In India, most people adhere to a vegetarian diet, which may lead to cobalamin deficiency. About 75% of the subjects had metabolic signs of cobalamin deficiency, which was only partly explained by the vegetarian diet.
The study population included 204 men and women aged 27–55 y from Pune, Maharashtra, India, categorized into 4 groups:
- patients with cardiovascular disease (CVD) and diabetes,
- patients with CVD but no diabetes,
- patients with diabetes but no CVD,
- healthy subjects.
Data on medical history, lifestyle, and diet were obtained by interviews and questionnaires. Blood samples were collected for measurement of serum or plasma total cobalamin, holotranscobalamin (holoTC), methylmalonic acid (MMA), and total homocysteine (tHcy) and hemetologic indexes.
- Methylmalonic acid, total homocysteine, total cobalamin, and holotranscobalamin did not differ significantly among the 4 groups.
- Total cobalamin showed a strong inverse correlation with total homocysteine (r = −0.59) and methylmalonic acid (r = −0.54).
- 47% of the subjects had cobalamin deficiency (total cobalamin <150 pmol/L),
- 73% had low holotranscobalamin (<35 pmol/L),
- 77% had hyperhomocysteinemia (total homocysteine >15 μmol/L),
- 73% had elevated serum methylmalonic acid (>0.26 μmol/L).
These indicators of impaired cobalamin status were observed in both vegetarians and nonvegetarians.
Folate deficiency was rare and only 2.5% of the subjects were homozygous for the MTHFR 677C→T polymorphism.
Marked ethnic differences in cobalamin metabolism have been reported (40); therefore, the possibility that Indians have adapted to a chronic low cobalamin concentrations through genetic mechanisms should be considered.
This finding agrees with our observation that even subjects with relatively high cobalamin concentrations can have high tHcy and MMA concentrations. Notably, in the study by Lindenbaum et al, the high MMA concentration was related to anaerobic gut flora and the high tHcy concentration was explained by a low cobalamin concentration. Some studies suggest that overgrowth of intestinal bacteria may lead to formation and absorption of inactive cobalamin analogues.