Pre- and Postnatal Health: Evidence of Increased Choline Needs
ABSTRACT Choline, a micronutrient found in food, serves as the starting material for several important metabolites that play key roles in fetal development, particularly the brain. Although human beings' requirement for choline is unknown, an Adequate Intake level of 425 mg/day was established for women with upward adjustments to 450 and 550 mg/day during pregnancy and lactation, respectively. The importance of choline in human development is supported by observations that a human fetus receives a large supply of choline during gestation; pregnancy causes depletion of hepatic choline pools in rats consuming a normal diet; human neonates are born with blood levels that are three times higher than maternal blood concentrations; and large amounts of choline are present in human milk. The development of the central nervous system is particularly sensitive to choline availability with evidence of effects on neural tube closure and cognition. Existing data show that the majority of pregnant (and presumably lactating) women are not achieving the target intake levels and that certain common genetic variants may increase requirements for choline beyond current recommendations. Because choline is not found in most varieties of prenatal vitamins (or regular multivitamins), increased consumption of choline-rich foods may be needed to meet the high pre- and postnatal demands for choline.
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- "Long sleep (9+hrs) was also associated with reduced consumption of theobromine, a methylxanthine found in tea and chocolate and a metabolite of caffeine thought to have some stimulant effects but likely has no psychotropic effects in humans (Benton, 2004). It was also associated with choline, which is an essential micronutrient that is particularly important for fetal development (Caudill, 2010). "
ABSTRACT: Short sleep duration is associated with weight gain and obesity, diabetes, cardiovascular disease, psychiatric illness, and performance deficits. Likewise, long sleep duration is also associated with poor physical and mental health. The role of a healthy diet in habitual sleep duration represents a largely unexplored pathway linking sleep and health. This study evaluated associations between habitual sleep parameters and dietary/nutritional variables obtained via the National Health and Nutrition Examination Survey (NHANES), 2007-2008. We hypothesized that habitual very short (<5hrs) short (5-6hrs) and long (9+hrs) sleep durations are associated with intake of a number of dietary nutrient variables. Overall, energy intake varied across very short (2036kcal), short (2201kcal), and long (1926kcal) sleep duration, relative to normal (2151kcal) sleep duration (p=0.001). Normal sleep duration was associated with the greatest food variety (17.8), compared to very short (14.0), short (26.5) and long (16.3) sleep duration (p<0.001). Associations between sleep duration were found across nutrient categories, with significant associations between habitual sleep duration and proteins, carbohydrates, vitamins and minerals. In stepwise analyses, significant contributors of unique variance included theobromine (long sleep RR=0.910,p<0.05), vitamin C (short sleep RR=0.890,p<0.05), tap water (short sleep RR=0.952,0<0.001; very short (<5hrs) sleep RR=0.941,p<0.05), lutein+zeaxanthin (short sleep RR=1.123,p<0.05), dodecanoic acid (long sleep RR=0.812,p<0.05), choline (long sleep RR=0.450,p=0.001), lycopene (very short (<5hrs) sleep RR=0.950,p<0.05), total carbohydrate (very short (<5hrs) sleep RR=0.494,p<0.05; long sleep RR=0.509,p<0.05), selenium (short sleep RR=0.670,p<0.01) and alcohol (long sleep RR=1.172,p<0.01). Overall, many nutrient variables were associated with short and/or long sleep duration, which may be explained by differences in food variety. Future studies should assess whether these associations are due to appetite dysregulation, due to short/long sleep and/or whether these nutrients have physiologic effects on sleep regulation. In addition, these data may help us better understand the complex relationship between diet and sleep and the potential role of diet in the relationship between sleep and obesity and other cardiometabolic risks.Appetite 01/2013; 64. DOI:10.1016/j.appet.2013.01.004 · 2.69 Impact Factor
- "B vitamins and methyl-group homeostasis have received considerable attention in recent years, providing a basis for understanding the complex interplay between nutrition and epigenetic modifications of disease-related genes, including those that are involved in aging and in Alzheimer's disease. For example, experimental modification of methyl-group homeostasis through dietary deficiency and supplementation of choline and folate has been shown to exert profound effects on brain development, function, and aging   , including epigenetic modification and/or aberrant expression of key AD genes . In light of this attention, it has been turned to the potential impact of food folic acid fortification and nutritional status in human metabolic programming  . "
Article: Nutrition and DementiaCurrent Gerontology and Geriatrics Research 06/2012; 2012:926082. DOI:10.1155/2012/926082
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- "Aside from diet, new choline molecules can only be derived from de novo synthesis of phosphatidylcholine that is catalyzed by phosphatidylethanolamine-N-methyltransferase (PEMT; catalyzes the methylation of phosphatidylethanolamine to phosphatidylcholine) . Many foods contain choline or choline-containing compounds  , these include eggs, beef, chicken, fish and milk as well as wheat germ and certain beans . See also http://www.nal.usda.gov/fnic/foodcomp/Data/Choline/Choline.html. "
ABSTRACT: Fetal progenitor cells proliferate, migrate, differentiate and undergo apoptosis at specific times during fetal development. Choline is needed by these cells for membrane synthesis and for methylation. There is growing evidence that this nutrient also modulates epigenetic regulation of gene expression in both neuronal and endothelial progenitor cells, thereby modifying brain development. It is likely that these mechanisms explain why, in rodent models, maternal dietary intake of choline influences both angiogenesis and neurogenesis in fetal hippocampus, and results in life-long changes in memory function. This also may explain why women eating diets low in choline have a greater risk of having a baby with a birth defect. Choline is mainly found in foods that contain fat and cholesterol, and intake of such foods has diminished in response dietary advice from nutritionists and physicians. Forty years ago, diets commonly contained choline-rich foods but now women in the USA tend to eat diets low in choline content. Premenopausal women normally may require less choline in their diet than do men and postmenopausal women, because estrogen induces the gene for the enzyme catalyzing endogenous biosynthesis of the choline-containing phospholipid phosphatidylcholine. However, many women have a single nucleotide polymorphism (SNP) that blocks the induction of endogenous biosynthesis, thereby making them require more dietary choline. When these women eat diets low in choline, the supply of this nutrient to the fetus is likely to be inadequate, and may perturb progenitor cell proliferation, migration, differentiation and apoptosis.Seminars in Cell and Developmental Biology 06/2011; 22(6):624-8. DOI:10.1016/j.semcdb.2011.06.002 · 5.97 Impact Factor