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marytabby
USA
545 Posts |
 Posted - 04/05/2005 : 17:02:19
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| My last appt. with an MD was almost two weeks ago, with a holistic doctor, the day after I started reading the MBP book. He was very supportive of me pursuing the mind/body approach and as a last ditch measure before I left his office after a full medical exam, he did a homocysteine test on me. Anyone know why he may have run that? I know it takes a month to get the results so I'm sure he'll be in touch in a few weeks. I'm just curious what he may have been looking for. I think he said something about fight or flight response but that could have been another conversation. Anyway, it's the last thing I had done as far as tests and I'm sure it's not going to reveal anything medical, but I couldn't find much online about that test. |
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kenny V
USA
268 Posts |
Posted - 04/05/2005 : 23:49:53
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Stay with reading Sarno’s book , journal, journal journal to break the pain cycle while understanding the MBP……….
Dr Sarno is a genius
Just for FYI only Homocysteine Has to do with detoxification
(very interesting stuff)
Methylation and Homocysteine
While there is a considerable amount we do not know about homocysteine (like why exercise reduces it), we do know how to use nutritional supplements to reduce homocysteine levels. This is done through three independent routes: (1) using folic acid with vitamin B-12, (2) using trimethylglycine (TMG), and (3) through B-6.
The first two are called methylation, and the last is called transsulfuration.
Methylation is the process of putting a methyl group (one carbon atom and three hydrogen atoms), on proteins, enzymes, chemicals, DNA, or amino acids like homocysteine. When a methyl group is transferred from folic acid to homocysteine, the homocystein is converted to the essential amino acid, methionine. When a methy group is transferred from TMG to homocysteine, the homocysteine is similarly converted to methionine (and TMG is converted to dimethylglycine). This process of methylation results in lower homocysteine and an increase in methionine. In fact, nearly twice the dietary level of methionine is produced during this conversion process. lencopyrighted lencopyrighted
Both folic acid and TMG have been used for nearly two decades to lower homocysteine. These two pathways are independent. Some people are better at using TMG to lower homocysteine and others are better at utilizing folic acid. That is why the literature suggests using both TMG and folic acid to lower homocysteine (folic acid requires B-12 for this activity). Such a combined approch, in conjunction with vitamin B-6, can normalize homocysteine in 95% of the people studied (Choline is also used as a methyl donor, as has been noted in JAMA, although its role is secondary to TMG).
Vitamin B-6 and Transsulfuration
The remaining method of lowering homocysteine is through a process using vitamin B-6. This is a separate process from methylation. Using B-6, the cells convert homocysteine to cystathionine and then to cysteine where it is either further processed and excreatedk or used in protein metabolism. This important method of lowering homocysteine is particularly relevant in the U.S. because B-6 is very unstable, and in today's diet of processed foods B-6 is destroyed and usually needs to be supplemented. In addition, B-6 is destroyed by smoking or birth control pills, which can explain the recent rise in vascular disease in women (remember vascular disease is cumulative, so women who started the pill in the 60's are now showing the results).
Supplemental B-6 is usually supplied in the form of pyridoxine HCL, even though the body uses B-6 in the form of pyridoxal 5' phosphate. Some people are not as efficient in converting pyridoxine HCL to pyridoxal 5' phophate, so a combined formulation is often suggested to insure that the B-6 is utilized.
Who's at Risk for Disorders Related to Homocysteine and Poor Methylation
1. Do you excercise less than three times a week? While excercise has long been known to help prevent many diseases including cardiovascular disease, there was no biological explanation until recently, when it was discovered that the risk factor known as homocysteine is reduced during exercise. lencopyrighted lencopyrighted
2. Is a significant amount of your diet derived from a box, a can, a bag, a freezer, or fast food? Processing foods removes vital nutrients required to maintain health. Processed foods contain a fraction of the critical vitamins, B-6, B-12, and folic acid. These nutrients are required to lower homocysteine and prevent cardiovascular disease. In addition, lack of these nutrients is related to carpal tunnel syndrome, anemia, polyp formation, rickets, and a variety of neurological and developmental conditions.
3. Did anyone in your family suffer from vascular disease? Recently, a genetic weakness in the body's ability to lower homocysteine has been linked to premature vascular disease. If your parents, grandparents, aunts, or uncles suffered from strokes, heart attack, angina, or any vascular disease, you are at an increased risk for vascular disease even if all your standard risk factors are normal. Fortunately, researchers have discovered that betain (TMG), combined with B-6, B12, and folic acid, can prevent much of the damage created by this silent genetic defect.
