The Truth about Cholesterol

In most major long-term studies, lowering cholesterol has done more harm than good.

Despite modern medicine’s decided shortcomings in the treatment of chronic diseases, we are led to believe that doctors have enough understanding of the human body to eradicate illness before it has begun. Increasingly doctors have turned their hand to what they like to call “ preventive medicine”.

Since the sixties, when doctors first hypothesised, that lowering blood cholesterol levels would prevent heart attacks, the focus has been on lowering high cholesterol either through diets low in saturated fats and cholesterol and/or cholesterol lowering drugs.

In fact, cholesterol lowering may be one of the biggest red herrings of the century. After 40 years or more of this” preventive medicine”, evidence is emerging that neither cholesterol-lowering drugs, nor any of the recommended low saturated fat and low cholesterol diets help at all in lowering overall mortality rates from coronary heart disease (CHD) over time.

In many cases the number of heart attacks may have dropped, but deaths from heart problems have not lowered significantly, and overall mortality from other causes have risen. An abundance of published research has shown, that lowering the blood cholesterol levels, can actually increase the risk of dying prematurely.

Approximately 90% of CHD is seen in patients older than sixty years. Most studies have shown that cholesterol is not a risk factor for CHD in older people and study after study have confirmed that high cholesterol is not a risk factor for women.(Quarterly J. of Medicine 2003; 96: 927) .

Although a staggering amount of money has been spent on research to conclusively prove the link between saturated fat, cholesterol and CHD, there exists a massive volume of scientific evidence published in peer-reviewed journals that completely absolves dietary cholesterol, saturated fat and elevated blood cholesterol of any harmful role in CHD.

Despite the fact that this research, contradicting the orthodox hypothesis, has been published in prestigious journals, and despite the complete failure of the massive low-fat, anti-cholesterol campaign to lower the overall incidence of CHD, the cholesterol/saturated fat theory of CHD enjoys almost unanimous acceptance among health authorities. There is no doubt that the present notoriety of cholesterol has all but obscured its physiological importance and necessity in our bodies.

Far from being a poisonous substance that must be avoided at all cost, cholesterol is a versatile compound, vital to the function of the human body.

Cholesterol, a steroid in its chemical structure, is metabolised into other essential body steroids, and is the indispensable chemical precursor for the manufacture of a number of critical steroid hormones. These hormones include the sex hormones, testosterone and estrogen, and the adrenal hormones, glucocorticoids (blood sugar regulation) and mineralocorticoids (mineral balance and blood pressure) Combined these hormones control a myriad of functions. Many of the disease of advancing age, are directly linked to the declining levels and imbalances of these critical hormones. For example low testosterone levels in males, may be a more significant risk factor for CHD than raised cholesterol levels.

Cholesterol is the main component of bile acids, which are needed to emulsify fats, enabling them to be digested and absorbed. Without cholesterol, the essential fat-soluble Vitamins A,D,E and K, could not be absorbed from food.

Only 7% of cholesterol is in the blood. The other 93% is located in every cell of the body, where its unique, waxy soapy consistency provides the cells with their structural integrity. Because cholesterol’s unique structure makes it impossible to dissolve in water, it forms a crucial component of the membrane surrounding every cell. Cholesterol acts to interlock lipid molecules, which stabilise our cell walls. The presence of cholesterol in the fatty double layer of the cell wall membrane adjusts the fluid level and rigidity to the proper value needed for both cell stability and function. Therefore, cholesterol is a vital building block and structural component for all bodily tissues.

The highest concentration of cholesterol is found in the brain and nerve cells. Most notably, cholesterol is an essential part of the myelin sheath, which allows neurons to conduct impulses necessary to communicate with each other. The myelin sheath, similar to the coating on copper wire, ensures that the nervous system functions properly by aiding the passage of electrical impulses. Cholesterol is the ‘synaptogenic factor,’ responsible for the development of highly specialised contact sites between adjacent neurons in the brain, known as synapses. (Announced in 2001 by researchers from the Max Planck Society for the Advancement of Science)

The formation of synapses is necessary for learning and the formation of memory. Cholesterol has been found to be the rate-limiting factor in the formation of synapse, Cholesterol not only helps guide the connecting parts of neurons to the right places, but is necessary for their ability to grow in the first place. The brain cannot tap the cholesterol in the blood, since lipoproteins, that mediate the transport of cholesterol, are too large to pass the blood-brain-barrier. The glial cells in the brain therefore produce their own cholesterol, to provide nerve cells with this vital component.

