Archive for December, 2007

Dec 18 2007

Creatine, Astragalus and Ginseng May Enhance Strength Training in Seniors

Older strength trainers who supplement with a combination of creatine, ginseng and astragalus experience increased strength, vigor and lean mass, researchers recently reported. The scientists investigated the effects of these supplements on 44 adults aged 55 to 84 years who were participating in a 12-week strength-training program. Continue Reading »

No responses yet

Dec 18 2007

Creatine Review Investigates Amino Acid’s Supportive Role in Muscular Dystrophy Patients

A new review of the medical literature indicates that the amino acid creatine may increase muscle strength in muscular dystrophy patients. There are 30 or more genetic and hereditary muscle diseases that fall under the category of muscular dystrophies. Continue Reading »

No responses yet

Dec 18 2007

Creatine and Whey Protein: Consuming Before Load-Bearing Exercise Produces Best Results

Consuming creatine monohydrate and whey protein immediately prior to load-bearing exercise results in greater gains in muscle and strength compared to taking the supplements at other times during the day, a soon-to-be-published study reports. Continue Reading »

No responses yet

Dec 18 2007

Selenium and Vitamins B6 and B12 Levels Linked to Active Life in Seniors

A new study indicates that women who have high serum concentrations of selenium and vitamins B6 and B12 have a significantly reduced risk of age-related disability in conducting daily activities, leading researchers to suggest that nutritional status is an important factor in helping the elderly live an active life longer. Continue Reading »

No responses yet

Dec 18 2007

Folic Acid and Vitamin B12 Linked to Healthy Bones in Japanese Study

Folic acid and vitamin B12 supplements reduce the risk of hip fractures in elderly Japanese patients following a stroke, researchers report in a new study in the Journal of the American Medical Association(JAMA). Stroke increases the risk of subsequent hip fracture by 2 to 4 times. Continue Reading »

No responses yet

Dec 04 2007

Homocysteine

Published by under Cardiovascular

Homocysteine

Its Destructive Role in Cardiovascular, Cognitive and Bone Health

Homocysteine is one of the most destructive compounds found in the human body. Although oxidized LDL cholesterol (the “bad” cholesterol) is commonly considered the arteries’ worst enemy, homocysteine has emerged as an equally powerful threat to heart health. In fact, research now shows that damage from homocysteine paves the way for LDL to have an even more destructive effect on the vascular system, indicating these two agents can work together to cause heart disease. Furthermore, as time goes on, more and more research is uncovering homocysteine’s role in other health conditions such as infertility, depression, cognitive decline and bone fractures.

Homocysteine is considered a primary risk factor for cardiovascular disease including stroke and deep vein thrombosis.1 Elevated blood levels of homocysteine also are considered an independent risk factor for atherosclerosis and thromboembolism (the obstruction of a blood vessel by a clot), and are correlated with a significant risk for coronary, cerebral and peripheral vascular disease, myocardial infarction (heart attacks), peripheral vascular occlusive disease, cerebral vascular occlusive disease, and retinal vascular disease.2 In fact, high homocysteine, even in the absence of other risks, such as smoking and obesity, is a serious but controllable risk factor for heart disease.

Homocysteine is an amino acid commonly found in the blood as a result of protein metabolism. It is mainly derived from another amino acid known as methionine, which is found in a number of food sources primary among them being meat. Blood levels of homocysteine can also be affected by genetic and physiologic factors.

Homocysteine is thought to cause vascular disease because of its effect on blood vessel walls. Homocysteine binds to certain proteins in the body affecting their structure and function. The binding of homocysteine to proteins will degrade and inhibit repair and maintenance of three main vascular connective tissue structures—cartilage, elastin and proteolgycans—making them more susceptible to disease processes, including vascular disease. Homocysteine can damage the cells lining the artery walls (known as the endothelium) in the vascular system. Homocysteine causes a reduction in nitric oxide activity, impairing blood vessels’ ability to dilate and leaving the endothelium more susceptible to oxidative damage.3 Damaged vascular walls will then allow more low density lipoprotein (LDL) to be absorbed, further harming the vessel. This damage then promotes the growth of new smooth muscle cells within the vessel, which then narrows it. Endothelial damage also allows for increased platelet adhesiveness and activation of the clotting cascade, increasing the risk of cardiac arrest (heart attack) or cerebrovascular accident (stroke).

