Fat and cholesterol are virtually interchangeable words these days and both have negative connotations, neither of which is strictly correct. I have talked basically about fats in a previous chapter, so now it is the turn of cholesterol! Cholesterol is vital to health – it is a precursor for the manufacture of many other substances. Around 80% of circulating cholesterol is made in the liver, the remainder coming from the diet. Obviously excessive amounts of it are undesirable and this is usually due to problems elsewhere in the body that require more of it than normal to be manufactured.
A very high proportion of those who die from heart attack do not have high cholesterol, therefore, we do not have the truth of the matter. The truth is that cholesterol is not the major risk factor for heart attack that is has been made out to be over the last forty of fifty years. Blood vessels can be damaged in differing ways such as free radical attack, loss of elasticity and become structurally inferior due to poor nutrition. In these instances, the body uses cholesterol to repair this damage and to stiffen the weakened vessels.
It is very important to understand that cholesterol also acts as an antioxidant when, it appears, that the normal dietary antioxidants such as vitamins A, C, E and selenium are at low levels or absent. (Antioxidants neutralize free radicals that can wreak havoc everywhere in the body). With this lack of antioxidants and the other common nutritional deficiencies, more and more cholesterol will be manufactured, eventually leading to an excess circulating in the blood. This can obviously impede blood flow through the arteries. Significantly cutting down on all fats is not the answer, it will reduce cholesterol by a small margin but the liver will keep on manufacturing cholesterol until the root cause is addressed. Research has also shown that an excess of ‘good’ cholesterol can be turned into ‘bad’ by the oxidation process if antioxidants are not present in the body.
I have brought high cholesterol down to normal in dozens of my clients by giving them a high strength antioxidant complex together with other ‘fat dissolving’ agents such as lecithin, as part of an overall treatment plan.
There are two types of cholesterol, LDLs (low-density lipoproteins) are ‘bad’ and HDLs (high-density lipoproteins) are ‘good’. High levels of LDL in relation to HDL is one the causes of cholesterol related problems, not the overall cholesterol level, unless it is ‘through the roof’! Home test kits that measure overall cholesterol are of little use, as they do not show this ratio or overall triglycerides. It is very useful to undertake a proper cholesterol test and insist on seeing the results and have the ratios explained.
The results of a study undertaken by the Honolulu Heart Programme are now out (9/01). The lipid and cholesterol levels were measured in 3572 Japanese/American men aged 71-93 years. The researchers compared changes in these levels over 20 years with all-cause death rates. Only the group with low cholesterol concentrations at both examinations had a significant association with an increased risk of death. The researchers stated that “the earlier that patients start to have lower cholesterol concentrations, the greater the risk of death”! Source: Schatz IJ et al, Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Programme: a cohort study, Lancet 358:9279, 351-5,2001.
The drugs used to control or block cholesterol synthesis have been found to be carcinogenic in some instances! I treated a female G.P. for a high cholesterol problem; she came to me because she would not consider taking the drugs commonly prescribed for this condition!
German drug company Bayer AG has announced the withdrawal of its cholesterol-lowering drug Cerivastatin also known as Baycol and Lipobay after the deaths of 52 people. Source: Drug firm withdraws statin from the market, Wim Webber, lancet Volume 358 issue 9281, page 568 August 18, 2001.
So if cholesterol is not the major risk factor for heart disease, what is? The ‘new kid’ on the block is homocysteine. Please study this carefully as a high homocysteine level is said to be up to 40 times more predictive of heart disease than one’s cholesterol level.
Two times Nobel Prize winner Linus Pauling invented a cure for heart disease in 1991. This incredible information was released to the public in 1993 and then virtually ignored, which is a travesty. Heart disease is THE major killer in the Western world and huge sums of money are generated by all sorts of companies and individuals in the treatment of it. Pauling’s work is based on experimental proof with guinea pigs who as well as humans cannot make vitamin C in their body. Pauling claimed that specific nontoxic substances called Lp(a) binding inhibitors taken orally will prevent and even dissolve existing atherosclerotic plaque. These substances are vitamin C, proline and lysine. Indeed, three US patents have been granted on the Pauling/Rath method of treatment – a rare occurrence.
Atherosclerotic plaque form in the blood vessels due to some type of insult. Early scientists recognized that these plaques usually form in the same places – where the blood vessels are stretched and bent. This scenario implicated high blood pressure and the stresses caused by the heart beating. Plaques deposition is a response to structural injury and other insults, it is a healing process that ultimately becomes worse than the disease.
It has now been confirmed that high levels of LP(a) convey 70% higher risk of heart attack than normal levels. These findings (The Oxford findings – Dr John Danesh of Oxford University) were published in Circulation, a journal of the American Heart Association.
