Homoscysteine Formula is designed to convert homocysteine into useful substances such as cysteine and glutathione, which will render homocysteine non-toxic. This product is so important we highly encourage you to read Dr. Preston’s full report. There he explains the full benefits of using the Homoscysteine Formula and Cholesterol Balance in conjunction with one another for preventing and reversing heart disease.
Homocysteine is an amino acid. Amino acids are the building blocks from which proteins are made. Many amino acids are essential to health. Homocysteine, however, is toxic, damaging the walls of arteries and triggering the deposition of plaque. It is also known to induce DNA damage and accelerate cell death.
Detecting an increased risk of direct homocysteine toxicity may not be the most important reason for checking homocysteine levels, however. Researchers are beginning to realize that elevated levels of homocysteine often reflect the body’s inability to perform ongoing maintenance and repair through a process called methylation.
Although most people have never heard the term, methylation is extremely important. Biochemically it is the transfer of a methyl group, which is comprised of one carbon atom and three hydrogen atoms (CH3), from one molecule to another.
Practically it is the process the body uses to manufacture critical hormones like adrenaline and melatonin, to tell genes when to exert their influence, to detoxify foreign substances in the liver, to manufacture new cells, and to repair free radical damage.
Homocysteine forms when methionine, an amino acid obtained from various foods, is used as a source of methyl groups. Diet does not play a major role in the process, however. It has been demonstrated that dietary intakes of methionine up to five times that typically consumed do not cause homocysteine levels to rise. The primary reason levels rise is a loss of methylation capacity. When the body’s methylation reserve is adequate, homocysteine is converted to either glutathione, an important antioxidant, or back to methionine. When the body’s methylation reserve is inadequate or methylation does not proceed normally, homocysteine accumulates. A wide range of diseases are associated with methylation deficiencies. Over 1500 published articles document the relationship to cardiovascular diseases including heart attack, stroke, hypertension, peripheral vascular disease, congestive heart failure, ischemic cardiomyopathy, venous thrombosis, and retinal vein occlusion.
Alzheimer’s disease and vascular dementia have both been shown to be associated with high homocysteine levels. Other neurological diseases including Parkinson’s Disease and multiple sclerosis show the same changes. Loss of methylation and elevated homocysteine levels have been found in chronic liver disease, depression, osteoporosis, acral purpura, and polycystic ovary disease.
Complications of pregnancy including premature birth, toxemia, and stillbirth are associated with elevations of homocysteine as are birth defects such as neural tube defects, heart defects, and Down’s Syndrome. Collagen diseases such as rheumatoid arthritis, lupus erythematosis, and scleroderma also commonly exhibit high levels of homocysteine. The same association has been found in many cancers, including those of the breast, cervix, colon, head and neck, and stomach. Failure of methylation appears to be one of the key factors triggering premature aging.
It is difficult to find a condition that is not linked to inadequate methylation. An analysis of elderly hospitalized patients in France, published in 2003, showed that 100 % had unsafe levels of homocysteine. A startling 45 % had levels above 15 mmol/L. A three-year study of elderly hospitalized patients in Italy, published in 2001, found that the mean homocysteine level was 16.8. Patients with the highest levels tended to present with the most serious diseases and had the highest incidence of atherosclerosis and impaired mental function. Analysis of homocysteine levels in population subgroups is revealing. Individuals who are receiving dialysis treatments have some of the highest homocysteine levels of any group, often above 50. They also have one of the highest rates of heart attack. An article published in the December 18, 2003 issue of the New England Journal of Medicine found the same to be true concerning a disease called Systemic Lupus Erythematous, often referred to simply as “lupus”. People who have SLE often die prematurely from a heart attack. The study found no increase in cholesterol or cholesterol risk ratios in lupus patients. What it did find was a significant increase in homocysteine levels. In contrast, people with Down’s syndrome have lower homocysteine levels than the general population, averaging between 2 and 3. This is due to the fact that a gene that regulates homocysteine metabolism is located on chromosome 21, an extra copy of which is carried by these individuals.
While heart birth defects are common in Down’s syndrome, heart attacks are not. I could find only one reported instance of an individual with Down’s syndrome having a heart attack.
A study of the cholesterol patterns of people with Down’s syndrome reveals something very interesting. The prevailing attitude is that high levels of cholesterol and LDL cholesterol (the so-called “bad” cholesterol) and low levels of HDL cholesterol (the so-called “good” cholesterol) cause heart attacks.