HomocysteineIn the Western world, homocysteine serum levels are most commonly found at 10-12 μmol/L. A level above 12 is generally considered elevated while levels below 6 are considered minimal. An increase of homocysteine levels by 5 μmol/L has been shown to increase the risk of cerebrovascular disease in the general population by 50 percent, and will increase the risk of coronary artery disease by 80 percent in women and 60 percent in men. In general, women have 10-15 percent less homocysteine than men during their reproductive years, which is thought in part to be the reason why women have fewer heart attacks than men, and why they tend to have them 10-15 years later than the time men commonly do.4

Genetic Causes of High Homocysteine

Dietary factors, while often cited as the chief cause for elevated homocysteine, are not the only factor. A rare hereditary disease known as homocystinuria results in several systemic disorders and is charachterized by the accumulation of homocysteine in the blood and an increased rate of excretion in the urine. Nearly 25 percent of people with this disorder die from cardiovascular complications before the age of thirty.

Ten percent of the population in general have another more common yet related condition where they are unable to effectively metabolize homocysteine and will be predisposed to the negative effects of elevated homocysteine levels, including blood clots and cardiovascular disease. This disorder is known as a methylenetetrahydrofolate-reductase (MTHFR) polymorphism genetic trait. People that have this condition are unable to effectively metabolize homocysteine and will be predisposed to the negative effects of elevated homocysteine levels, including blood clots and cardiovascular disease.

Homocysteine’s Widespread Role

Elevated homocysteine, also known as hyperhomocysteinemia, may contribute to many other conditions.

Infertility

Women who have high levels of homocysteine have been shown to have a more difficult time getting pregnant and are two times as likely to have complications during pregnancy. Furthermore, women with high homocysteine levels are at risk of having miscarriages early in pregnancy.5-6 Researchers are not sure what role homocysteine has in infertility, but it has been theorized that high homocysteine contributes to subfertility, or difficulty achieving a pregnancy.

Mental Health

Elevated levels of homocysteine are also a risk factor for diseases affecting the brain. Epidemiologic studies show a dose-dependent relationship between homocysteine levels and risk for neurodegenerative diseases such as stroke, Parkinson’s disease, multiple sclerosis, and depression.7 Researchers continue to collect evidence that correlates several cardiovascular disease risk factors, homocysteine being one, with the incidence of cognitive decline and Alzheimer’s disease.8 High homocysteine by itself is considered a strong independent risk factor for dementia and Alzheimer’s disease. A study looking at data collected from the Framingham Study showed that a homocysteine level over 14 μmol/L increased the risk of developing Alzheimer’s disease by 150 percent.9

Bone Fractures

Homocysteine is considered an independent risk factor for osteoporosis fractures in the elderly.10 It is thought that homocysteine leads to fractures in the same way in which it contributes to heart disease in that homocysteine affects certain connective tissue proteins and prevents them from functioning correctly. In the case of fractures, homocysteine interferes with the cross-linking ability of collagen (a major connective tissue protein) with the tissues it supports such as the skeletal system. Because homocysteine affects the structural proteins of which bone is comprised, it does not actually affect bone density. Therefore, traditional measures used to build bones (weight bearing exercise, adequate calcium and vitamin D, etc.) will not necessarily correct the damage from homocysteine on the bones.

Controlling Elevated Homocysteine

HomocysteineCurrently, there is no standard recommendation that all people have their homocysteine levels checked. Despite this, the American Heart Association does encourage testing for homocysteine in people with a personal or family history of heart disease. In order to address all possible aspects of heart disease (and other conditions), testing homocysteine levels is a good idea.

