Celiac.com 03/10/2009 - A recent study confirms that B-vitamin supplements are helpful in raising vitamin B6, B12 and folate levels and in reducing homocysteine levels in people with celiac disease.
Celiac disease is a typical malabsorption syndrome, and is associated with higher rates of numerous deficiencies, including folate and vitamin B12. People with celiac disease face higher rates of Hyperhomocysteinemia than do healthy controls.
The study measured levels of vitamin B6, folate, vitamin B12, and fasting plasma homocysteine in 51 adults with celiac disease and 50 healthy control subjects of similar age and sex.
The results show that the celiac disease subjects who used vitamin supplements had higher blood levels of vitamin B6 (P = 0.003), folate (P < 0.001), and vitamin B12 (P = 0.012) than celiac patients who did not use supplements, or healthy controls (P = 0.035, P < 0.001, P = 0.007, for vitamin B6, folate, and vitamin B12, respectively).
Patients who use vitamin supplements also showed lower levels of plasma homocysteine than in patients who did not (P = 0.001) or healthy controls (P = 0.003). Vitamin B6 and folate were both associated with homocysteine levels, whereas vitamin B12 was not. Twenty-four (48%) of 50 controls and 23 (50%) of 46 of the celiac disease patients carried the MTHFR thermolabile variant T-allele (P = 0.89).
The research team concludes that Homocysteine levels are dependent on Marsh classification and the regular use of B-vitamin supplements reduces of homocysteine levels in patients with celiac disease.The study confirms earlier studies suggesting that both the presence and severity of celiac disease determined homocysteine levels.
The regular use of supplemental B vitamins resulted in higher levels of serum vitamin B6, folate, vitamin B12 and lower levels of plasma homocysteine in patients with celiac disease. Moreover, supplemental B vitamins seem to offer protection against the effects of villous atrophy on homocysteine levels, independent of the genetic susceptibility status as determined by carriage of the C677T polymorphism of 5,10 methylenetetrahydrofolate reductase.
World J Gastroenterol. 2009;15:955–960