Cholesterol has beneficial effects on the immune system. Men with high cholesterol levels have stronger immune systems, than those with low cholesterol, as can be seen by the fact that they have more lymphocytes, total T-cells, helper T-cells and CD8+ cells. Researchers have also identified cholesterol as an inactivator/neutriliser of multiple bacterial toxins.

Further, many strains of disease-causing bacteria, are almost totally inactivated by Low Density Lipoprotein (LDL) cholesterol (Ravnskov 2003; Quarterly J of Medicine; 96)
Cholesterol, or more precisely 7-dehydrocholesterol, is the precursor to Vitamin D. Vitamin D has long been recognised for its role in maintaining calcium balance and promoting bone health. More recently it is becoming known for a wide range of other functions, including the maintenance of mental health, a strong immune system, blood sugar regulation and the prevention of cancer.

Cholesterol also acts as an anti-oxidant, protecting cell membranes from free radical damage.

The amount of cholesterol formed by the liver, is controlled according to the needs of the body. If dietary cholesterol is increased, a healthy liver responds by making less cholesterol.
But, if the cholesterol in the diet is decreased, the liver makes more. In this way the body regulates how much cholesterol is produced for its needs.

Because cholesterol is water resistant, and blood is a water-based medium, cholesterol shuttles through the blood inside an array of water soluble packages, known as lipoproteins. The two most abundant cholesterol transporting lipoproteins are, high density lipoprotein (HDL) and low density lipoprotein (LDL). The main function of LDL is to transport cholesterol from the liver to the organs and tissues where it is incorporated into cell membranes etc.

In contrast, the HDL carries the old cholesterol, that has been discarded by the cells, back to the liver for recycling or excretion.

Cholesterol and atherosclerosis

The medical profession would have us believe that high cholesterol causes coronary artery disease(CAD), by triggering the build up of atherosclerotic(hardening and degeneration of arterial walls) plaque along the arterial wall, eventually blocking blood flow to the heart. If cholesterol did indeed cause atherosclerosis, the number one cause of coronary heart disease, then one would logically expect at post-mortem examinations of heart attack victims, to find a strong correlation between blood cholesterol and degree of plaque build up in the coronary arteries.

Already in 1936, Kurt Lande and Walter Sperry concluded “After thorough and methodical post-mortem investigation in victims of heart attacks , it was clear that no relationship was evident. It is concluded that the incidence and severity of atherosclerosis are not directly affected by the level of cholesterol in the blood serum. (Archives of Pathology 1936;22)

In 1961, researchers studied the levels of cholesterol and the degree of atherosclerosis seen at autopsy. No correlation could be observed between the blood cholesterol levels and the amount or severity of atherosclerotic plaque within the arteries – cholesterol levels, whether high or low, had no impact on the growth of atherosclerotic plaque, the major cause of CAD. (Mathur et al 1961;Circulation: 23)

In 1962 autopsy studies by Polish researchers found that 2/3 of those who died from confirmed CAD, had serum cholesterol in normal to low ranges. They could find no correlation between blood cholesterol content and the cholesterol content of arterial plaque. (Marek et al 1962; American Heart Journal). Subsequent autopsy studies from the USA and Gautemala confirmed these findings.

Continuing the search for a correlation between cholesterol levels and atherosclerotic plaque, we can use state-of-the-art technology. Rather than looking at arteries after death, we can simply look at them while the patient is alive. Utilising a special X-ray imaging technique known as electron beam computed tomography (EBCT), scientists are able to look at both cholesterol levels and atherosclerotic build up in living patients.

Utilising EBCT technology, researchers at the Beth Israel Medical Centre in New York set out to determine if increased cholesterol levels, specifically LDL cholesterol, led to plaque build up. Looking at 182 individuals who may develop CAD, over 1-2 years of treatment with cholesterol lowering drugs, it was discovered that despite lower cholesterol levels there were ZERO differences in the development of atherosclerotic plaque. The researchers concluded “with respect to LDL cholesterol-lowering, ‘lower is better’ is not supported by changes in calcified plague progression.” (American J. of Cardiology 2003; 92:3)

Also, whether cholesterol goes up, or down, by itself or due to medical intervention, the changes in cholesterol have never been followed by parallel changes in the atherosclerotic plaques; there is no dose-response.

