Dietary and supplementary betaine: Effects on betaine and homocysteine concentrations in males☆
Received 15 November 2008; received in revised form 13 January 2009; accepted 16 January 2009. published online 06 April 2009.
Abstract
Background and aims
Betaine is an osmolyte that when catabolised decreases plasma total homocysteine. A betaine-rich meal has acute effects similar to a supplement, but the effects of a longer-term increase in dietary betaine intake need clarification. We compared the effects of two weeks of dietary and supplementary betaine on plasma betaine and homocysteine concentrations both fasting and after a methionine load.
Methods and results
In a randomized crossover study, 8 healthy males (22–36y) consumed either a betaine-rich diet (∼800mg/day) or a betaine supplement (0.5g twice daily) for 14 days. Fasting blood samples were collected on day −5, −1 (pre-treatment) 0, 2, 6, 9, 13 (treatment), 14 and 18 (post-treatment). Post-methionine load blood samples were collected on day −5, 0, 6 and 13, while 24h urine samples were collected on day −5, 0, 6, 13 and 14. Plasma betaine, dimethylglycine, homocysteine and urine betaine, dimethylglycine and creatinine concentrations were measured. Plasma betaine concentrations significantly increased for both treatments compared to pre-treatment values (P<0.001). Fasting homocysteine levels were minimally affected. Both treatments reduced post-methionine load homocysteine and this effect tended to be greater following a betaine-rich diet (P=0.108). Small increases in urinary betaine excretion were observed following both treatments (≈1.5% of supplement; ≈1.3% of dietary betaine). Most was attributable to increased excretion of betaine as dimethylglycine.
Conclusions
Supplemental or dietary betaine similarly increase circulating betaine concentrations and attenuate the post-methionine load rise in homocysteine concentrations.
☆ Research Support: This study was supported by a grant from the National Heart Foundation of New Zealand (to PMG) and S. Slow was supported by a grant from the Neurological Foundation of New Zealand.
ABSTRACT