Homocysteine is a toxic amino acid produced during the body's break-down of the amino acid methionine. The substance is involved in many serious diseases.
Most likely, methionine is the prerequisite for all forms of life and entirely indispensable for our own physical existence. At the same time it is one of the most toxic amino acids. During its natural decomposition in the body it produces an intermediate. This intermediate is homocysteine, which is also an amino acid but not a vital nutrient.
Homocysteine is actually poisonous! The healthy reaction of the body is to get rid of it as fast as possible by breaking it down into cystathione, a harmless substance. The decomposition requires the enzyme cystathione synthase.
If you lack this enzyme or have too little of it, the homocysteine can accumulate in the body - and thereby also in the blood. This accumulation is too much - or "hyper" as the Greeks put it - and then the patient suffers from hyperhomocysteinemia, or in more common English: too much homocysteine in the blood. Severe hyperhomocysteinemia is a hereditary enzyme deficiency disease.
From the blood, the toxic substance enters the urine and therefore the condition is also known as homocysteinuria.
Homocysteine attacks the central nervous system, the circulation, the bones, the eyes, and other organs.
Also fertility problems, pregnancy problems, miscarriage, and spinal hernia can be the results of this condition. In severe cases, people become mentally retarded and many of these die at an early age.
Severe cases of hyperhomocysteinemia are easily diagnosed because they are so apparent: birth traumas, abnormal development, and mental retardation. However, the illness can break out at many different stages in life and in very different degrees of severity.
In many cases, it is not a matter of either/or as it is with some hereditary illnesses, and it cannot be said that either you have hyperhomocysteinemia or you are "normal" and are 100 % sure of not having it.
The research also indicates that the biochemical picture is much more complicated. In reality, there are 4 different kinds of hyperhomocysteinemia, and in practice there are patients who are completely without the enzyme and who are actually doomed, others who at birth or early in their lives become hopelessly crippled and who will live short lives, and finally the ones who do not feel the symptoms until late in life, and for whom the symptoms vary greatly.
Somewhere on this scale we can therefore expect to find people who have an almost sufficient enzyme production, sufficient enough that no remarkable symptoms are noted, and for these people to appear healthy and normal. However, in practice, these people are still strained enough to carry a risk factor, and under unfavourable conditions it can provoke illnesses which are really caused by a "mild" form of - almost always undiagnosed - hyperhomocysteinemia!
Therefore, the question arises: How many of us may suffer from such a "mild" form of undiagnosed hyperhomocysteinemia?
So far, research indicates that we are talking about a fair amount of people. The amount is probably so large that undiagnosed hyperhomocysteinemia may very contribute for one the greatest killer diseases of our time: arteriosclerosis. Moreover, it may also be a factor for a number of other illnesses.
The reason why these less distinct cases of hyperhomocysteinemia remain undiagnosed is first and foremost because they can be hard to spot, but also that conventional doctors expect that these cases have been diagnosed earlier in the patients' lives, and therefore they are not on the lookout for this disease in the ordinary practice.
Most medical laboratories are actually not geared to take the blood tests that can reveal the condition. Moreover, there is little understanding for the fact that a relatively low degree of hyperhomocysteinemia can easily be worsened, because the illness - just like any other enzyme dependent relation - is susceptible to age, stress, and malnutrition. However, the involved enzymes do not work within a vacuum; in the body they depend on the presence of concurrent factors which in this case is mainly the B-vitamins. A vitamin B deficiency is therefore a great strain even in cases of a mild condition of hyperhomocysteinemia, and especially among the middle-aged it is often the real reason why the illness breaks out and manifests itself as arteriosclerosis, brittleness of the bones, or another one of the degeneration illnesses. We often tend to look elsewhere for the reason for theses illnesses. .
As one would expect, most cases of adult or late hyperhomocysteinemia is affected positively by B-vitamins. We are mainly talking about vitamin B6 (pyridoxine), folic acid, and vitamin B12 (cobalamin). Other nutrients, e.g. zinc, also play a significant part. The sensitive enzyme mechanism and its level of activity is stimulated by these factors, and thereby the accumulation of homocysteine in the tissue is reduced.
This is the good news that in many cases allows us to treat hyperhomocysteinemia as an ordinary deficiency condition - along with scurvy, beri-beri and pellagra - and thereby cure the illnesses which accompany the condition. It also gives us an opportunity to acknowledge the widespread hidden presence of hyperhomocystenemia and from this awareness prevent one of the most severe and often lethal illnesses of our time.
But before we proceed it may be wise to ask: How new is this piece of news? - In 1998 a team of scientists wrote: "Since the first reports from Rinehart and Greenberg in 1948 concerning the connection between arteriosclerosis and a pyrodoxine defiency, numerous tests have further extended the role of pyrodoxine in the prevention of arteriosclerosis. A pyrodoxine deficiency (B6) leads to an accumulation of homocysteine which damages the parietal cells (the endothelium) and this causes arteriosclerosis."
Some people have both in writing and in speech had the opportunity early to point out the inconsistencies in the theory that cholesterol is the sole factor in developing atherosclerosis at a time when this kind of heresy caused a foaming rage among the true believers. Since then this theory has crackled severely, and the large cracks in the foundation have become only too apparent. A Danish doctor has performed a very accurate and critical analysis of this foundation - that is, the large surveys that supported the theory - and he found them not viable. His book on the subject has, interestingly enough, come out in Swedish but not in Danish! He is, however, not alone. Numerous surveys performed on clearly defined groups of people with clearly defined dietary patterns contradict the cholesterol theory.
Moreover, there are all the cases of arteriosclerosis and heart disease where the "cause" - the villain cholesterol - could not be traced in the body affected. However, an abnormal accumulation of homocysteine was found.
Hyperhomocysteinemia is a word that most of us would rather not have to learn and be forced to handle in writing and in speech. Until recently, the 9 syllables have been a problem in the media. Even in medical reference books the word is often missing. However, there is much indicating that we need to know this word and it is bound to come up more often in the future. In the more advanced circles of therapists, hyperhomocysteinemia is already a hot topic, and it can become important for one's own health to know what lies behind the name.
There are many good reasons to learn the 9 syllables by heart.
