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. 2011 Mar 29;2(2):e00022-11. doi: 10.1128/mBio.00022-11

Adequate Vitamin D during Pregnancy Reduces the Risk of Premature Birth by Reducing Placental Colonization by Bacterial Vaginosis Species

William B Grant 1
PMCID: PMC3065193  PMID: 21447701

The recent paper by Fichorova et al. (1) reported that placental colonization by bacterial species common in bacterial vaginosis (BV) was linked to an increased risk of premature birth and that targeting this colonization could reduce the risk of premature birth and subsequent inflammation-provoked late sequelae.

Overlooked in the paper was any mention of vitamin D. At least two papers have reported that maternal vitamin D deficiency during pregnancy is associated with an increased risk of BV. In one, a statistically significant inverse correlation between serum 25-hydroxyvitamin D [25(OH)D] and BV was found for black women but not white women (2). In another, vitamin D deficiency was associated with BV only in pregnant women; however, for nonpregnant women, black race was associated with risk (3).

Vitamin D reduces the risk of bacterial infections through induction of cathelicidin and defensins (4) and has been found associated with reduced risks for several types of diseases linked to bacterial infections, including dental caries, pneumonia, severe sepsis, and tuberculosis (5). Serum 25(OH)D levels of 30 to 40 ng/ml are indicated for reduced risk of bacterial infections (6).

Pregnant women are generally not advised to obtain sufficient vitamin D during pregnancy. According to Hollis, pregnant women require up to 6,400 IU/day of vitamin D3 (7). His group conducted a randomized controlled trial of vitamin D supplementation with up to 6,000 IU/day and found no adverse effects, including effects on serum or urine calcium levels (8).

William B. Grant, Sunlight, Nutrition, and Health Research Center, San Francisco, California, USA

Footnotes

Citation Grant WB. 2011. Adequate vitamin D during pregnancy reduces the risk of premature birth by reducing placental colonization by bacterial vaginosis species. mBio 2(2):e00022-11. doi:10.1128/mBio.00022-11.

REFERENCES

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Articles from mBio are provided here courtesy of American Society for Microbiology (ASM)

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