Manipulation of estrogen during specific critical windows of development throughout gestation and early infancy leads to a myriad of adverse health outcomes including malformations in the ovary, uterus, mammary gland and prostate, early puberty, reduced fertility, disrupted brain organization, and reproductive tract cancers
Another study showed that infant boys born to vegetarian mothers had increased incidence of hypospadias (malformation of the male external genitalia) [186] suggesting that dietary components (perhaps phytoestrogens) cross the placenta and cause adverse effects on the developing fetus
].
Infants fed soy formula have circulating phytoestrogen concentrations of approximately 1000 ng/ml, 13,000–22,000 times higher than their own endogenous estrogen levels, 50–100 times higher than estradiol levels in pregnant women and 3000 times higher than estradiol levels at ovulation [249,14,295]. These blood levels are high enough to produce many of the physiological effects observed in research animals and human adults. In addition, they are at least a level of magnitude higher than those reported for other endocrine disruptors including BPA (Table 3) and the phthalates [50]. A recent prospective study in human infants observed that female infants on soy-based infant formulas exhibit estrogenized vaginal epithelium at times when their breast fed or cow based formula counterparts did not, suggesting estrogenic activity of the soy infant formula [28]. Determining if use of soy infant formulas can have long term reproductive health effects is a public health imperative
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Unfortunately, many children, both male and female, born to women prescribed DES (ein Stoff der ähnlich wirkt wie Genistein aus Stoff in Soja) during pregnancy subsequently developed reproductive health problems as adults. Adverse effects were first detected in 1971, decades after DES use had become commonplace. Two physicians noted that an extremely rare form of vaginal clear cell carcinoma was appearing in DES daughters more frequently than in unexposed women, and at a much younger age [100,101]. It was subsequently established that DES exposure in utero can also result in vaginal dysplasia, vaginal and/or cervical adenosis, malformations of the uterus, cervix and vagina, increased risk of testicular cancer, lower sperm count, undescended testes, infertility, late spontaneous abortion, premature delivery, and other pregnancy complications [183,232,197]. In general, the severity of the health effects correspond with timing and level of exposure, an observation which was the first, clear demonstration of how important it is to consider “critical windows of exposure” when attempting to predict potential consequences of human exposure to endocrine disruptors, such as the phytoestrogens.
In rodents, neonatal exposure to genistein alters ovarian differentiation, reduces fertility and causes uterine cancer later in life. Most of these studies have been done with subcutaneous injections of the aglycone form of the compound, genistein. Mice treated by subcutaneous injection of genistein at a dose of 50 mg/kg/day have peak serum circulating levels of genistein of 3.4–6.2 µM [61]. These levels are similar to infants on soy-based infant formulas.
(Was ich wichtig finde ist, dass im Falle dieser Hormongeschichten bei trächtigen Tieren das Ergebnis scheinbar sehr gut auf den Mensch zu übertragen ist, da die Vorgänge fast identisch sind und sich Erfahrungen im Tierversuch mit denen am Menschen decken. Das ist ja nicht immer der Fall)
The National Toxicology Program recently completed its most recent safety assessment of soy infant formula (available at
http://cerhr.niehs.nih.gov/chemicals/ge ... rt_508.pdf) and concluded there is “minimal concern for adverse developmental effects.”It is the same level of concern initially expressed for BPA
So is another reproductive health tragedy silently unfolding with the use of soy infant formula? Most of the reproductive outcomes following fetal exposure to DES were predicted by or replicated in animal models [183,168] emphasizing the importance of animal models for adumbrating potential adverse effects of endocrine disruptors in humans. Evidence for concern is emerging from a steady stream of laboratory animal data. The difficulty for public health agencies, parents and physicians is determining if the observed effects reliably predict what is likely to be happening in humans.
