Concentrations of Choline-Containing Compounds and Betaine in Common Foods

Zeisel, Steven H.; Mar, Mei Heng; Howe, Juliette C.; Holden, Joanne M.

doi:10.1093/jn/133.5.1302

Cited by 633 publications

(555 citation statements)

References 30 publications

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“…For example, 100 g of spinach, one of the richest vegetable sources of folate, contains only B50 mg of folate, 74 but has B600 mg of betaine and 22 mg of choline. 77 Therefore, diet-induced folate deficiency may be accompanied by a more severe deficiency of methyl-group donors. Thus, it seems that the importance of folate in the increasing prevalence of metabolic syndrome and its related diseases is overestimated.…”

Section: Folic Acidmentioning

confidence: 99%

Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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The metabolic syndrome, a major risk factor for type 2 diabetes and cardiovascular disease, is a cluster of metabolic abnormalities including obesity, insulin resistance, hypertension and dyslipidemia. Although systemic oxidative stress and aberrant methylation status are known to have important roles in the development of metabolic syndrome, how they occur remains unclear. The metabolism of methyl-consuming compounds generates reactive oxygen species and consumes labile methyl groups; therefore, a chronic increase in the levels of methyl-consuming compounds in the body can induce not only oxidative stress and subsequent tissue injury, but also methyl-group pool depletion and subsequent aberrant methylation status. In the past few decades, the intake amount of methyl-consuming compounds has substantially increased primarily due to pollution, food additives, niacin fortification and high meat consumption. Thus, increased methyl consumers might have a causal role in the development and prevalence of metabolic syndrome and its related diseases. Moreover, factors that decrease the elimination/ metabolism of methyl-consuming compounds and other xenobiotics (for example, sweat gland inactivity and decreased liver function) or increase the generation of endogenous methyl-consuming compounds (for example, mental stress-induced increase in catecholamine release) may accelerate the progression of metabolic syndrome. Based on current nutrition knowledge and the available evidence from epidemiological, ecological, clinical and laboratory studies on metabolic syndrome and its related diseases, this review outlines the relationship between methyl supply-consumption imbalance and metabolic syndrome, and proposes a novel mechanism for the pathogenesis and prevalence of metabolic syndrome and its related diseases.

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Section: Folic Acidmentioning

confidence: 99%

Dietary methyl-consuming compounds and metabolic syndrome

Zhou

et al. 2011

Hypertens Res

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“…Main food sources of betaine are wheat bran, wheat germ, spinach, pretzels, shrimps and wheat bread (Zeisel et al, 2003). Choline is present in the human diet primarily as lecithin, which is the trivial name for phosphatidylcholine.…”

Section: Introductionmentioning

confidence: 99%

“…Intake of choline moieties from foods is estimated at 400-600 mg/day (Shaw et al, 2004;Fischer et al, 2005). Main food sources of choline are beef liver, chicken liver, eggs, wheat germ, bacon, dried soybeans and pork (Zeisel et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Prospective study on dietary intakes of folate, betaine, and choline and cardiovascular disease risk in women

et al. 2007

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Objective: To investigate the association between dietary intakes of folate, betaine and choline and the risk of cardiovascular disease (CVD). Design: Prospective cohort study. Subjects: A total of 16 165 women aged 49-70 years without prior CVD. Subjects were breast cancer screening participants in the PROSPECT-EPIC cohort, which is 1 of the 2 Dutch contributions to the European Prospective Investigation into Cancer and Nutrition (EPIC). Methods: Each participant completed a validated food frequency questionnaire. Folate intake was calculated with the Dutch National Food Database. Betaine and choline intakes were calculated with the USDA database containing choline and betaine contents of common US foods. Data on coronary heart disease (CHD) events and cerebrovascular accident (CVA) events morbidity data were obtained from the Dutch Centre for Health Care Information. Results: During a median follow-up period of 97 months, 717 women were diagnosed with CVD. After adjustment, neither folate, nor betaine, nor choline intakes were associated with CVD (hazard ratios for highest versus lowest quartile were 1.23 (95% confidence interval 0.75; 2.01), 0.90 (0.69; 1.17), 1.04 (0.71; 1.53), respectively). In a subsample of the population, high folate and choline intakes were statistically significantly associated with lower homocysteine levels. High betaine intake was associated with slightly lower high-density lipoprotein (HDL)-cholesterol concentrations. Conclusion: Regular dietary intakes of folate, betaine and choline were not associated with CVD risk in post-menopausal Dutch women. However, the effect of doses of betaine and choline beyond regular dietary intake -for example, via supplementation or fortification -remains unknown.

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“…The flux through MTHFR determines the amount of newly formed one-carbon units that are directed towards nucleotide synthesis or towards the de novo synthesis of transferable methyl groups, following the activation of methionine to SAM (S-adenosylmethionine). Other sources of transferable methyl groups are the dietary preformed donors -methionine, betaine and choline [1]. Choline can be metabolized to betaine, which serves as an alternative methyl donor for the remethylation of homocysteine to methionine, by the enzyme BHMT (betaine-homocysteine methyltransferase; EC 2.1.1.5) [2].…”

Section: Introductionmentioning

confidence: 99%

Betaine rescue of an animal model with methylenetetrahydrofolate reductase deficiency

Schwahn

Laryea

Chen

et al. 2004

Biochemical Journal

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MTHFR (methylenetetrahydrofolate reductase) catalyses the synthesis of 5-methyltetrahydrofolate, the folate derivative utilized in homocysteine remethylation to methionine. A severe deficiency of MTHFR results in hyperhomocysteinaemia and homocystinuria. Betaine supplementation has proven effective in ameliorating the biochemical abnormalities and the clinical course in patients with this deficiency. Mice with a complete knockout of MTHFR serve as a good animal model for homocystinuria; early postnatal death of these mice is common, as with some neonates with low residual MTHFR activity. We attempted to rescue Mthfr−/− mice from postnatal death by betaine supplementation to their mothers throughout pregnancy and lactation. Betaine decreased the mortality of Mthfr−/− mice from 83 % to 26 % and significantly improved somatic development from postnatal day 1, compared with Mthfr−/− mice from unsupplemented dams. Biochemical evaluations demonstrated higher availability of betaine in suckling pups, decreased accumulation of homocysteine, and decreased flux through the trans-sulphuration pathway in liver and brain of Mthfr−/− pups from betaine-supplemented dams. We observed disturbances in proliferation and differentiation in the cerebellum and hippocampus in the knockout mice; these changes were ameliorated by betaine supplementation. The dramatic effects of betaine on survival and growth, and the partial reversibility of the biochemical and developmental anomalies in the brains of MTHFR-deficient mice, emphasize an important role for choline and betaine depletion in the pathogenesis of homocystinuria due to MTHFR deficiency.

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Concentrations of Choline-Containing Compounds and Betaine in Common Foods

Cited by 633 publications

References 30 publications

Dietary methyl-consuming compounds and metabolic syndrome

Dietary methyl-consuming compounds and metabolic syndrome

Prospective study on dietary intakes of folate, betaine, and choline and cardiovascular disease risk in women

Betaine rescue of an animal model with methylenetetrahydrofolate reductase deficiency

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