Most coronary events are not due to progressive blockage of an artery by gradual accumulation of lipid material, but to thrombosis(clot formation) and disruption of an asymptomatic fibrous plaque with minimal protrusion… Human atherosclerotic plaque has all the hallmarks of an inflammatory response to infection, and there is considerable evidence to support such an etiology. For many years scientists have suspected that viruses and bacteria, in particular cytomegalovirus and Clamydia pneumonia participate in the development of artherosclerosis. A protein secreted by the liver during infection, named C-reactive protein, is a much stronger risk factor for CHD than cholesterol. Research within this area has exploded during the last decade, and by 2004, at least 200 reviews of this issue have been published in medical journals.

The dangers of low blood cholesterol

Countries with diets high in saturated fat also tend to have high levels of colon cancer. In 1974 a review of the Framingham data and those from the Keys’ Seven Countries’ study was carried out, expecting to show that the cancer could also be blamed on high cholesterol. However the opposite was found – those with colon cancer had cholesterol levels that were lower than the average. Reports of more than twenty studies into the relation between blood cholesterol and cancer have been published since 1972. Most have reported a an association between low blood cholesterol and cancer.

Cholesterol studies in patients who developed colon cancer, conclude that it is the long term lowering of cholesterol levels, which increases the risk of developing cancer. The average blood cholesterol level of those who developed cancer declined to 5.56mmol/L, and yet the medical guidelines remain to reduce everyone’s levels to below 5.2mmol/L (Winawer et al 1990; JAMA: 263.) The results of a 3-year study , involving 11,500 patients, published in the European Heart Journal in 2003, found that the low cholesterol group – total cholesterol below 4.5mmol/L – had a relative risk of death 2.27 times higher than those with high cholesterol. The most common cause of death in the low cholesterol group was cancer, while the risk of cardiac death was the same in both groups.

A very large study from Japan, covering two decades, concluded that low levels of blood cholesterol also increased the incidence of stroke.(Takashi Shimamoto et al 1989; Circulation: 3) Supporting their findings were the results of a follow-up of 350,000 men screened for the MRFIT study in the United States that showed that the risk of death from cerebral haemorrhage in middle-aged men was six times greater if they had low cholesterol levels. In 1997, results from a study entitled Cholesterol and Mortality: 30 Years of Follow-up from the Framingham Study were published. The researchers from the Framingham study group said that ” High serum cholesterol level is not related to the incidence of stroke.” This in-depth study showed that after the age of 50, there is no increased overall death rate associated with high cholesterol! There was however a direct association between low levels(or dropping levels) of cholesterol and increased death. They concluded that “ Intakes of fat and type of fat were not related to the incidence of the combined outcome of all cardiovascular diseases or to total cardiovascular mortality” (Gillman et al 1997; JAMA :278)

Two studies which considered total blood cholesterol levels and mortality in the elderly, were published in the Lancet almost simultaneously in 1997. In the first, scientists working at the Leiden University Medical Centre found that “each 1mmol/L increase in total cholesterol corresponded to a 15% decrease in mortality” (Weverling-Rijnsburger et al 1997; Lancet :350)

Similarly, doctors at Reykjavik Hospital and Heart Preventive Clinic in Iceland noted that the major epidemiological studies had not included the elderly. They too studied total mortality and blood cholesterol in the over 80’s to show that men with blood cholesterol levels over 6.5mmol/L had less than half the mortality of those whose cholesterol level was around the 5.2mmol/L we are told is “healthy” (Jonsson et al 1997; Lancet; 350)

Researchers at the University of San Diego School of Medicine point out that high cholesterol in those over 75 years of age is protective, rather than harmful in that low cholesterol is a risk factor for heart arrhytmia (irregular heart beat), the leading cause of death if a heart attack occurs. An important study by Dr Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, revealed that persons older than 70, with low cholesterol levels, died twice as often from a heart attack as did old people with a high cholesterol. (JAMA 1994;272)

A study published in 2003 in the Journal of the American Geriatrics Society, studying the total cholesterol levels of 3,295 participants age 65-84 years over a 4 year period, concluded that those with total cholesterol levels below 5mmol/L,had a higher risk of dying, even when many related factors were taken into account

Recent(2006) research from the University of Hull in England. has linked low cholesterol with higher death rates in people with heart failure. A study of 10,701 patients with suspected heart failure found that those with low cholesterol were 1.7 times more likely to die within 12 weeks of being hospitalised. The study was based on the Euro Heart Failure survey, which involved 115 hospitals in 24 European countries. Researchers from Germany also found that the strongest predictor for death in patients with heart failure, was the concentration of cytokines(hormones secreted from white blood cells responding to an inflammatory process in the body) In addition the mortality rate was higher in those patients who had the lowest cholesterol, LDL and triglyceride blood levels. Patients with cholesterol levels above 5.6 mmol/L had half the mortality.