4. Do you eat less than three courses of vegetables and fruits per day, or consume a typical high protein diet? While the benefits of moderate protein intake and an abundance of fruits and vegetables have long been advocated by health professionals, it is often unrealistic. Recently, the government reduced the reccommended daily allowance (RDA) for folic acid simply because so few people were obtaining the required amount for proper health -- not because the body suddenly rrquired less vitamins. Only a diet high in fresh vegetables and fruits combined with moderate protein can keep our homocysteine levels low and allow for optimal health and longevity. In response to the reality of the American diet, the government has advocated using supplements in many foods, especially the methyl donor folic acid and B-6. lencopyright
5. Do You eat commercial non-organic vegetables and fail to eat foods high in minerals? Foods high in minerals include organic vegetables and sea vegetables. Both are common in Japan where both vascular disease and many of the types of cancer found in the U.S. are significantly less common. Minerals such as Zinc, Copper, and Magnesium are required to allow the enzymes that lower homocysteine to function properly and maintain proper DNA methylation (described later).
6. Is there a history of depression, neurological disease, fatty-liver, or "weak" liver in your family? Often, depression and neurological disease are related to low S-adenosylmethionine levels (SAM), which are directly related to high homocysteine levels and poor methlation. Research journals have shown that the nutritional supplement betaine and the other methyl donors can significantly elevate the level of SAM. SAM is beneficial not only for depression, but has proven useful for some liver problems as well.
7. Do you smoke, or use birth control pills? Both smoking and birth controls pills elevate homocysteine levels.
If you answer 'YES" to ANY of the questions above, you are at risk for disorders related to homocysteine and poor methylation.
Scientific References
1. JAMA1 (vol. 277, No. 22, pg. 1776-1781, 1997)"In this study, users of vitamin preparations containing these nutrients appear to experience substantial protection from vascular disease, with a relative risk of 0.38 (95% CI 0.2-0.72) compared with nonusers of vitamins." [Interpretation: If a group of nonusers of vitamins contained 100 people with vascular disease, the same size group of vitamin users would expect only 38 people with vascular disease.]
2. Lancet2 (vol. 349, pg. 397. Feb 8, 1997) The present data extend the previous view that an increased level of plasma Hcy (homocysteine) may be a risk factor for CVD (cardiovascular disease)."
3. JAMA3 (vol. 268, pg. 877-881. Aug. 12, 1992) "Moderately high levels of plasma homocyst(e)ine are associated with subsequent risk of MI (myrocardial infarction) independent of other coronary risk factors. Because high levels can often be easily treated with vitamin supplements, homocyst(e)ine may be an independent, modifiable, risk factor." "Elevated homocyst(e)ine levels can often be normalized by modest doses of folate (1 to 5 mg/d). For cases that are resistant to this therapy, the addition of vitamin B6, choline, or betaine, is often effective. These supplements at the recommended dosages have few or no side effects under most circumstances."
4. Journal of Nutrition4 (vol. 126, pg. 1295s-1300s, 1996) "Long-term betain (TMG) supplementation of 10 patients, who had pyridoxine-resistant homocystinuria and gross hyperhomocysteinemia due to a deficiency of cystathionine ß-synthase activity, caused a substantial lowering of plasma homocysteine, which has now been maintained for periods of up to 13 years...We have found that prolonged betaine treatment, taken with concurrent vitamin B-6 and folic acid therapy, maintained its initial promise of lowering plasma homocysteine concentrations substantially in all patients."
5. JAMA5 (vol. 274, No. 19, pg. 1532, 1995) "(the data suggest) that exercise, especially heavy physical activity exerts its most favorable effect in subjects with hyperhomocysteinemia. Several studies have shown that there is a dose-dependent reduction in risk for coronary heart disease with physical activity, and a greater benefit has been demonstrated in older age groups. Since this effect cannot be fully explained by changes in other established risk factors, decreased plasma tHcy (total homocysteine) level may contribute to the beneficial effect of physical activity on coronary risk." "...in patients with homocystinuria, the risk of a fatal thromboembolic event is substantially reduced after Hcy-lowering therapy." lencopyright
6. Lancet6 (vol. 346, pg. 1395-98, 1995) "These findings suggest that tHcy (homocysteine) is a strong and independent risk factor for stroke." "Moderately elevated Hcy concentrations, reflecting less severe genetic defects and deficiency of nutritional factors required for Hcy metabolism (folic acid, vitamin B12, vitamin B6) are common in the general population. There are consistent data from more than 20 cross-sectional and case-control studies linking moderate hyperhomocysteinaemia with vascular disease, including peripheral vascular disease, ischaemic heart disease and stroke."
