Periconceptual consumption of folic acid has been shown to decrease the incidence of neural tube defects. The strategy of universal fortification of staple foodstuffs with folic acid presents the possibility of life-long exposure to unmetabolized folic acid. Chief among the risks of exposure to folic acid in the circulation is that of masking the diagnosis of cobalamin deficiency in pernicious anemia and the progression of neurologic disease. Other effects are unknown. For instance, the effect of in vivo chronic exposure of adult and fetal cells to the synthetic form of the vitamin has never been investigated at the population level. This study examined the acute appearance of unmetabolized folic acid in serum in response to the consumption of some fortified foodstuffs by young and elderly volunteers. Subjects on a 5-d regimen of fortified ready-to-eat-cereal and bread in addition to their normal diet had a threshold intake of 266 micrograms folic acid per meal at which unaltered folic acid appeared in the serum. Subjects given folic acid in either isotonic saline, milk, or white bread also had a threshold > 200 micrograms. From patterns of food consumption in the United States, the implementation of flour fortification at 1.4 mg/kg is unlikely to lead to folic acid appearance in serum, assuming that consumption is spread throughout the day. Increasing this level of fortification, however, as has been advocated by some agencies, may result in the repeated appearance of folic acid in serum over many years, particularly in consumers in nontargeted populations of large amounts of fortified foods. The "safe level of intake" of 1 mg folate/d set by the US Food and Drug Administration may cause a serum folic acid effect. Furthermore, a repeated serum folic acid response is likely to be found in many women complying with the advice to take 400 micrograms folic acid/d to prevent the occurrence of neural tube defects.

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Oral ingestion of sodium bicarbonate (bicarbonate loading) has acute ergogenic effects on short-duration, high-intensity exercise. Because sodium bicarbonate is 27% sodium, ergogenic doses (i.e. 300 mg·kg−1) result in sodium intakes well above the Dietary Reference Intakes upper limit of 2300 mg/day. Therefore, it is conceivable that bicarbonate loading could have hypertensive effects. Therefore, we performed a double-blind cross-over trial to evaluate the hypothesis that bicarbonate loading increases resting and exercise blood pressure (BP). A secondary hypothesis was that bicarbonate loading causes gastrointestinal distress. Eleven endurance-trained men and women (exercise frequency, 4.6±0.4 sessions/wk; duration, 65±6 min/session) underwent testing on two occasions in random sequence: once after bicarbonate loading (300 mg·kg−1) and once after placebo ingestion. BP and heart rate (HR) were measured before bicarbonate or placebo consumption, 30 minutes after consumption, during 20 min of steady state submaximal cycling exercise, and during recovery. Bicarbonate loading did not affect systolic BP during rest, exercise, or recovery (p=0.38 for main treatment effect). However, it resulted in modestly higher diastolic BP (main treatment effect, +3.3±1.1 mmHg, p=0.01) and higher HR (main treatment effect, +10.1±2.4 bpm, p=0.002). Global ratings of gastrointestinal distress severity (0–10 scale) were greater after bicarbonate ingestion (5.1±0.5 vs. 0.5±0.2, p<0.0001). Furthermore, 10 of the 11 subjects (91%) experienced diarrhea, 64% experience bloating and thirst, and 45% experienced nausea after bicarbonate loading. In conclusion, although a single, ergogenic dose of sodium bicarbonate does not appear to have acute, clinically important effects on resting or exercise BP, it does cause substantial GI distress.

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The findings suggest that active BAT detected by F-FDG PET/CT is associated with less central obesity and liver fat. The presence of foci of BAT may be protective against features of the metabolic syndrome.

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