This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance. Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers.1 But let us take a look at heart mortality,the risk of dying from a heart attack if cholesterol is high.
Consider for instance the finding by Dr.Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported that old people with low cholesterol died twice as often from a heart attack as did old people with high cholesterol.2 Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, the result of chance among a huge number of studies finding the opposite.
But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis. To be more specific, almost all studies of old people have shown that high cholesterol is not a risk fact for coronary heart disease. This was the result of my search in the Medline database for studies addressing that question.3 Eleven studies of old people came up with that result, and a further seven found that high cholesterol did not predict all-cause mortality either, and more such studies have been published since then.
I have mentioned it before, but it is worth repeating, that more than 90 percent of those who die from a heart attack or a stroke have passed the age of 65. You may also recall that high cholesterol is not a risk factor for women, nor for a number of other population groups.
But there is more comfort for those who have high cholesterol. At least fifteen studies have found that total mortality is inversely associated with either total or LDL-cholesterol, or both. This means that it is actually much better to have high than to have low cholesterol if you want to be very old.
Many studies have found that low cholesterol in certain respects is worse than high cholesterol. For instance, in nineteen large studies of more than 68,000 deaths, reviewed by David R. Jacobs and his co-workers from the Division of Epidemiologyat the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.4 Most gastrointestinal and respiratory diseases have an infectious origin. Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposesto infection? You have probably already guessed what the directors of the cholesterol campaign have said, but is it true?
To answer that question David Jacobs´ group followed more than 100,000 healthy individuals in the San Francisco area for fifteen years. At the end of the study those who had low cholesterol at the start of the study had been admitted more often to hospital because of an infectious disease of the respiratory system or because of another type of infection.5,6 This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol be caused by a disease they had not yet encountered? Isn´t it much more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation.
Young, unmarried men with a previous sexually transmitted disease or liver disease run a much greater risk of becoming infected with HIV virus than other people.7
Similar results came from a study of the MRFIT screenees. Sixteen years later four times more among those with the lowest cholesterol had died from AIDS compared with those who had the highest.8
Heart disease may lead to a weakening of the heart muscle. A weak heart means that less blood and therefore less oxygen is delivered to the arteries. To compensate for the decreased power, the heart beat goes up, but in severe heart failure this is not sufficient. Such patients become short of breath because too little oxygen is delivered to the tissues, the pressure in their veins increases because the heart cannot deliver the blood away from the heart with sufficient power, and they become edematous, meaning that fluid accumulates in the legs and in serious cases also in the lungs and other parts of the body. This condition is called congestive or chronic heart failure.
There are many indications that bacteria or other microorganisms play an important role in chronic heart failure, and also that the risk of heart failure is much greater in people with low cholesterol.9–13
Furthermore, children born with very high cholesterol, so-called familial hypercholesterolemia, are protected against infection. But if inborn high cholesterol protects against infections, inborn low cholesterol should have the opposite effect. Indeed, this seems to be true.
Children with the Smith-Lemli-Opitz syndrome have very low cholesterol because the enzyme that is necessary for the last step in the body’s synthesis of cholesterol does not function properly. Most children with this syndrome are either stillborn or they die early because of serious malformations of the brain .Those who survive are imbecile, they have extremely low cholesterol, and they suffer from frequent and severe infections. However, if their diet is supplemented with pure cholesterol or extra eggs, their cholesterol goes up and their bouts of infection become less serious and less frequent.14
There is no contradictory observation that can´t beexplained away by the believers. One of the most striking aberrations appeared in two recent studies from the US. The first one came from the medical departmentat the University of California in LA.15 A total of 137,000 patients from 541 hospitals in the US had been admitted because of an acute heart attack. In all of them, their cholesterol was analysed within the first 24 hours of admission. To their surprise, the authors found that their cholesterol was lower than normal. To be precise, their mean total cholesterol was 174 (4.46 mmol/l) and the ‘bad’ LDL cholesterol was also much lower than normal.
It is not possible to explain away the result by using the argument that it was a result of chance, considering that this is the largest study of the cholesterol levels of heart patients, which has ever been published. The researchers were of course surprised. One explanation could be the well-known fact that cholesterol goes down in patients with an acute myocardial infarction, but they rejected it, because this happens first after two-three days and the reduction is only fifteen percent at most.16,17
Did the authors, three of whom were supported by eight drug companies, realize that they had stumbled upon something important? That high cholesterol may not be the cause of heart disease?
Of course not. What they concluded was that cholesterol must be reduced even further.
A few months later a research group from Henry Ford Heart and Vascular Institute in Detroit came up with a similar result.18Again, LDL cholesterol measured within the first 24 hours of admission was lower than normal, not higher. To be precise, in half of the 500 patients LDL-cholesterol was lower than 105 (2.69 mmol/l). They thought that something had gone wrong and were convinced that those whose LDL was below 105 had a much better chance to survive than those whose LDL was higher, because this is what all of us have been told by the American Heart Association and the drug companies repeatedly.
