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Cholesterol a Symptom, not the Disease

by Peter Dingle PhD(more info)

listed in heart, originally published in issue 179 - February 2011

Cardiovascular disease (CVD) in the UK, US, Australia and other Western nations accounts for between 30% and 40% of all registered deaths each year. It is the single biggest killer. However, since the advent of cholesterol-lowering drugs, cholesterol has become 'public enemy number one' and has wrongly taken all the blame for the increase in CVD. There is widespread belief that the lower one's cholesterol, the healthier he or she will be. The world has become fixated on lowering cholesterol through medication. Unfortunately this has led to a lot of misinformation and misdirection in treating the real illness. As a result, the rates of CVD continue to rise.

Cholesterol diagram

This focus on medication to lower cholesterol can be dangerous or even deadly, particularly since the overwhelming evidence shows that CVD is a result of lifestyle and dietary choices that lead to inflammation. CVD is no longer considered a disorder of lipid (fat) accumulation, but rather a disease process characterized by low-grade inflammation of the vascular (artery) lining and an inappropriate wound healing of the blood vessels. It is similar to a low-grade wound on your skin that does not heal but it is on the inside. There is now extensive and rapidly growing evidence that inflammation, which is what you get with every wound, plays a critical role in all stages of CVD.[1,2,3,4] It is not a disease of cholesterol or cholesterol accumulation; it is a disease of inflammation. Treating cholesterol is treating the symptom.

CVD is an inflammatory illness linked with many inflammatory conditions including diabetes, psoriasis, Alzheimer's, Parkinson's, rheumatoid arthritis, migraines, periodontal disease, sleep apnoea and chronic kidney failure. The common link is inflammation. One of my students recently remarked that when she was a trainee nurse in the cardiovascular ward she could not believe the rates of chronic inflammatory diseases of patients there who suffered from not one, but multiple inflammatory diseases. We are living in the inflammation age. A person with CVD very likely has underlying inflammation and, as a result, many other inflammation-related health problems, not just high cholesterol.

So when treating CVD one should also treat all these related diseases. However, as a culture we don't. Modern medicine has become one-dimensional and unable to look at the big, multidimensional picture. We treat cholesterol and we continue to get sicker. More people suffer and more people die from CVD and a raft of other inflammatory illnesses. Only when we treat the inflammation and stress on the body do we treat the illness.

Modern Medicine has Failed

The best way to describe the medical field's obsession with cholesterol is as a decades-old failing protocol, hanging by a thread and looking for more science or another change in the cholesterol theory to justify it. The whole basis of using statin drugs to lower cholesterol in the body is a chameleon theory. It keeps changing to suit the argument. There is no evidence that cholesterol causes heart attack or stroke even if you include HDL, LDL, VLDL or any thing else. There is just no science to support it. But it keeps changing to suit the pharmaceutical market place and keep its sales up for just another year or two to make a bit more money. Modern medicine has focused too much on the economics of health care and has lost sight of the real goal: to prevent and reverse illness.

The promotion of a drug-dependent cure for high cholesterol by multinational pharmaceutical companies has done nothing to stem the pain and suffering caused by chronic illness. Medical institutions have failed miserably to turn around chronic illness despite billions of dollars spent each year.

As a result, our population is over-medicated, our health system is financially strained and no one is actually healthier. The tragedy is that CVD is a totally preventable illness. The promotion of a drug-dependent cure is the real global epidemic.

A Few People Make a Lot of Money

Unfortunately illness has become one of the most profitable businesses of the 21st century. Many big companies earn too much money on chronic illness to have any interest in disease prevention. Profit is made from treating an illness that is not cured.

The whole system is flawed, starting from the philosophy of modern drug use to research, right through to regulation and administering drugs. The pharmaceutical industry now defines much of the medical profession's practice. We have a compromised medical research and academic community that has become dependent on industry money for its existence.

