Can PCOS be fully treated without western medicine? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
PCOS is multifactorial in causes. Can you effect a change for what is innate? We can detox from plastics or EDCs by how much if we are exposed to it inside our mother’s womb. I have seen some lab results when I was a nutritionist for women who undergo hysterectomies. And the presence of many microbes suggest a probiotic/prebiotic regimen of whole foods, raw garlic and raw carrots and many other dietary supplementations.
Reprod Sci. 2016 Jun 23. pii: 1933719116654992. [Epub ahead of print]
Prenatal Exposure to Endocrine Disruptors: A Developmental Etiology for Polycystic Ovary Syndrome.
Hewlett M1, Chow E1, Aschengrau A2, Mahalingaiah S3.
Polycystic ovary syndrome (PCOS) is one of the most common and complex endocrinopathies among reproductive-age women. Polycystic ovary syndrome is characterized by symptomatology of oligomenorrhea and androgen excess, with or without presence of polycystic ovarian morphology. The etiology of PCOS is multifactorial, including genetic and environmental components. It has been previously established that prenatal androgen exposure results in a PCOS phenotype in experimental animal models and epidemiologic human studies. Investigators hypothesize that prenatal exposure to endocrine-disrupting chemicals (EDCs) may contribute to PCOS development. This review examines the emerging research investigating prenatal exposure to 3 major classes of EDCs-bisphenol A (BPA), phthalates, and androgenic EDCs-and the development of PCOS and/or PCOS-related abnormalities in humans and animal models. Highlights of this review are as follows: (1) In rodent studies, maternal BPA exposure alters postnatal development and sexual maturation;, (2) gestational exposure to dibutyl phthalate and di(2-ethylhexyl)phthalate results in polycystic ovaries and a hormonal profile similar to PCOS; and (3) androgenic EDCs, nicotine and 3,4,4′-trichlorocarbanilide, create a hyperandrogenic fetal environment and may pose a potential concern. In summary, prenatal exposure to EDCs may contribute to the altered fetal programming hypothesis and explain the significant variability in severity and presentation.