In 1962, doctors at the Royal Belfast Hospital for Sick Children uncovered a previously unseen metabolic disorder while performing biochemical screening of mentally retarded children. The disorder inhibited the breakdown of a compound called homocysteine. What the doctors didn’t know at the time was that their discovery would lead to, what is arguably, the most significant medical revelation this century. Forty years of follow-up research has uncovered the true gravity of this discovery – homocysteine is the major cause of cardiovascular and cerebrovascular disease.
The first clues
During the screening, the Irish doctors found that two sisters, aged 6 and 4, suffered with an enzymatic abnormality that caused them to excrete significant amounts of homocystine, an oxidized form of the protein metabolite homocysteine, in the urine. When the older sister died at age 9 the autopsy revealed the shocking truth – she had died of advanced atherosclerotic heart disease. Numerous other cases of childhood homocystinuria surfaced soon after, culminating in the same tragic result. Nevertheless, this particular type of homocystinuria was exceedingly rare (affecting one in 200,000), and hence attracted little scientific attention.
However, in 1969 a Harvard researcher, Dr Kilmer McCully, began the first serious scientific investigation of this phenomenon when he came across the cases of two homocysteine-related fatalities in children, one was aged eight and the other was only two months old. Both children presented with severe atherosclerosis.
The theory is born
Although these children suffered from rare enzyme defects, his analysis of the autopsies showed that the arterial damage was essentially identical to that seen in elderly people with atherosclerosis. McCully also established that it was the homocysteine itself that had damaged the arteries. At the time almost all the scientific focus on atherosclerosis was related to cholesterol, yet these children all had normal cholesterol levels. McCully’s early investigation led to the publication of a paper in the American Journal of Pathology in which he proposed that homocysteine could cause cardiovascular disease in normal people, even in the absence of enzymatic abnormalities.
Research by McCully and other scientists on animals soon established a `cause and effect’ relationship between blood homocysteine levels and atherosclerosis. If homocysteine levels were lowered in animals with high homocysteine then premature death was avoided. The cholesterol theory, in spite of its massive allocation of research funding, was severely flawed and had not successfully established a common link to cardiovascular or cerebrovascular disease. By 1978, McCully had accumulated a compelling body of work that clearly warranted a shift in emphasis, to make homocysteine the major priority for large-scale human cardiovascular research funding.
Political and scientific injustice
So why are we only hearing about homocysteine now? When Dr McCully originally presented his theory virtually all the funding for heart disease research was being allocated to the erroneous belief that cholesterol was the most important risk factor. Since no one would fund what was needed to take homocysteine research to the critical stage of large-scale human studies, McCully was forced to leave Harvard.
McCully’s work flew in the face of the established views of the time, and certainly threatened the viability of those commercial interests dependent on anti-cholesterol awareness becoming mainstream. It could be argued that this is still the case. McCully was made a scientific outcast in 1979 and it was two years before he found a job as a pathologist at the Veterans Affairs Hospital in Providence, Rhode Island, where he works today. However, it was not until the early 1990s, when large-scale human studies by various scientists throughout the world corroborated his theory, that homocysteine started to be taken seriously.
The mechanism of destruction
Homocysteine is formed when the essential amino acid methionine is metabolized from dietary protein. In spite of its clear association with disease, homocysteine is a normal intermediary metabolite that is formed in the bodies of all people, whether healthy or not. The key is that homocysteine is only a stepping-stone between methionine and its beneficial (and safe) end products such as cystathionine. In other words, you cannot metabolize methionine completely without homocysteine being formed. However, homocysteine is only genetically intended to be a temporary stage.
It is when homocysteine becomes elevated in the blood that problems begin to occur and atherosclerotic processes are triggered and/or accelerated. As it happens, the atherogenic mechanisms of homocysteine are quite diverse. In fact, in a recent interview with renowned biochemist Richard Passwater Ph.D., McCully commented, “As we understand it at the present time, homocysteine is involved in virtually all of the pathogenic processes that result in arteriosclerotic plaques:’
Primary pathogenic processes associated with homocysteine are:
The formation of lesions in blood vessel walls.
The formation of arterial lesions is the initiating factor in atherosclerosis development. Homocysteine interferes with the way the arterial cells utilize oxygen, in a manner that leads to a greatly accelerated accumulation of free radicals. Free radicals damage artery tissue proteins such as elastin and cause excessive cross-linking of collagen in the lining of the vascular wall. Also, LDL cholesterol and triglycerides are oxidized more rapidly in these conditions.
The thickening and hardening of vascular walls.
The damage to elastin and collagen combines with the fact that homocysteine stimulates abnormal production of smooth muscle cells, leading to excessive extracellular deposition of matrix proteins.
The triggering of various clotting factors, increasing reactivity, and ultimately the aggregation, of blood platelets The increase in the atherogenic capabilities of lipoprotein (a) or LP(a)
Lp(a) is considered to carry an atherosclerotic risk that is ten times greater than LDL cholesterol. LP(a) is similar to LDL cholesterol in its artery-damaging mechanism – the difference being that it adheres to the vascular walls much easier than LDL cholesterol due to an adhesive protein that it contains. High homocysteine levels cause LP(a) to more readily bind to fibrin, a protein found in high concentrations in blood clots and plaque.