The power exercised by the pharmaceutical industry has created conflicts of interest that have undermined the credibility of medical research and education. As a simple example, a quick visit to any medical journal website will more than likely come up with an advertisement for a drug. This excessive power has, in fact, undermined ethics. It has even undermined the credibility of the front line GPs who see the patients. As a whole, many GPs have become the retail arm of the pharmaceutical industry.

Cholesterol is a Symptom, Not the Disease

High cholesterol is a symptom of an underlying health problem. It predicts less than 35% of cardiovascular disease. In fact, most heart attack and stroke events occur in individuals without elevated cholesterol. At least half of all cardiac arrests occur in people with normal cholesterol levels, and 20% occur in people without any traditional risk factors. Cholesterol is the messenger telling us that there is stress on the liver; cholesterol is not the killer it is made out to be.

A significantly better (than cholesterol) predictor of the risk of heart attack or stroke is the concentration of omega 3 oils in the blood. The higher the concentrations, the lower the risks.[5,6,7,8,9,10,11,12] Omega 3 concentrations predict up to 90% of CVD compared to a 35% prediction rate from cholesterol readings. But there is no money to be made in prescribing omega 3 oils. Omega 3 oils also reduce triglycerides and other risk factors for CVD, as well as reducing the risk of many other forms of chronic illness - from Alzheimer's to arthritis and cancer. This is due to the anti-inflammatory effect of fish oils. Fish oils have only positive side effects and far outweigh any benefit from statin drugs.

Another marker of inflammation in the body is C-reactive protein (CRP). C-reactive protein is a better predictor of CVD than cholesterol. People with elevated CRP run twice the risk of dying from cardiovascular-related problems compared to those who have elevated cholesterol levels. However, CRP is just a marker and, like cholesterol, it is not the cause.[13] We want to get CRP lower but not by a drug that lowers CRP only; we want to lower it by lowering inflammation. When inflammation is reduced, one result is CRP comes down.

C-reactive protein is produced in the liver and other tissues in response to inflammation anywhere in the body. It is manufactured as part of the body's immune response against infection and injury, but this response can cause damage if it produces excess and chronic inflammation. CRP levels are improved by the same factors that improve cardiovascular health: exercise, good diet, maintaining a healthy weight and not smoking. One study[14] demonstrated that supplementing with 500 milligrams (mg) of vitamin C reduced CRP by 25%, while numerous other studies have shown that supplementing with vitamins and minerals also reduces CRP and the inflammatory process.[15,16]

So What is the Problem?

One possibility is that our diets are deficient in nutrients - such as omega 3 oils from fish as well as vitamins, minerals and antioxidants - needed to maintain a healthy balance between inflammatory and anti-inflammatory responses. Researchers have also found that low levels of vitamin D are linked to higher levels of inflammation markers such as C-reactive protein.[17] Interestingly, extensive research has shown a direct inverse correlation with vitamin D levels and the risk of cardiovascular disease; a serious problem is that many people are now deficient in vitamin D. Simply getting outside and getting more sun (if it is around) reduces your risk of CVD better than any drug.

It's All in the Liver

Along with other signalling molecules, insulin controls the production of fats such as cholesterol and triglycerides. It also controls the packaging of cholesterol and triglycerides into LDL, VLDL, HDL and other lipoproteins. Glucagon inhibits the enzyme HMG-CoA reductase that creates VLDL and LDL cholesterol; insulin activates the enzyme. To control cholesterol production, it is important to increase glucagon and decrease insulin. The result of eating more sugar or processed carbohydrates (or other high-GI foods such as white bread and breakfast cereals) is the production of more insulin hormone. Increased insulin stimulates more HMG-CoA reductase enzyme and, as a consequence, more cholesterol and triglycerides are produced. Simple carbohydrates are the main culprits. We have known this since the early 1970s and there are hundreds of studies since that show the higher the GI, the higher the cholesterol. One study in 1976 of more than 2,000 school children found that those on a high-sugar diet had elevated cholesterol; the study predicted that the high sugar group had a higher future risk of heart attack and stroke. People with type 2 diabetes have elevated fasting insulin as well as elevated cholesterol and are two to four times as likely to have coronary heart disease (CHD) as a person without diabetes.[18] In fact, elevated fasting insulin is a better predictor of cardiovascular disease than cholesterol. Glucagon, when present in the bloodstream, lowers insulin levels. Glucagon is released every time you eat lean protein, especially from fish and plant sources.