Individuals with Down’s syndrome have cholesterol and LDL levels that are no different than those in the general population and actually have LOWER than average levels of HDL cholesterol. If the cholesterol and heart disease theory is correct, people with Down’s syndrome should be having more heart attacks than the rest of the population, not less. It is therefore disappointing that the American Heart Association states, “The American Heart Association has not yet called hyperhomocysteinemia (high homocysteine level in the blood) a major risk factor for cardiovascular disease. We don’t recommend widespread use of folic acid and B vitamin supplements to reduce the risk of heart disease and stroke.” A clear and strong correlation of homocysteine levels to Alzheimer’s Disease has also been discovered. Studies in the International Journal of Geriatric Psychiatry, April 1998, and the Journal of Gerontology and Biological Sciences, March 1997, confirmed that people with Alzheimer’s disease have much higher homocysteine levels than others in their age group. A number of similar studies have confirmed the link. Despite the mounting evidence that high levels of homocysteine are associated with Alzheimer’s disease, the Alzheimer’s Disease Society has criticized the recommendation that people take folic acid supplements to lower their homocysteine levels. Their official position is, “No one knows whether taking (folic acid) supplements will help prevent the disease or whether it will affect the rate at which the disease progresses. The only way this will be discovered is by doing further studies on many, many more patients over a long period of time.”
The American Heart Association and the Alzheimer’s Disease Society are not alone in their resistance to homocysteine testing. Medicare excludes homocysteine testing as a benefit. The official Medicare position is that homocysteine testing is “not medically necessary.” Skeptics support the position that any link between homocysteine and disease is unproven by pointing to studies that appear to be inconclusive. These studies typically compare homocysteine levels in people having a particular disease with the levels in a control group of people without the disease using a “normal” cutoff of 15 mmol/L. These studies are failing to recognize an important fact, which is that there is no “normal” level of homocysteine. The American Journal of Epidemiology reported in 1996 that when homocysteine rises from 7 mmol/L to 10 mmol/L the risk of heart attack jumps 35 percent. Other studies looking at the incidence of disease at progressively rising homocysteine level have shown similar results.
With the average level of homocysteine standing at 10, it is not surprising that studies comparing people who have had a heart attack or have developed Alzheimer’s disease with the population at large have reported inconclusive results. One must compare the disease incidence in individuals with high levels of homocysteine with that in those with low levels to draw a logical conclusion. If it were not possible to support methylation and control homocysteine levels the reluctance of physicians and organizations to accept the link between homocysteine and degenerative diseases might be understandable. The truth, however, is that elevated homocysteine levels Methylation requires adequate numbers of methyl groups along with optimum levels of folic acid, B-12, and zinc. Taking a broad-spectrum nutritional supplement that contains optimum levels of B vitamins and zinc will assure safe homocysteine levels in approximately 40 percent of those doing so.
Homocysteine can be converted to useful substances such as cysteine and glutathione, provided that adequate levels of B-6 and magnesium are present. This process is limited by genetic deficiencies in cystathionine-B-synthase and B-6 conversion enzyme, however. While some advocate increasing the amount of B-6, B-12, and folic acid further when homocysteine levels remain elevated, this is rarely effective. Adding other nutrients is usually necessary and much more efficient in achieving the desired result.One of these additional nutrients is N-acetyl cysteine.N-acetyl cysteine is an amino acid that combines with homocysteine to form a substance that is efficiently excreted by the kidneys. 500 mg. of N-acetyl cysteine should be taken twice daily.The other beneficial nutrient is N-N, dimethylglycine (DMG). This is a rich source of methyl groups. While some advocate the use of trimethylglycine, the body must convert this to dimethylglycine using an enzyme called betaine-homocysteine methyl transferase (BHMT). As DMG accumulates this process slows down. This limits the effectiveness of supplemental trimethylglycine. 400 mg. of DMG twice daily is usually effective. The combination of B vitamins, N-acetyl cysteine, zinc, magnesium and DMG will reduce homocysteine levels to a safe range in nearly all cases. These nutrients are present in HCY Formula, a product formulated to address methylation failure and homocysteine accumulation. The connection between Vitamin B-6 and heart diseasewas reported as early as 1948 and the connection between B-12 deficiencies and dementia was reported in 1969. The homocysteine connection was recognized as early as 1980. The suggestion that people should wait to lower homocysteine until the results of long-term studies conclusively prove the consequences of ineffective methylation to everyone’s satisfaction is absurd.
If you do not know your homocysteine level I encourage you to have it checked immediately and, if it is over 7, take steps to bring it into a safer range. Because the body’s methylation capacity tends to diminish with age and can fall off quickly, everyone over the age of 70 should check their homocysteine level annually. The mechanisms that trigger and direct the aging processare complex, but a great deal has been learned in the past two decades. The free radical theory of aging, which states that aging occurs primarily because the cells and tissues of the body are attacked and damaged by unbalanced molecules has led to a greater understanding of the body’s antioxidant defense system and the nutrients that must be provided to maintain its effectiveness. It has become clear that methylation is the primary mechanism the body uses to repair free radical damage and that homocysteine levels are a reliable indicator of the body’s ability or inability to perform maintenance and repair tasks.
By providing antioxidant nutrients to minimize free radical damage and methylation nutrients to support the repair of the damage that does occur, each of us can expect to age gracefully and die biologically young at an advanced chronological age.