The increase in the atherogenic capabilities of dietary fat and cholesterol intake
When levels of homocysteine are high there is a significant increase in accumulation of oxidized lipids in the formed plaque. Only about 2% of healthy people have elevated homocysteine levels. Research suggests that 30% of those with either coronary artery or peripheral artery disease and more than 40% of those with cerebrovascular disease have severely elevated homocysteine levels. On the other hand, of those people who die of a heart attack, 80-85% have normal cholesterol levels. Although much of the publicity about homocysteine risks has focused on very high elevation, evidence suggests that even moderate elevation may well carry risks. In fact, Dr Egil Arnesen, author of a 1995 study in the International Journal of Epidemiology, stated, ..”.there is no threshold level below which homocysteine is not associated with a risk of myocardial infarction” (heart attack). Interestingly, current research shows that one’s level of homocysteine is 40 times more predictive of heart disease than one’s cholesterol level.
As it happens, the harmful biochemical influences of homocysteine are not limited to the pathology of cardiovascular and cerebrovascular disease. Elevated levels can also be a major factor in osteoporosis, Alzheimer’s disease and certain forms of cancer.
When one is optimally nourished, homocysteine is converted into harmless compounds. When certain nutritional deficiencies are present, the conversion is impaired, hence the elevation. Research shows that the essential nutrients required for homocysteine metabolism are vitamin B6, B12 and folic acid.
Vitamin B6 is needed for the forward conversion of homocysteine into the innocuous end product cystathionine. It is interesting to note that a 1949 study showed that when monkeys were fed a diet that was only deficient in B6 they developed atherosclerosis. Oddly enough, McCully was the first scientist to follow the strand of this widely reported study – more than 20 years later. It brought to his attention that B6 is necessary for methionine metabolism.
Converting methionine into homocysteine involves the loss of methyl groups from methionine. Once converted into their active forms in the body, folic acid and B12 carry molecules of methyl in their structure, donating methyl to homocysteine, thus causing it to be recycled back into methionine.
Of the three, folic acid has been shown to be the most effective. However, it appears that the most clinically effective tool in lowering homocysteine is the methyl donor called trimethylglycine (TMG). Studies show that TMG, also known as betaine, lowers homocysteine in cases that do not respond to folic acid or B6.
Please note: Betaine hydrochloride, the supplemental form of hydrochloric acid, should not be used as a source of TMG.
One can’t help but wonder how many lives could have been saved if homocysteine had not been relegated to the status of `interesting, but unimportant’. Although recent major studies have created widespread acceptance of the homocysteine theory within the scientific community, this has not yet filtered down into the awareness of the large majority of physicians, much less the public – at least not in Britain.
This would probably still be the case in the US if it hadn’t been for a deluge of media coverage in 1998 throughout the country. This focused on the significance of homocysteine in heart disease and stroke, and exposed the truth about the suppression of the acceptance of McCully’s theory due to the dynamics of the pro-cholesterol lobby. Justice was finally served and McCully was virtually made a national hero overnight. Homocysteine has since gained a prominent place in the awareness of the medical establishment and public alike. Ever since, homocysteine testing has become increasingly common in the US and is well on its way to eventually becoming the first line of diagnosis for cardiovascular and cerebrovascular risk.
Lowering homocysteine in the general populace could save countless lives and billions of pounds in healthcare costs each year. The proven method for lowering even the worst cases of elevated homocysteine is safe, easy to administer and is very inexpensive. It is essential that the incredible momentum of homocysteine awareness currently seen in America should somehow be accomplished in Britain.
The foregoing article on homocysteine by Dr Stephen Terras was first published in The Nutrition Practitioner – The ONC journal, volume 1, February 1999. – The Nutrition Practitioner – The ONC journal (01344 301344). It is reproduced with the kind permission of both parties.
Several companies are now producing a supplement to counter high homocysteine levels. These normally contain vitamin B6, B12, folic acid and TMG (trimethylglycine) at least. If you feel or know you are at risk from heart disease it would be prudent to have your homocysteine levels checked. This can be done from a simple blood test.
The two theories of heart disease summarized above both have extremely important ramifications for every single person who consumes a Western-style diet. In my view, the two theories are interlinked, and therefore do not contradict one another. If you want to maximize your chances of NOT getting heart disease, not only take serious notice, but also make sure that you are getting adequate and regular amounts of Vitamin B12, B6, folic acid, vitamin C, TMG and the amino acids proline and lysine. The Pauling/Rath regimen uses mega doses of vitamin C, proline and lysine. If you wish to undertake this particular regimen it must be under the supervision of a health professional.