There is also strong evidence to show that stress increases a person's inflammatory markers and cholesterol.[19,20,21] Not to mention increasing the levels of cortisol and their risk of heart attack and stroke. One possibility may be that stress encourages the body to produce more energy in the form of metabolic fuels, e.g., fatty acids and glucose. These substances require the liver to produce and secrete more LDL, which is the principal carrier of cholesterol in the blood.[22] Both adrenaline and cortisol trigger the production of cholesterol. Cortisol has the additional effect of releasing more sugar into the blood, which increases the insulin and, as a consequence, increases LDL cholesterol. To highlight the importance of this, we also know that there is a strong association between stress and cardiovascular disease. The higher the stress, the higher the risk of CVD. Stress causes inflammation in the body, and inflammation is the underlying cause of heart attack and stroke. Stress is probably the single biggest causal factor in cardiovascular disease and linked to just about every other form of chronic illness. So why are we worrying about cholesterol?

Elevated fibrinogen in the blood, another indicator of inflammation, is linked to an increased risk of stroke, heart attack and cardiovascular death. Fibrinogen is a protein involved in clotting, and it seems to make platelets stick more readily to atherosclerotic plaques or to form clots when these plaques rupture. The aim is not to find a drug to reduce fibrinogen but to lower inflammation through a healthy diet and lifestyle. Trying to lower just one or two of the indicators is like shooting the messenger. It does not work.

Cholesterol is an Essential Nutrient

Cholesterol is not the enemy. In fact, it is essential to good health and wellbeing. Every cell in the body needs cholesterol in its membrane, where it plays a critical role in cell communication. Without cholesterol, cell membranes are incomplete and, as a result, their functional role deteriorates.

Cholesterol is also used in the mitochondria, the powerhouse of the cell, and plays a vital role in cell energy production, not to mention its essential role in the brain structure and function. Cholesterol is the starting material of many essential chemicals including vitamin D, steroid hormones and bile acids for digestion. Do you see how important it is? Without adequate cholesterol and sunlight your body can't make vitamin D. Vitamin D deficiency is one of the major nutrient deficiencies in the Western world and is linked to many diseases and disorders, including type 2 diabetes, osteoporosis, CVD and the process of inflammation.

Cholesterol is metabolized into vital body steroids such as the steroid hormones, including: sex hormones, oestrogen, progesterone, testosterone and DHEA, as well as the adrenal hormones aldosterone and cortisol. These are essential to your health and wellbeing; none of these can be made without cholesterol. Their production changes in relation to the levels of cholesterol in the blood.[23] Low levels of these hormones can have a significant impact on an individual's health and, in fact, low testosterone is associated with an elevated risk of all-cause mortality[24] as well as other chronic illnesses including insulin resistance.[25]

It is in the best interests of large drug companies for the public to believe that the lower their cholesterol levels, the healthier they are, as this would amount to more sales of cholesterol-lowering drugs. Unfortunately this message has gone too far. Recent studies show that cholesterol may have protective properties against cancer.[26] An inverse relationship between low LDL cholesterol (low-density lipoprotein cholesterol, often referred to as 'bad cholesterol') levels and cancer is shown when statins inhibit the normal levels of cholesterol production in the liver. That is, the lower the levels of LDL cholesterol, the higher the rates of cancer.