Controlling homocysteine can be achieved by supplementing with 4 common nutrients: vitamins B6, B12, folic acid and betaine. Vitamins B6, B12, and folic acid blood levels are found to be inversely related to plasma homocysteine concentration. Combination therapy with the aforementioned vitamins provides an effective way to reduce homocysteine levels,11 and side effects of this therapy are relatively unknown.12 Another supplement that has demonstrated usefulness in lowering homocysteine levels is betaine, also known as trimethylglycine.

High dietary consumption of methionine, which can be found in meats and dairy products, can result in the overproduction of homocysteine. Once homocysteine is produced it is metabolized in the body through one of two possible pathways—remethylation or transsulfuration. Remethylation is a process that utilizes folate, vitamin B12 or betaine (trimethylglycine) to convert homocysteine back to methionine. Alternately, transsulfuration utilizes vitamin B6 (pyridoxal-5-phosphate) to break down excess homocysteine into a number of metabolites for eventual excretion from the body.13,3 B6 has been shown to be effective in reducing homocysteine levels following the ingestion of significant amounts of methionine.14

Vitamin B12 in the form of methylcobalamin is needed for the conversion (remethylation) of homocysteine back to methionine.15 This remethylation reaction also requires folic acid. B12 is thought to provide an additive effect to the lowering of homocysteine when supplied in conjunction with folic acid.16

Folic acid is needed for the metabolism of homocysteine; low levels of folate in the blood are associated with higher levels of homocysteine. Folic acid is involved in one of the two pathways (remethylation) by which homocysteine is metabolized; this pathway also requires vitamin B12. Enzymes involved in remethylation of homocysteine are dependent upon folate and vitamin B12.17-18 Supplementation with folic acid will increase the activity of the remethylation pathway and thereby reduce homocysteine levels.19

Betaine is derived from choline and occurs naturally in the body. It can also be found in foods like cereal, seafood, spinach and beets, to name a few. Betaine acts as a methyl donor and contributes in the remethylation pathway when converting homocysteine back to methionine,20 thereby reducing homocysteine levels. Betaine has been shown to lower homocysteine levels in the majority of patients unresponsive to vitamin B6 therapy. In one study, daily doses of 250 mg of vitamin B6, 5 mg of folic acid, and 6 gm of betaine by themselves or in combination normalized the majority of high homocysteine levels in patients administered high doses of methionine.21

Homocysteine-lowering strategies also include a diet low in methionine since homocysteine is an intermediate product of methionine metabolism in the body. Foods rich in methionine include cheddar cheese, eggs, chicken, and beef.


Conclusion

Homocysteine is considered a primary, independent risk factor for cardiovascular disease and is thought to contribute to a host of other conditions such as miscarriages and difficult pregnancy, bone fractures, strokes, blood clots, depression, dementia, Alzheimer’s and Parkinson’s diseases. Due to this amino acid’s role in a host of diseases, individuals at risk for high homocysteine levels should consider a supplement regimen that includes vitamins B12 and B6, folic acid, and betaine. The physicians at Griffin Medical Group can prescribe a treatment protocol to help lower homocysteine levels.

References

1. Blum A, Hijazi I, Eizenberg MM, Blum N. Homocysteine (Hcy) follow-up study. Clin Invest Med. 2007;30(1):21-5.

2. Lentz SR. Mechanisms of homocysteine-induced atherothrombosis. J Thromb Haemost. 2005 Aug;3(8):1646-54.

3. Keebler ME, De Souza C, Fonesca V. Diagnosis and treatment of hyperhomocysteinemia. Curr Atheroscler Rep. 2001;3:54-63.

4. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A quantitative assessment of plasma homocysteine as a risk factor for vascular disease. Probable benefits of increasing folic acid intakes. JAMA. 1995;274:1049-57.

5. D’Uva M, Di Micco P, Strina I, et al. Hyperhomocysteinemia in women with unexplained sterility or recurrent early pregnancy loss from Southern Italy: a preliminary report. Thromb J. 2007 Jul 11;5:10.

