Skip to content

Betaine supplementation decreases post-methionine hyperhomocysteinemia in chronic renal failure.

Kidney international
Q1
Mar 2002
Citations: 87
Influential: 6
Interventional (Human) Studies
84

What this study found

Glycine betaine improved post-methionine hyperhomocysteinemia but did not meaningfully change fasting total homocysteine. After betaine, fasting tHcy fell by 4.17 ± 0.59 μmol/L and the post-methionine tHcy increment was 14.2 ± 0.68 μmol/L; the corresponding post-methionine increment without betaine was 19.9 ± 1.3 μmol/L. The absolute post-methionine tHcy concentration difference between treatments was 6.02 μmol/L (3.55, 8.49), while the mean fasting tHcy difference between treatments was 1.78 μmol/L (−1.17, 4.74). Plasma betaine rose from 29.3 ± 2.1 to 392 ± 34 μmol/L, and no adverse effects…

Study & population
Randomized crossover trial in 36 adults with chronic renal failure, including ESRD, who were not on dialysis and were already receiving stable folate and pyridoxine therapy.
Intervention
Oral glycine betaine 4 g/day was given for 3 months per treatment phase in a randomized crossover design.
Key limitation
The study was small, short term, and conducted in a highly selected population of mostly older Caucasian adults with chronic renal failure, limiting generalizability.
View sourceOpen PDF

Original abstract

BACKGROUND Fasting and post-methionine load hyperhomocysteinemia are independent risk factors for vascular disease that are common in chronic renal failure. Folate decreases but seldom normalizes fasting total homocysteine (tHcy) concentrations in such patients. Glycine betaine (GB) is known to decrease tHcy in other clinical settings, but whether it is beneficial in chronic renal failure has not been established. METHODS We conducted a crossover-controlled trial in 36 patients with chronic renal failure to determine if oral GB decreased fasting or post-methionine tHcy concentrations. All subjects received, in randomized sequence, 5-mg folic acid and 50-mg pyridoxine daily, with or without GB 4-g daily, for three months each. Fasting plasma tHcy, GB, folate, B vitamins, serum lipids and creatinine were measured at one and three months, and methionine load tests were performed at the end of each three-month treatment phase. RESULTS GB and N,N-dimethylglycine (DMG) levels in plasma and urine increased markedly during GB treatment. Fasting tHcy decreased from baseline with both treatments but did not differ between treatments. Post-methionine tHcy decreased with both treatments and was 18% lower on GB than on folate and pyridoxine alone (P < 0.001). There were small increases in lipids during treatment with GB but the ratio of total: HDL cholesterol was unchanged. CONCLUSIONS GB supplementation had no effect on fasting tHcy in patients with chronic renal failure who were folate and pyridoxine replete, but it significantly decreased tHcy concentrations after methionine loading.