A recent study in Hong Kong[27] found an LDL level of 107 to be associated with a 33% increase in risk of cancer and death, while an LDL level of 87 was associated with a 50% increase. The risk of developing cancer is increased by statins that inhibit the production of cholesterol in the liver. Further, cholesterol-lowering drugs were found to inhibit the absorption of cholesterol across the digestive tract.[28]

Your Brain Needs Cholesterol

Cholesterol is the most abundant organic molecule in the brain,[29] which contains almost a quarter of the unesterified cholesterol present in the entire body. In 2001, in groundbreaking research and with media fanfare, cholesterol was identified as the synaptogenic factor responsible for the development of synapses, the nerve connections in the brain. The glial cells of the central nervous system, which perform the housekeeping functions in the brain, produce their own cholesterol for the specific purpose of providing nerve cells with the vital component required for synapse function.[30,31,32]

Cholesterol is also required for the function of serotonin receptors in the brain. Serotonin is the chemical in our brain that makes us feel happy. Low cholesterol level has been associated with mortality due to suicides and accidental deaths.[33,34,35,36,37] Studies have demonstrated the relationship between low cholesterol levels and physical aggression and impulsivity in both humans and primates.[38,39] The reasons set forth to account for this relationship between cholesterol levels and violence, aggression and suicide relate to cholesterol's role in serotonin activity.[40]

The brain depends on a supply of cholesterol, as the cholesterol in the blood is carried by large carrier proteins, such as low-density lipoprotein (LDL) and high-density lipoprotein (HDL), which are too large to pass through the blood-brain barrier.[41] Unfortunately the highly lipophilic (fat soluble) statin drugs can easily pass through the blood-brain barrier and can therefore directly interfere with the synthesis of cholesterol by the helper cells in the brain, the glial cells.[42] It's no wonder that a major side effect of the statin drugs is an impact on memory and thinking.

All Your Cells Need Cholesterol

Cholesterol is a significant component of the cell membrane that influences its fluidity. It therefore indirectly affects neurotransmitters by interacting with the neurotransmitter receptors on the membrane.[43] Cholesterol is essential for cellular communication. It also forms part of the myelin that surrounds our nerves, aiding in the fast transmission of nerve signals. Lower cholesterol levels in the blood correlate with slower visuomotor speed.[44]

Low cholesterol levels have been shown to increase a person's susceptibility to infections.[45] This is due to cholesterol's functional role in preventing infections in the body. The lipoproteins that carry cholesterol through our bloodstream aid in our protection against harmful effects of bacterial poisons (endotoxins) released during infection.

A thirty-year study published in 1987 provides evidence that elevated cholesterol in people over the age of 50 does not increase the risk of having a heart attack. Cholesterol levels of people free of CHD and cancer were measured and there was no increase in the death rate in people with high cholesterol and over the age of 50.[46] Research on the effects of cholesterol levels and age shows that high cholesterol levels in people over the age of 75 is protective, not harmful. A study published in the European Heart Journal (1997) found that the risk of cardiac death was the same in groups of people with low or normal cholesterol levels as in those with high cholesterol.[47]

The Great Cholesterol Deception book cover

Maybe we need to rethink the billion dollars we spend on lowering cholesterol each year and spend the money on the real risk factors associated with cardiovascular disease such as stress and our lifestyle, including nutritional and environmental factors that increase inflammation. At the same time, we would be lowering risk factors for all forms of chronic illness, including cancer.