7. Lancet7 (vol. 349, pg. 1102-1103, April, 1997) "Conversely, macroangiopathy at the level of the heart and legs is associated with clinical signs of microangiopathy, such as retinopathy and kidney disease. Thus, moderate hyperhomocysteinaemia may represent a mechanism that accounts for the concomitant presence of the two conditions in patients with insulin-dependent diabetes."
8. New England Journal of Medicine8 (vol. 337, pg. 230, July 24, 1997) "Plasma total homocysteine levels are a strong predictor of mortality in patients with angiographically confirmed coronary artery disease."
9. Frankel, P. and Madsen, F., Your Life Depends On It! Understanding Homocysteine Methylation and Your Health, TRC, Publications: Thousand Oaks, CA 1997.
10. Graham, I.M. et al. Plasma homocysteine as a risk factor for vascular disease. "Journal of the American Medical Association, 277(22):1775-1781, 1997.
11. Alfthan, G., et al. Plasma Homocysteine and cardiovascular disease mortality. Lancet 349:397, 1997.
12. Stampfer, Meir J., et al. A prospective study of plasma homocyst(e)ine and risk of myocarial infarction in US physicians.Journal of the American Medical Association, 268(7):877-81, 1992.
13. Dudman, Nicholas P.B., et al. Human homocysteine catabolism: Three major pathways and their relevance to development of arterial occlusive disease. Journal of Nutrition, 126(4S):1295S-1300S, 1996.
14. Nygârd, O., et al. Total plasma homocysteine and cardiovascular risk profile. The Hordaland homocysteine study. JAMA 274(19):1526-33, 1995.
15. Perry, I.J., et al. Prospective study of serum total homocystein concentration and risk of stroke in middle-aged British men. Lancet 346:1395-98, 1997.
16. Vaccaro, O., et al. Moderate hyperhomocysteinaemia and retinopathy in insulin-dependent diabetes. Lancet 349:1102-1103,1997.
17. Nygârd, O., et al. Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med 337:230-236, 1997.
18. Cooney, C.A. Are somatic cells inherently deficient in methylation metabolism? A proposed mechanism for DNA methylation loss, senescence and aging. Growth, Development and Aging, 57(4):261-73, 1993.
19. McCully, K.S. Vascular pathology of homocysteinemia:implications for the pathogenesis of arteriosclerosis. American Journalof Pathology 56:111-128, 1969.
20. McCully, D.S. Homocysteine and vascular disease. Nature Medicine 2:386-389, 1996.
21. Gruber, Edward R. and Raymond, Stephen A., Beyond Cholesterol:Vitamin B6, Arteriosclerosis, and Your Heart. St. Martin's Press: New York, N.Y., 1981.
22. Malinow, M.R. Plasma homocyst(e)ine and arterial occlusive diseases: a mini-review. Clinical Chemistry, 41(1):173-6, 1995.
23. Dudman, N.P., et al. Disordered methionine/homocysteine metabolism in premature vascular disease. Its occurrence, cofactor therapy, and enzymology. Arteriosclerosis and Thrombosis, 13(9):1253-60, 1993.
24. van den Berg, M., et al. Combined vitamin B6 plus folic acid therapy in young patients with arteriosclerosis and hyperhomocysteinemia. Journal of Vascular Surgery, 20(6):933-40, 1994.
25. Steegers-Theunissen, R.P., et al. Neural tube defects and elevated homocysteine levels in amniotic fluid. American Journal of Obstetrics and Gynecology, 172(5):1436-41, 1995.
26. Mills, J.L. et al. Homocysteine metabolism in pregnancies complicated by neural tube defects. Lancet 345(8943):149-51, January 21, 1995.
27. Kagan, B.L. et al. Oral S-adenosylmethionine in depression: a randomized double-blind, placebo-controlled trial. American Journal of Psychiatry, 147(5):591-5, 1990.
28. Brandes, L.J. et al. Stimulation of malignant growth in rodents by antidepressant drugs at clinically relevant doses.Cancer Research, 52(13):796-800, 1992.
