[ Diabetes Type 1 ]

Effect of B-Vitamin Therapy on Progression of Diabetic Nephropathy: A Randomized Controlled Trial

Diabetes mellitus is associated with diabetic impairment of testicular function, ultimately leading to reduced fertility. In a randomized, double-blind, placebo controlled clinical trial, 69 type 2 diabetic patients were randomly divided into four groups, each group receiving one of the following daily supplement for 3 months; group M: 200 mg Mg and 30 mg Zn (n = 16), group V: 200mg Vitamin C and 150 mg Vitamin E (n = 18), group MV: minerals plus vitamins (n = 17), group P: placebo (n = 18). Prevalent retinopathy (n = 224) was determined in 1993–1995 from graded fundus photographs. “If the homocysteine theory of atherosclerosis is to be proved or disproved with certainty, it may be necessary to find alternative, non-vitamin strategies to lower homocysteine, such as enhancing the conversion of homocysteine to cysteine in the liver or enhancing urinary excretion,” they add. Observational studies report a strong association between vitamin D deficiency and cardiovascular and metabolic disorders; however, there remains a paucity of large long-term randomized clinical trials showing a benefit with treatment. In a paper entitled “High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease”, published in Diabetologia on 4th August, the team found that thiamine concentration in blood plasma was decreased 76% in type 1 diabetic patients and 75% in type 2 diabetic patients. They examined whether there were any significant differences in serum vitamin D levels between patients with diabetic retinopathy and controls.

RESULTS The median (range) vitamin D level was 36.9 (3.8–118.6) nmol/L. Trial participants received a placebo (n = 119) OR a daily vitamin pill containing: 2.5 mg folic acid, 25 mg B6, 1mg B12 (n = 119) – that’s a lot of folic acid. Ideally, future studies would include frequent measurement of intake of these three nutrients through diet and supplements, standardized exams to identify DR, and agreed-upon biomarkers to assess DR progression,” Dr. Vitamin D3 is generated in the skin by sunlight and is present in animal sources, especially fatty fish or their liver oils. One VERY salient point which the examiners appear to have “overlooked” appears in the table of baseline characteristics under “History No%” the number of patients with peripheral vascular disease is SIGNIFICANTLY higher in the B-Vitamin group – 24 (20.2%) compared with the placebo group – 17 (14.3%). This is the first demonstration that MVT significantly attenuates the progression of diabetes in male rats with chronic experimental diabetes. Were these the same patients that had MIs and stokes in the treatment group?

Individual patient data are not published so we cannot check this, but this is 7 more people compared with placebo group. In the placebo group 12 more people had suffered previous heart attacks or angina. Maybe it is as simple as this – during the trial the treatment group “caught up” to the placebo group as a natural progression of CVD, i.e. Conclusion: The authors conclude that supplementation with high doses of B vitamins lowers plasma homocysteine levels but worsens diabetic nephropathy and increases the risk of cerebrovascular and cardiovascular events in patients with diabetes. were all pretty even over an entire lifetime. There is some experimental evidence on the preventive effect of vitamin D in the development of diabetic retinopathy in a rodent model [6]. Apparently the groups were randomised.

If the baseline characteristics (previous MI/angina and peripheral vascular disease) can be so different in the two groups, then if the groups really were random, this must be due to chance. The increase in “bad” endpoints (MI, stroke and revascularisation) seen in the Vitamin treated group is very small – in the placebo group (over 3 years) 4 people had a MI and 1 person had a stroke and in the treatment group 8 people had an MI and 6 people had a stroke. This is because visceral fat secretes a number of factors involved in a range of metabolic and physiological processes, some of these factors having been implicated in the pathologies associated with obesity including diabetes, hypertension and CVD [3, 4]. These total numbers are roughly the same as the differences between the groups to start with, so why can’t these be due to chance just like the baseline differences? Maybe the groups weren’t really correctly randomised to start with? That would make the whole trial invalid. Annals Academy of Medicines.

It claims a risk derived from very small numbers in groups who were significantly different to start with.

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