1. Dixon NC, TL Hurst et al. Active middle-aged men have lower fasting inflammatory markers but the postprandial inflammatory response is minimal and unaffected by physical activity status. Journal of Applied Physiology 107(1): 63-68. 2009.
2. Loppnow H, K Werdan, et al. Invited review: Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms. Innate Immunity 14(2): 63-87. 2008.
3. Packard RRS and P Libby. Inflammation in atherosclerosis: From vascular biology to biomarker discovery and risk prediction. Clinical Chemistry 54(1): 24-38. 2008.
4. Sukhanov S, Y Higashi, et al. IGF-1 reduces inflammatory responses, suppresses oxidative stress, and decreases atherosclerosis progression in ApoE-defficient mice. Arteriosclerosis, Thrombosis, and Vascular Biology 27(12): 2684-2690. 2007.
5. Kris-Etherton, PM, WS Harris, et al. Fish consumption, fish oil, omega-3 fatty acids, and cardiovascular disease. Circulation 106: 2747-2757. 2002.
6. Wang C, WS, Harris, et al. n-3 fatty acids from fish or fish-oil supplements, but not alpha-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: A systematic review. American Journal of Clinical Nutrition 84: 5-17. 2006.
7. Schacky, CV and WS Harris. Cardiovascular benefits of omega-3 fatty acids. Cardiovascular Research 73(2): 310-315. 2006.
8. Psota, TL, SK Gebauer, et al. Dietary omega-3 fatty acid intake and cardiovascular risk. American Journal of Cardiology 98: 3i-18i. 2006.
9. Harris WS, B Assaad, et al. Tissue omega-6/omega-3 fatty acid ratio and risk for coronary artery disease. American Journal of Cardiology 98: 19i-26i. 2006.
10. Robinson JG and NJ Stone Antiatherosclerotic and antithrombotic effects of omega-3 fatty acids. American Journal of Cardiology 98: 39i-49i. 2006.
11. Reiffel JA and A McDonald Antiarrhythmic effects of omega-3 fatty acids. American Journal of Cardiology 98: 50i-60i. 2006.
12. Jacobson TA Secondary prevention of coronary artery disease with omega-3 fatty acids. Amerian Journal of Cardiology 98: 61i-70i. 2006.
13. Elliott P, JC Chambers, et al. Genetic loci associated with C-reactive protein levels and risk of coronary heart disease. Journal of American Medical Association 302(1): 37-48. 2009.
14. Block G, CD Jensen, et al. Vitamin C treatment reduces elevated C-reactive protein. Free Radical Biology and Medicine 46(1): 70-77. 2009.
15. Scheurig AC, B Thorand, et al. Association between the intake of vitamins and trace elements from supplements and C-reactive protein: Results of the MONICA/KORA Augsburg study. European Journal of Clinical Nutrition 62: 127-137. 2008.
16. Nanri A, MA Moore, et al. Impact of C-reactive protein on disease risk and its relation to dietary factors: Literature Review. Asian Pacific Journal of Cancer Prevention 8: 167-177. 2007.
17. Dobnig H, S Pilz, et al. Independent association of low serum 25-Hydroxyvitamin D and 1,25-Dihydroxyvitamin D levels with all-cause and cardiovascular mortality. Archives of Internal Medicine 168(12): 1340-1349. 2008.
18. Malmberg K, S Yusuf, et al. Impact of diabetes on long-term prognosis in patients with unstable angina and non-Q-wave myocardial infarction: Results of the OASIS Organization to Assess Strategies for Ischemic Syndromes) Registry. Circulation 102: 1014-1019. 2000.
19. Steptoe A and L Brydon. Associations between acute lipid stress responses and fasting lipid levels 3 years later. Psychology 24(6): 601-607. 2005.
20. Coleman CA, AG Friedman, et al. The relationship of daily stress and health-related behaviors to adolescents' cholesterol levels. Adolescence 33(n130): 447-460. 1998.
21. Berger DF, JJ Starzec, et al. The effects of differential psychological stress on plasma cholesterol levels in rats. Psychosomatic Medicine 42(5): 481-492. 1980.
22. Steptoe A and L Brydon. Associations between acute lipid stress responses and fasting lipid levels 3 years later. Psychology 24(6): 601-607. 2005.
23. Khaw KT and E Barrett-Connor. Endogenous sex hormones, high density lipoprotein cholesterol, and other lipoprotein fractions in men. Arteriosclerosis and Thrombosis 11: 489-494. 1991.
24. Khaw KT, M Dowsett, et al. Endogenous testosterone and mortality due to all causes, cardiovascular disease, and cancer in men: European Prospective Investigation Into Cancer in Norfolk EPIC-Norfolk) Prospective Population Study. Circulation 116: 2694-2701. 2007.