29. Kishi, T. et al. Effect of betaine on S-adenosylmethionine levels in the cerebrospinal fluid in a patient with methylenetetrahydrofolate reductase deficiency and peripheral neuropathy. Journal of Inherited Metabolic Disease. 17(5):560-5, 1994.
30. Barak, A.J. et al. Dietary betaine promotes generation of hepatic S-adenosylmthionine and protects the liver from ethanol-induced fatty infilteration. Alcoholism, Clinical and Experimental Research, 17(3):552-5, 1993.
31. Bostom, A.G. et al. Post-methionine load nyperhomocysteinemia in persons with normal fasting total homocysteine: initial results from the NHLBI family heart study. Atherosclerosis,<?I> 116:147-151, 1995.
32. Henderson, L.M. Vitamin B6. In: Present knowledge in Nutrition,5th, Ed., pages 303-317, The Nutrition Foundation, Inc. Washington, D.C.
33. Leklem, J.E. Vitamin B6: Reservoirs, receptors, and red-cell reactions. Ann NY Acad. Sci, 669:34-43, 1992.
34. Lieu, P.L. et al. Phospholipids, phospholipid methylation and taurine content in synaptosomes of developing rat brain. In: Taurine. Editors: Lombardini, J.B., et al Plenum Press, New York, 1992.
35. Schwade, Steve. Prevention, p. 74, July 1994.
36. Baylin, S.B. et al. Abnormal patterns of DNA methylation in human neoplasia: potential consequence for tumor progression. Cancer Cells 383-390, 1991.
37. Boers, G.H. Hyperhomocysteinaemia: a newly recognized risk factor for vascular disease. Netherlands Journal of Medicine, 45(1):34-41, 1994.
38. Bottiglieri, T. et al. The clinical potential of ademetionine (S-adenosylmethionine) in neurological disorders. Drugs, 48(2):137-52, 1994.
39. Butterworth, C>E. Jr. Folate status, women's health, pregnancy outcome, and cancer, Journal of the American College of Nutrition, 12(4)438-41, 1993.
40. Eskes, T.K. Possible basis for primary prevention of birth defects with folic acid. Mills Fetal Diagnosis and Therapy, 9(3):149-54, 1994.
41. Franken, D.G. et al. Treatment of mild hyperhomocysteinemia in vascular disease patients. Arteriosclerosis and Thrombosis, 14(3):465-70, 1994.
42. Friedel, Heather et al. S-Adensoyl-L-Methionine: A review of its pharmacological properties and therapeutic potential in liver dysfunction and affective disorders in relation to its physiological role in cell metabolism. Drugs, 38(3):389-416, 1989.
43. Giovannucci, Edward et al. Folate, Methionine and Alcohol Intake and Risk of Colorectal Adenoma. Journal of the National Cancer Institute, 85(11):875-84, 1993.
44. Holme, E. et al. Betaine for treatment of homocystinuria caused by methylenetetrahydrofolate reductase deficiency. Archives of Disease in Childhood, 64:1061-4, 1989.
45. Lucock, M.D. et al. The methylfolate axis in neural tube defects: in vitro characterisation and clinical investigation. Biochemical Medicine and Metabolic Biology, 52(2):101-14, 1994.
46. Montero, Brens C. et al. Homocystinuria: effectiveness of the treatment with pyridoxine, folic acid, and betaine. Anales Espanoles de Pediatria, 39(1):37-41, 1993.
47. Reynolds, E.H. and Stramentinoli, G. Folic acid, S-adenosylmethionine and affective disorder. Psychological Medicine,13:705-710, 1983.
48. Reed, S.M. Glick, J.N. Fluoxetine and reactivation of the herpes simplex virus. Am. J. Psychiatry 49:949-950, 1991.Scott, J.M. et al. Folic acid metabolism and mechanisms of neural tube defects. CIBA Foundation Symposium, 181:180-91,1994.
49. Steegers-Theunissen, R.P. et al. Maternal hyperhomocysteinemia: a risk factor for neural-tube defects? Metabolism:Clinical and Experimental, 43(12):1475-80, 1994.
50. Ueland, P.M. and Refsum, H. Plasma Homocysteine, a risk factor for vascular disease: plasma levels in health, disease,and drug therapy. Journal of Laboratory and Clinical Medicine, 144(5):473-501, 1989.
Always Hope For Recovery
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Anyone know why a homocysteine test is done?
