NTP-CERHR Expert Panel Report on the reproductive and developmental toxicity of soy formula

Department of Pharmacology and Toxicology, University of Kansas Medical Center, Kansas City, KS, USA.
Birth Defects Research Part B Developmental and Reproductive Toxicology (Impact Factor: 1.17). 08/2006; 77(4):280-397. DOI: 10.1002/bdrb.20086
Source: PubMed
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Available from: Patricia B Hoyer, Jun 19, 2015
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    ABSTRACT: Soy formula containing estrogenic isoflavones is widely used in the United States. Infants consuming soy formula exclusively have high isoflavone exposures. We wanted to study whether soy formula prolonged the physiologic estrogenization of newborns, but available quantitative descriptions of the natural history of breast and genital development are inadequate for study design. We piloted techniques for assessing infants' responses to the withdrawal from maternal estrogen and gathered data on breast and genital development in infants at different ages. We studied 37 boys and 35 girls, from term pregnancies with normal birth weights, who were < 48 hr to 6 months of age, and residents of Philadelphia, Pennsylvania, during 2004-2005. One-third of the children of each sex and age interval were exclusively fed breast milk, soy formula, or cow-milk formula. Our cross-sectional study measured breast adipose tissue, breast buds, and testicular volume; observed breast and genital development; and collected vaginal wall cells and information on vaginal discharge. We assessed reliability of the measures. Breast tissue was maximal at birth and disappeared in older children, consistent with waning maternal estrogen. Genital development did not change by age. Breast-milk secretion and withdrawal bleeding were unusual. Vaginal wall cells showed maximal estrogen effect at birth and then reverted; girls on soy appeared to show reestrogenization at 6 months. Examination of infants for plausible effects of estrogens is valid and repeatable. Measurement of breast tissue and characterization of vaginal wall cells could be used to evaluate exposures with estrogen-like effects.
    Environmental Health Perspectives 03/2008; 116(3):416-20. DOI:10.1289/ehp.10409 · 7.03 Impact Factor
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    Birth Defects Research Part B Developmental and Reproductive Toxicology 12/2006; 77(6):485-638. DOI:10.1002/bdrb.20087 · 1.17 Impact Factor
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    ABSTRACT: Polycystic ovarian syndrome (PCOS) is the most common female endocrine disorder with a prevalence as high as 8 -15% depending on ethnicity and the diagnostic criteria employed. The basic pathophysiology and mode of inheritance remain unclear, but environmental factors such as diet, stress and chemical exposures are thought to be contributory. Developmental exposure to endocrine disrupting compounds (EDCs) have been hypothesized to exacerbate risk, in part because PCOS hallmarks and associated metabolic co-morbidities can be reliably induced in animal models by perinatal androgen exposure. Here we show that lifetime exposure to a soy diet, containing endocrine active phytoestrogens, but not developmental exposure (gestational day 6–lactational day 40) to the endocrine disrupting monomer Bisphenol A (BPA), can induce key features of PCOS in the rat; results which support the hypothesis that hormonally active diets may contribute to risk when consumed throughout gestation and post-natal life.
    Reproductive Toxicology 09/2014; 49. DOI:10.1016/j.reprotox.2014.09.003 · 2.77 Impact Factor