B Complex & Intermittent Claudication
BiGol...@aol.com
extremities. With the increased incidence of HIV-related and
HAART-related vascular disease, these problems may be increasing.
In a 1/99 review, as concerns homocysteine and cardiovascular disease,
Prasad states: "Folic acid, vitamin B12 and B6 have been shown to be
beneficial in reducing plasma homocysteine levels. Folic acid is
specifically very effective, safe and inexpensive."
Apparently, there is a relationship between increased levels of
homocysteine and intermittent claudication (Molgaard et al., 1992).
On 1/15/99, the FDA approved Pletal (cilostazol) for the painful leg
syndrome known as intermittent claudication. The disorder causes severe
pain or cramping in patients who have poor blood circulation in their
legs. It results from the hardened fatty blockages that mark heart
disease and related arterial disease.
There is some criticism that the drug may endanger certain heart
patients. Patients with any degree of heart failure have been warned
not to take the drug because of the known danger of similar medication.
It has only been approved for intermittent pain and not for more severe
conditions.
It has been shown that B complex can reduce nocturnal leg cramps caused
by hypertension (Chan et al., Journal of Clinical Pharmacology 1998
Dec;38:1151-1154).
Would B complex (folate/folic acid + vitamin B12 + vitamin B6 +
choline), used two or three times a day, be of value as a therapy for
intermittent claudication and less toxic than the newly approved drug
Pletal (cilostazol)?
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Prasad K. Homocysteine, a Risk Factor for Cardiovascular Disease.
International Journal of Angiology 1999 Jan;8(1):76-86
Department of Physiology and Associate Member, Department of Medicine,
College of Medicine, University of Saskatchewan, Saskatoon, Canada
Abstract: Fasting hyperhomocysteinemia is an independent risk factor for
coronary artery disease, stroke, peripheral vascular atherosclerosis,
and for arterial and venous thromboembolism. The risk for cardiovascular
disease with homocysteine is similar to conventional risk factors. The
interaction of hyperhomocysteinemia with hypertension and smoking is
strong and the combined effect is more than multiplicative. The combined
effect of homocysteine and cholesterol is additive. Homocysteine
produces atherosclerosis, thromboembolism, and vascular endothelial cell
injury. Vascular dysfunction produced by homocysteine may be due to
endothelial cell damage. Homocysteinemia-induced atherosclerosis is
probably due to various factors including endothelial cell injury,
inability to sustain S-nitroso-homocysteine formation because of
imbalance between production of nitric oxide by dysfunctional
endothelium and homocysteine, smooth muscle cell proliferation, and
thromboembolism. There is strong evidence that endothelial cell injury
is associated with oxidative stress produced by homocysteine.
Hyperhomocysteinemia is associated with numerous conditions, including
coronary disease, stroke, peripheral vascular disease (carotid artery
and cerebrovascular atherosclerosis), venous thrombosis, renal disease,
diabetes mellitus, and organ transplant. Folic acid, vitamin B12 and B6
have been shown to be beneficial in reducing plasma homocysteine levels.
Folic acid is specifically very effective, safe and inexpensive.
=============================
Molgaard J, Malinow MR, Lassvik C, Holm AC, Upson B, Olsson AG.
Hyperhomocyst(e)inaemia: an independent risk factor for intermittent
claudication. J Intern Med 1992 Mar;231(3):273-9
Department of Internal Medicine, Faculty of Health Sciences, University
Hospital, Linkoping, Sweden.
Abstract: The aim of this study was to test the question of
hyperhomocyst(e)inaemia as a risk factor for intermittent claudication
(IC) independent of other important risk factors for peripheral
atherosclerotic disease, such as smoking, hypertension, diabetes mellitu
s, hypercholesterolaemia, hypertriglyceridaemia, low levels of
high-density-lipoprotein (HLD) cholesterol and age. The study population
was recruited from an epidemiological study in Linkoping County, Sweden,
where all middle-aged men (n = 15,253, 45-69 years of age) were screened
for IC. Seventy-eight subjects with verified IC and 98 healthy sex- and
age-matched controls were randomly selected. Plasma levels of
homocyst(e)ine (including the sum of free and bound forms of
homocysteine and their disulphide oxidation products, homocystine, and
homocysteine-cysteine mixed disulphide) were significantly higher (16.74
+/- 5.45 mumol l-1, mean value +/- SD, P = 0.0002) in IC subjects than
in controls (13.80 +/- 3.21 mumol l-1), with 23% of the claudicants
above the 95th percentile for controls. Stepwise logistic regression
analysis revealed that the difference in plasma homocyst(e)ine was
independent of the other above-mentioned risk factors. Moreover, the
elevation of plasma homocyst(e)ine in claudicants was mainly confined to
subjects with serum folate levels of less than or equal to 11.0 nmol
l-1. The results suggest that folic acid supplementation should be tried
in IC subjects with hyperhomocyst(e)inaemia.