Homocystein
Homocysteine
 
By  Dr. Steve Windley, MD
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TAKE YOUR MARK

Homocysteine as a natural internal indicator.

Although its importance has fallen in and out of favor in recent years, integrative physicians maintain that homocysteine values can help determine risk for inflammatory conditions such as heart disease, stroke and Alzheimer’s disease. This naturally-occurring amino acid has potential as a clinical indicator of disease in the blood vessels as well.
      Homocysteine should be utilized like other markers, such as cholesterol, to better understand one’s health and potential areas for intervention. Research has gone on for decades, but too few patients realize what homocysteine is in relation to their body. This article is geared toward educating patients on the role of homocysteine in their wellness program.
      While all of us have some homocysteine in our system, experts believe that too much can be a marker of potential damage to the blood vessel walls. Patients with higher levels of homocysteine in their blood have been shown to have a higher risk of stroke [1,2]. Additionally, high levels have been connected to depression, dementia, osteoporosis, heart disease and macular degeneration [3,4,5,6,7,8,9,10,11,12,13].
      A simple blood test is needed to check your homocysteine level. This can be done through most medical labs, and is commonly administered as a fasting test. The reference range for homocysteine will vary, but commonly goes from 0-13, with optimal values recommended at less than 9 (umol/liter) [10]. The homocysteine test should be considered for all adults. Patients with a normal homocysteine level can continue this evaluation in coordination with other annual screening markers like cholesterol. Patients who are not at goal levels need to have their status followed to achieve appropriate treatment and maintenance therapy.
      The best part about homocysteine is that treatment of an imbalance is very simple, cost-effective and safe. Homocysteine levels can be successfully lowered with a combination of B vitamins, particularly B-6 (pyridoxine), B-12 (cobalamin) and folic acid. Dosing for this regimen should include:

• B-12. 1000 mcg daily.
B-6. 20-50 mg daily
• Folic acid. 400-800 mcg daily

Some patients may not see adequate results from the above regimen. Typically, these patients need specific types of these nutrients, particularly B-12 and folic acid. The ability to absorb and use folic acid and B-12 will be enhanced by using the methyl- forms of these vitamins, methylcobalamin and 5-methyltetrahydrofolate. Dosage can be adjusted based on response.
      Homocysteine does not cause symptoms, whether its value is high or low. Because of its relationship with chronic illness, homocysteine offers a simple variable that patients can use to lower their risk of disease. It is yet another tool to help you stay on the path to optimal wellness.

References:
1. Virtanen, J.K., Voutilainen, S., Happonen, P., et al. (2005). Serum homocysteine, folate and risk of stroke: Kuopio Ischaemic Heart Disease Risk Factor (KIHD) Study. Eur J Cardiovasc Prev Rehabil, 12(4):369-75.
2. Clarke, R., Daly, L., Robinson, K., et al. (1991). Hyperhomocysteinemia: an independent risk factor for vascular disease. N Engl J Med, 25;324(17):1149-55.
3. Bottiglieri, T., Laundy, M., Crellin, R., et al. (2000). Homocysteine, folate, methylation and monoamine metabolism in depression. J Neurol Neurosurg Psychiatry. 69(2):228-32.
4. Sachdev, P.S., Parslow, R.A., Lux, O., et al. (2005). Relationship of homocysteine, folic acid and vitamin B-12 with depression in a middle-aged community sample. Psychol Med, 35(4):529-38.
5. Postiglione, A., Milan, G., Ruocco, A., et al. (2001). Plasma folate, vitamin B-12, and total homocysteine and homozygosity for the C677T mutation of the 5,10-methylene tetrahydrofolate reductase gene in patients with Alzheimer’s dementia. A case control study. Gerontology, 47(6):324-9.
6. Quadri, P., Fragiacomo, C., Pezzati, R., et al. (2004). Homocysteine, folate, and vitamin B-12 in mild cognitive impairment, Alzheimer disease, and vascular dementia. Am J Clin Nutr, 80(1):114-22.
7. Seshadri, S., Beiser, A., Selhub, J., et al. (2002). Plasma homocysteine as a risk factor dementia and Alzheimer’s disease. N Engl J Med, 346(7):476-83.
8. van Meurs, J.B., Dhonukshe-Rutten, R.A., Pluijm, S.M., et al. (2004). Homocysteine levels and the risk of osteoporotic fracture. N Engl J Med, 350(20):2033-41.
9. Stampfer, M.J., Malinow, M.R., Willett, W.C., et al. (1992). A prospective study of plasma homocysteine and risk of myocardial infarction in U.S. physicians. JAMA, 268(7):877-81.
10. Nygård, O., Nordrehaug, J.E., Refsum, H., et al. (1997). Plasma homocysteine levels and mortality in patients with coronary artery disease. N Engl J Med, 337(4):230-6.
11. Wald, N.J., Watt, H.C., Law, M.R., et al. (1998). Homocysteine and ischemic heart disease: results of a prospective study with implications regarding prevention. Arch Intern Med, 158(8):862-7.
12. Seddon, J.M., Gensler, G., Klein, M.L., Milton, R.C. (2006). Evaluation of plasma homocysteine and risk of age related macular degeneration. Am J Ophthalmol, 141(1):201-3.
13. Kamburoglu, G., Gumus, K., Kadayifcilar, S., Eldern, B. (2006). Plasma homocysteine, vitamin B-12 and folate levels in age-related macular degeneration. Graefes Arch Clin Exp Ophthalmol, 244(5):565-9.

Other Trusted Sources:
American Heart Association
Web MD

 
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