. A heart attack is associated with a rise in cholesterol, probably because extra cholesterol is being sent to help cellular repair.[14]

There's no question that the majority of heart attacks are the result of blocked arteries caused by a build up of plaque. The bulk of the plaque (68%) is fibrous repair tissue, mainly collagen. Calcium deposits are also present (8%) and the lipid-rich core of the plaque makes up 16%. Cholesterol also makes up a small part of this plaque and has been chemically damaged rather than being in its normal healthy form.

The original cause of the plaque build up is likely to be damage to the artery wall by agents such as bacteria, viruses, chemicals, toxins or undigested food. This causes inflammation and plaque formation which is the 'fall out' from the inflammatory process. Excess insulin production stimulated by too many refined carbohydrates in the diet also contributes to inflammatory damage. Cholesterol is attracted to the site as a healing agent. If there is no inflammation, blood cholesterol will not be deposited but will stay in circulation.

There is a clear link between stress and cholesterol since cholesterol is the raw material for making stress hormones. So when we are stressed, cholesterol production will increase. Cholesterol will test high after stressful events such as surgery. Then it will decrease again. Stress produces a high amount of free radicals which cause oxidative damage.

So we should see cholesterol as an indicator of damage in the body. If the damage is ongoing, the cholesterol production will continue to be high. We should look to the cause of the damage rather than seeking to attack the cholesterol. As Dr Mcbride says "cholesterol has been mistakenly blamed for the crime just because it was found at the scene".

Insulin Balance

Metabolic Syndrome consists of abdominal obesity, high blood pressure and glucose/insulin disturbances, and is clearly linked with increased risk of cardiovascular disease. Rather than concentrating on saturated fat and cholesterol, health advice should focus on reducing consumption of high amounts of refined sugar and carbohydrates (these foods will anyway be turned into fat if eaten in excess and increase cholesterol and triglycerides). Their frequent consumption in Western diets causes insulin resistance as the cells, continuously flooded with insulin, become desensitized to it so more and more is produced. Excessive insulin has damaging effects on blood vessels, causing them to contract. It is interesting to note that the increase in CVD parallels the increase in sugar consumption over the last century.

Conclusion

To maintain a healthy heart and arteries, concentration should be on preventing inflammation, treating oxidative stress and maintaining healthy blood sugar levels. Key nutrients for cardiovascular health are the omega 3 and 6 fats, vitamin D, B complex, plant sterols and CO Q10. Part two of this article will focus on nutrition based treatment strategies in more detail.

References

1. Keys A. Atherosclerosis: A problem in newer public health. Journal of Mount Sinai Hospital 20: 118-139. 1953.
2. Garrett HE et al. Serum Cholesterol Values in Patients Treated Surgically for Atherosclerosis. JAMA 189(9):655-659. 1964.
3. Werko L. Analysis of the MRFIT screenees: a methodological study. Journal of Internal Medicine 237: 507-518. 1995.
4. Kannel WB, Gordon T. The Framingham diet study: diet and the regulation of serum cholesterol. The Framingham study. An Epidemiological Investigation of Cardiovascular Disease. Section 24. Washington, DC, 1970.
5. Nichols AB et al. Daily nutritional intake and serum lipid levels. The Tecumseh study. American Journal of Clinical Nutrition 29:1384-1392. 1976.
6. Peskin BS, Sim S, Carter MJ. The failure of vytorin and statins to improve cardiovascular health: bad cholesterol or bad theory? J Am Phys Surg:13:82-87. 2008.
7. Becker JD et al. Simvastatin vs Therapeutic Lifestyle Changes and Supplements: Randomized Primary Prevention Trial. Mayo Clin Proc. 83:758-64. 2008.
8. Abramson J, Wright JM. Are lipid-lowering guidelines evidence based? Lancet 369:168-9.
2007.
9. Rosch PJ. Statin Associated Peripheral Neuropathy. Lancet, in press.
10. Wagstaff LR, Mitton MW, Arvik BM, Doraiswamy PM. Statin-associated memory loss: analysis of 60 case reports and review of the literature. Pharmacotherapy 23(7):871-80. 2003.
11. Golomb BA, Kane T, Dimsdale JE. Severe irritability associated with statin cholesterol-lowering drugs. Quart JM 97:229-235. 2004.
12. Rundek T, Naini A, Sacco R, Coates K, KiMauro S. Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke. Arch Neurol. 61:889-92. 2004.
13. Put You Heart In Your Mouth. What Really Is Heart Disease and What We Can Do to Prevent and Even Reverse It. Dr Natasha Campbell-Mcbride. Medinform Publishing. 2007.
14. Pfohl M et al. Upregulation of cholesterol synthesis after acute myocardial infarction--is cholesterol a positive acute phase reactant? Atherosclerosis 142(2):389-93. 1999.