25. Yeap BB, SAP Chubb, et al. Lower serum testosterone is independently associated with insulin resistance in non-diabetic older men: the Health In Men Study. European Journal of Endocrinology 161(4): 591-598. 2009.
26. Goldstein MR and L Mascitelli. Do statins decrease cardiovascular disease at the expense of increasing cancer? International Journal of Cardiology 133(2): 254-256. 2009.
27. Yang X, W So, et al. Independent associations between low-density lipoprotein cholesterol and cancer among patients with type 2 diabetes mellitus. Canadian Medical Association Journal 179(5): 427-437. 2008.
28. Drazen JM, RB D'Agostino, et al. Ezetimibe and cancer: An uncertain Association. The New England Journal of Medicine 359: 1398-1399. 2008.
29. Guyton AC and JE Hall. The adrenocortical hormones. Textbook of Medical Physiology. Philadelphia, Saunders: 957-971. 1996.
30. Mauch DH, K Nägler, et al. CNS synaptogenesis promoted by glia-derived cholesterol. Science 294(5545): 1354-1357. 2001.
31. Koudinov AR and NV Koudinova. Essential role for cholesterol in synaptic plasticity and neuronal degeneration. The Federation of American Societies for Experimental Biology Journal 15: 1858-1860. 2001.
32. Göritz C, DH Mauch, et al. Role of glia-derived cholesterol in synaptogenesis: new revelations in the synapse-glia affair. Journal of Physiology - Paris 96(3-4): 257-263. 2002.
33. Jacobs D, H Blackburn, et al. Report of the conference on low blood cholesterol: Mortality associations. Circulation 86: 1046-1060. 1992.
34. Muldoon MF, JE Rossouw, et al. Low or lowered cholesterol and risk of death from suicide and trauma. Metabolism 42(1): 45-46. 1993.
35. Lindberg G, L Rastam, et al. Low serum cholesterol concentration and short term mortality from injuries in men and women. British Medical Journal 305: 277-279. 1992.
36. Steegmans PHA, AW Hoes, et al. Higher prevalence of depressive symptoms in middle-aged men with low serum cholesterol levels. Psychosomatic Medicine 62(2): 205-211. 2000.
37. Ibid.
38. Freedman DS, T Byers, et al. Plasma lipid levels and psychologic characteristics in men. American Journal of Epidemiology 141: 507-517. 1995.
39.Golomb B, H Stattin, et al. Low cholesterol and violent crime. Journal of Psychiatric Research 34: 301-309. 2000.
40. Roy A, J DeJong, et al. Cerebrospinal fluid monoamine metabolites and suicidial behavior in depressed patients: a five-year follow-up study. Archive Genetics Psychiatry 46: 609-612. 1989.
41. Graveline D. Alzheimer's disease and statins. Accessed 4th April 2009. 2009.
42. Hayashi T, K Hamakawa, et al. HMG CoA reductase inhibitors reduce ischemic brain injury of Wistar rats through decreasing oxidative stress on neurons. Brain Research 1037(1-2): 52-58. 2004.
43. Heron DS, M Shinitzky, et al. Lipid fluidity markedly modulates the binding of serotonin to mouse brain membranes. Proceedings of the National Academy of Sciences of the United States of America 77(12): 7463-7467. 1980.
44. Zhang J, MF Muldoon, et al. Serum cholesterol concentrations are associated with visuomotor sped in men: Findings from the third National Health and Nutrition Examination Survey, 1988-1994. American Journal of Clinical Nutrition 80(2): 291-298. 2004.
45. Leardi S, F Altilia, et al. Blood levels of cholesterol and postoperative septic complications. Annali Italiani di Chirurgia 71(2): 233-237. 2000.
46. Anderson KM, WP Castelli, et al. Cholesterol and mortality: 30 years of follow-up from the Framingham study. Journal of American Medical Association 257(16): 2176-2180. 1987.
47. Behar S, E Graff, et al. Low total cholesterol is associated with high total mortality in patients with coronary heart disease. The Bezafibrate Infarction Prevention BIP) Study Group. European Heart Journal 18(1): 52-59. 1997.



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About Peter Dingle PhD

Peter Dingle PhD is Environmental and Nutritional Toxicologist at School of Environmental Science at Murdoch University, Australia and may be contacted via Tel: +61 08 9360 2569; Fax: +61 08 9310 4997;

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