Vitamin treatment improves ED in men with elevated homocysteine
Vitamin treatment improves ED in men with elevated homocysteine
An article published online on August 17, 2009 in the Journal of Sexual Medicine describes research conducted at the University of Rome which found that it may be necessary to reduce homocysteine before treatment with erectile dysfunction (ED) can be effective.
The study included 75 men aged 25 to 65 with erectile dysfunction who were treated with sildenafil citrate (“Viagra”) for 2 months. Nonresponders to the drug were treated with a course of 600 milligrams vitamin B6 per week and 15 milligrams folic acid per day along with sildenafil for 6 weeks. Questionnaires concerning erectile function were administered before and after treatment.
Participants were evaluated for the presence of the MTHFR 677T mutation which is present in a higher percentage of heart disease patients than in those without the disease. Individuals with two copies of the mutation have levels of homocysteine that average 25 percent higher than the rest of the population, and which increase significantly when blood levels of folate are low. Twenty-seven percent of the subjects had both copies of the MTHFR 677T mutation and 48 percent had one copy, which is a greater frequency than the general populace.
All of the 18 patients who initially failed to respond to drug treatment had high levels of homocysteine and low folic acid levels. Subsequent to the 6 week course of vitamin therapy, folic acid levels increased, homocysteine concentrations declined, and all but two participants experienced improvement in ED.
The association of hyperhomocysteinemia with vascular disease supports the mechanism for homocysteine-reducing agents in improving ED, which is caused primarily by the same factors that affect the coronary arteries. “Measurement of plasma homocysteine and folic acid levels and molecular analysis of the MTHFR genotype should be added to the ED diagnostic procedure, especially in young patients or in those with a family history of cardiovascular disease," the authors conclude. "When this mechanism is implicated, treatment should first aim to reduce homocysteine levels through administration of folic acid, alone or in combination with vitamin B6 or B12, and then proceed to treatment with phosphodiesterase-5 inhibitors.”
Since the introduction of Viagra® (sildenafil citrate) in 1998, several other drugs for the treatment of ED have been introduced; it has become clear that ED is far more prevalent than may have been suspected previously. A study conducted in the Boston area from 1987 to 1989 found that 52 percent of men between the ages of 40 and 70 suffered some degree of ED (Feldman HA et al 1994). By extrapolation, about 30 million men are affected by ED in the United States (McKay D 2004). And given men’s ever increasing life span, it has been further estimated that the incidence of ED worldwide will more than double in the next quarter century (Goldstein I 2000).
Arginine is an amino acid the body uses to produce nitric oxide, which relaxes smooth muscle, thus allowing for increased blood flow in many parts of the body. This action may explain why ED is more common in men with forms of vascular disease in which disorders of nitric oxide play a role, such as ischemic heart disease and stroke. For example, 75 percent of men with ischemic heart disease suffer from ED (Kloner RA et al 2003).
Risk factors for ED include conditions such as high blood pressure, abnormally high blood lipids (i.e., elevated low-density lipoprotein cholesterol and triglycerides), obesity, diabetes, and smoking (McKay D 2004). Recently, some US scientists reported that it may be necessary to add aging itself to the list of risk factors that produce vascular dysfunction of the kind associated with ED. “The normal aging process may induce significant global vascular dysfunction (involving the endothelium and the vascular smooth muscle),” wrote scientists published in the International Journal of Cardiology. This age-associated dysfunction was judged to occur even in the absence of clinically diagnosed atherosclerosis and was related to alterations in the production of endothelial nitric oxide (Al-Shaer MH et al 2006).
The link between ED and vascular disease is so strong that physicians are advised to consider men who present with ED but no diagnosis of heart disease as undiagnosed cardiovascular patients until proven otherwise (Jackson G et al 2006). It is believed that alterations in the availability of vascular endothelial nitric oxide represent the common thread linking these interrelated pathologies (Sullivan ME et al 1999).
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