Three years later it appeared that among those with the lowest LDL-cholesterol twenty-six patients had died, but only twelve among those with the highest LDL-cholesterol. The authors considered their finding very salient. They warned their readers against feeling a false sense of security in patients with low LDL. Although more of those with low LDL were on statin treatment, they wrote , ”these patients may in fact need more aggressive risk modification.”
Recently I published a paper together with 15 international colleagues, where we reviewed 19 studies of elderly people (>60 years) who had been followed for several years. None of these studies found that LDL-cholesterol (the “bad” one) predisposes to cardiovascular disease; on the contrary, most of them showed that those with high LDL cholesterol lived the longest.19
There is a logical explanation. What very few know is that LDL, the molecule that transport cholesterol in the blood, partake in the immune system by adhering to and inactivating all kionds of miocroorganisms and their toxic products. You can read more about that in two papers that I have published together with Kilmer McCully, he who discovered the association between homocystein and atherosclerosis.20,21
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Salonen JT et al. HDL, HDL2, and HDL3 subfractions, and the risk of acute myocardial infarction. A prospective population study in eastern Finnish men. Circulation 1991;84:129-39.
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Ulmer H et al. Why Eve is not Adam: prospective follow-up in 149650 women and men of cholesterol and other risk factors related to cardiovascular and all-cause mortality. J Womens Health 2004;13(1):41-53.
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Sritara P et al. Associations between serum lipids and causes of mortality in a cohort of 3,499 urban Thais: The Electricity Generating Authority of Thailand (EGAT) study. Angiology 2007;58:757-63.
Åkerblom JL et al. Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders. Age Ageing. 2008;37:207-13.
Noda H et al. Gender difference of association between LDL cholesterol concentrations and mortality from coronary heart disease amongst Japanese: the Ibaraki Prefectural Health Study. J Intern Med 2010;267:576– 87
Newson RS et al. Association between serum cholesterol and noncardiovascular mortality in older age. J Am Geriatr Soc.2011;59:1779-85.
- Krumholz HM et al. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years..272, 1335-40, 1994.
- Ravnskov U. High cholesterol may protect against infections and atherosclerosis. 96, 927-934, 2003.
- Jacobs D et al. Report ofthe Conference on Low Blood Cholesterol: MortalityAssociations. Circulation 86, 1046–60, 1992
- Iribarren C et al. Serum total cholesterol and risk of hospitalization, and death from respiratory disease J Epidemiol 26, 1191–202, 1997.
- Iribarren C et al. Cohort study of serum total cholesterol and in-hospital incidence of infectious diseases. Epidemiol Infect 121, 335–47, 1998.
- Claxton AJ et al. Association between serum total cholesterol and HIV infection in a high-risk cohort of young men. J Acquir Immune Defic Syndr Hum Retrovirol 17, 51–7, 1998.
- Neaton JD, Wentworth DN. Endotoxin and immune activation in chronic heart failure: a prospective cohort study AIDS 11,929–30, 1997.
- Rauchhaus M et al. The endotoxin-lipoprotein hypothesis Lancet 356, 930–3, 2000.
- NiebauerJ er al. Endotoxin and immune activation in chronic heart failure: a prospective cohort study Lancet 353, 1838-1842, 1999.
- Vredevoe DL et al. Skin test anergy in advanced heart failure secondary to either ischemic or idiopathic dilated cardiomyopathy. Am J Cardiol 82, 323-8, 1998.
- Rauchhaus M et al. The relationship between cholesterol and survival in patients with chronic heart failure. J Am Coll Cardiol 42, 1933-40, 2003.
- Kalantar-Zadeh K et al. Reverse epidemiology of conventional cardiovascular risk factors in patients with chronic heart failure J Am Coll Cardiol 43, 1439-44, 2004.
- Elias ER et al. Clinical effects of cholesterol supplementation in six patients with the Smith-Lemli-Opitz syndrome (SLOS) Am J Med Genet 68, 305-10, 1997.
- Sachdeva A et al. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in Get With The Guidelines. Am Heart J 2009;157:111-7.
- Gore JM et al. Validity of serum total cholesterol level obtained within 24 hours of acute myocardial infarction. Am J Cardiol 1984;54:722-5.
- Sewdarsen M et al. Plasma lipids can be reliably assessed within 24 hours after acute myocardial infarction Postgrad Med J 1988;64;352-6.
- Al-Mallah MH et al. Low admission LDL-cholesterol is associated with increased 3-year all-cause mortality in patients with non ST segment elevation myocardial infarction Cardiol J 2009;16:227-33
- Ravnskov U 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 2016;6(6):e010401
- Ravnskov U, McCully KS. Vulnerable plaque formation from obstruction of vasa vasorum by homocysteinylated and oxidized lipoprotein aggregates complexed with microbial remnants and LDL autoantibodies. Ann Clin Lab Sci 2009;39:3–16.
- Ravnskov U, McCully KS. Infections may be causal in the pathogenesis of atherosclerosis. Am J Med Sci. 2012;344(5):391-4.