LOW CHOLESTEROL, AGGRESSIVE BEHAVIOUR AND SUICIDE Since 1992 several observers have noted increases in suicides among those undertaking cholesterol -lowering regimes. Decreases in blood cholesterol cause decreases in serotonin receptors and affect the balance of cerebral lipid metabolism, leading to increased microviscosity, which could have profound effects on brain function.: In institutions, aggressive people and those with antisocial personalities have been found to have lower than normal blood choleterol levels Mental patients with high blood cholesterol (7.55 mmol/L) were less regressed and withdrawn than those with lower (4.8 mmol/L) .(Engleberg 1992; Lancet 339)(Modai et al 1994 J, Clin, Psychiatry ; 55)

Approximately half of the brain is made up of fats. Dr F.M. Corrigan and colleagues, writing in 1990 about relief of Alzheimer‘s Disease, ask that “strategies for increasing the delivery of cholesterol to the brain should be identified“. In the fight against Alzheimer’s Disease, they recommended increasing fat intake (Corrigan et al 1991; J. Nutr. Med: 2)

The benefits of high cholesterol

There seems to be certain benefits to high cholesterol that medical authority is very reluctant to tell us about.
In his article, The Benefits of High Cholesterol, Uffe Ravnskov MD PhD says that people with high cholesterol live longest. “This statement seems so incredible that it takes a long time to clear one’s brainwashed mind to fully understand its importance” he continues , adding “ yet the fact that people with high cholesterol live the longest, emerges clearly from many scientific papers.“ (Ravnskov 2003; Quarterly J. of Medicine: 96).

Most studies of old people have shown that high cholesterol is not a risk factor for CHD, and is indeed associated with longevity. In a Medline database search, eleven studies of old people came up with this result, and a further seven found that high cholesterol did not predict all-cause mortality either.(Quarterly J. of Medicine 2003;96) Six of the studies found total mortality was inversely associated with either total or LDL- cholesterol. This means that it is actually much better to have high, rather than low cholesterol, if you want to live to be very old.

In 19 large studies of more than 68,000 deaths, reviewed by Professor David Jacobs and co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastro-intestinal and respiratory disease (Circulation 1997; 26)(International J. of Epidemiology 1997; 26) (Epidemiology and Infection 1998; 121

Researchers from the University of California at Los Angeles found a higher mortality in patients with severe heart failure, with the lowest lipid values, including total cholesterol, LDL-cholesterol and HDL- cholesterol.(American J. of Cardiology 1998; 82) This finding was confirmed by Dr. Rauchhaus, in cooperation with researchers at several German and British University hospitals. They found that the risk of dying, in patients with chronic heart failure, was strongly and inversely associated with total cholesterol and LDH- cholesterol; those with high lipid values lived much longer than those with low values. (Lancet 200; 356)(Journal of the American College Cardiology 2003; 42) The largest study included more than 1,000 patients with severe heart failure. After five years 62% of the patients with total cholesterol below 4.5mmol/L had died, but only half as many of the patients with cholesterol above 4.4mmol/L. (Journal of Cardiac Failure 2002; 8 )

The immune supporting properties of LDH- cholesterol plays an important role in human health. High cholesterol protects against infection – LDL-cholesterol binds and inactivates dangerous bacterial toxins.(Infection and Immunity 1989; 57 and 1995; 63)(Arteriosclerosis and Thrombosis 1992; 12)

Researchers at the University of Pittsburgh, Pennsylvania, studying a group of healthy middle-aged men, found that the number of various types of white blood cells were significantly lower in the men with serum cholesterol below 4.5mmpl/L,, than in men with serum cholesterol above 4.5mmol/L.(Clinical Immunology and Immunopathology 1997; 84)

The International Network of Cholesterol Sceptics (THINCS), a steadily growing group of scientist, physicians, other academicians and science writers are questioning the common dogma that dietary saturated fat and cholesterol cause CHD. Not only is there no proof to support this hypothesis, says spokesman Dr Uffe Ravnskov of Lund, Sweden, but the available scientific evidence clearly contradicts this claim.

Cholesterol has been wrongfully convicted as the oily villain in CHD – it deserves redemption!

Next Issue: Hidden truth about cholesterol-lowering drugs.

The Great Cholesterol Con: ANTHONY COLPO
The Cholesterol Myth: UFFE RAVNSKO
Fats that Harm, Fats that Heal: UDO ERASMUS
Know your Fats: MARY G. ENIG