6. Forges T, Monnier-Barbarino P, Alberto JM, et al. Impact of folate and homocysteine metabolism on human reproductive health. Hum Reprod Update. 2007 May-Jun;13(3):225-38. Epub 2007 Feb 16.

7. Herrmann W, Lorenzl S, Obeid R. Review of the role of hyperhomocysteinemia and B-vitamin deficiency in neurological and psychiatric disorders–current evidence and preliminary recommendations] Fortschr Neurol Psychiatr. 2007 Sep;75(9):515-27.

8. Rosendorff C, Beeri MS, Silverman JM. Cardiovascular risk factors for Alzheimer’s disease. Am J Geriatr Cardiol. 2007 May-Jun;16(3):143-9.

9. Seshadri S, Beiser A, Selhub J, et al. Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. N Engl J Med. 2002 Feb 14;346(7):476-83.

10. Perier MA, Gineyts E, Munoz F, Sornay-Rendu E, Delmas PD. Homocysteine and fracture risk in postmenopausal women: the OFELY study. Osteoporos Int. 2007 Oct;18(10):1329-36.

11. Krishnaswamy K, Lakshmi AV. Role of nutritional supplementation in reducing the levels of homocysteine. J Assoc Physicians India 2002 May;50 Suppl:36-42.

12. O’Connor JJ, Meurer LN. Should patients with coronary disease and high homocysteine take folic acid? J Fam Pract. 2003 Jan;52(1):16-8.

13. Sunder-Plassmann G, Winkelmayer WC, Fodinger M. Therapeutic potential of total homocysteine-lowering drugs on cardiovascular disease. Exp Opin Invest Drugs. 2000;9:2637-51.

14. Mayer EL, Jacobsen DW, Robinson K. Homocysteine and coronary atherosclerosis. J Am Coll Cardiol. 1996;27:517-27.

15. Selhub J, Jacques PF, Bostom AG, et al. Relationship between plasma homocysteine and vitamin status in the Framingham study population. Impact of folic acid fortification. Publ Health Rev. 2000;28:117-45.

16. Landgren F, Israelsson B, Lindgren A, et al. Plasma homocysteine in acute myocardial infarction: homocysteine-lowering effect of folic acid. J Intern Med. 1995;237:381-8.

17. Woodside JV, Yarnell JW, McMaster D, et al. Effect of B-group vitamins and antioxidant vitamins on hyperhomocysteinemia: a double-blind, randomized, factorial-design, controlled trial. Am J Clin Nutr. 1998;67:858-66.

18. Fohr IP, Prinz-Langenohl R, Bronstrup A, et al. 5,10-Methylenetetrahydrofolate reductase genotype determines the plasma homocysteine-lowering effect of supplementation with 5-methyltetrahydrofolate or folic acid in healthy young women. Am J Clin Nutr. 2002;75:275-82.

19. Vermeulen EG, Stehouwer CD, Twisk JW, et al. Effect of homocysteine-lowering treatment with folic acid plus vitamin B6 on progression of subclinical atherosclerosis: a randomised, placebo-controlled trial. Lancet. 2000;355:517-22.

20. Brouwer IA, Verhoef P, Urgert R. Betaine supplementation and plasma homocysteine in healthy volunteers (letter). Arch Intern Med. 2000;160:2546-7.

21. Boers GHJ. Hyperhomocystinemia: A Newly Recognized Risk Factor For Vascular Disease. Netherlands Journal of Medicine. 1994; 45:34-41.

No responses yet

Supply of hospital pharmacies operating externally due to cost savings will continue to grow all over the next years. Even today, 90% of all pharmacies pribolnichnyh organized in cooperation provisioning This shows that the Canadian pharmacy online has become not take seriously the business partner compared with the pharmaceutical industry. However, the development of recent years shows that the industry sees its price registration stronger with the number of sales, thus strengthening the competitiveness of supplying hospital pharmacies in the long term due to more efficient logistics and a lot of sales.