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Dx Environmental Toxins Exposure Risks:

(1). Polycystic Ovary Syndrome (PCOS) is a complex and enigmatic (confusing) syndrome of unknown origin..
(2). Experimental exposure to industrial endocrine disruptors has been related with the impairment of normal reproductive (and metabolic) function.[Both BPA and organophosphates]
(3). The author hypothesizes that "industrial chemicals may".. help "unveil PCOS characteristics in a genetically predisposed individual"...

(4). There is a gender difference: male to female and phenotype difference between PCOS and normal women.
(5). Prolactin may be elevated.
(6). Metformin may lower insulin resistance, TSH(Thyroid Stimulating Hormone), as well as Androgen levels and Free Androgen Index (implying a not yet confirmed change in SHBG).
(7). Topical progesterone is offered as a treatment although no article is referenced,
(8). The Androgen-Receptor can be blocked. But the "PPARγ mRNA expression is down-regulated by testosterone, and up-regulated by insulin and rosiglitazone with different dosages. Decreased PPARγ mRNA in the Granulosa Cells of PCOS is related to the clinical characteristics of PCOS.

Exposure to Organo-Phosphates (OP) affect Male Hormone Levels

Journal of Toxicology: May 2013
"There is a growing concern about the endocrine effects of long-term, low-level exposure to organophosphate (OP) compounds. Studies on experimental animals have found that OP pesticides have an impact on the endocrine system and a few clinical and epidemiological studies have also shown that OPs may affect the male hormone profile, although results are inconsistent. We have evaluated the effect of exposure to OP pesticides, measured through urinary levels of six dialkylphosphate (DAP) metabolites, on male hormone profile in 136 floriculture workers from the State of Mexico and Morelos during two agricultural periods with different degree of pesticide exposure. Generalized estimated equations (GEE) models were developed and adjusted for several potential confounders, including PON1 enzyme activity, as a biomarker of susceptibility, and serum levels of p,p'-DDE, a metabolite of the pesticide DDT widely used in Mexico until 1999 for control of agricultural pests and malaria. Exposure of male floriculture workers to OP pesticides was associated with increased serum levels of follicle-stimulating hormone (FSH) and prolactin and with decreased serum testosterone and inhibin B levels. Among all DAPs tested, only DETP was inversely associated with luteinizing hormone (LH). Estradiol showed a marginally significant positive trend with DEP and DETP derivatives.

In conclusion, OP pesticides may have an impact on the endocrine function because of their potential to modify the male hormone profile as a function of the type of pesticide *[Editor] ""

Virgina Hopkins, M.D. explains the connection between xeno-estrogens (environmental toxins) that makes sense and parallels the Editor's work with Endometriosis, Diabetes and inflammatory diseases. She explains:
"But what causes dysfunctional follicles that won’t release eggs? I am convinced, from wildlife studies and from what I have observed in my practice, this is due to the exposure of female embryos to xenobiotics, environmental pollutants which chemically act like estrogen on the developing baby’s tissues.

When a female embryo develops in the womb, 500 to 800 thousand follicles are created, each enclosing an immature ovum. Studies show that the creation of ovarian follicles during this embryo stage is exquisitely sensitive to the toxicity of xenobiotics. When the mother is exposed to these chemicals, she experiences no apparent damage. But the baby she is carrying is far more susceptible, and these chemicals may damage a female embryo’s ovarian follicles and make them dysfunctional; unable to complete ovulation or manufacture sufficient progesterone. This damage is not apparent until after puberty."
Makes sense.

Literature Search:
Which Environmental Toxins?
Several endocrine Disrupting Chemicals (EDCs), such as pesticides, bisphenol A, phthalates, dioxins, and phytoestrogens, can interact with the female reproductive system and lead to endocrine disruption.
How do the Environmental Toxins Work?
Initially, it was assumed that EDCs exert their effects by binding to hormone receptors and transcription factors, but it is currently known that they may also alter the expression of enzymes involved in the synthesis or catabolism of steroids.

Correlation to Testosterone Levels
There were significant positive correlations between serum BPA and total testosterone (r = 0.391, p<0.001), free testosterone (r = 0.504, p<0.001), androstenedione (r = 0.684, p<0.001), and DHEAS (r = 0.514, p<0.001) concentrations in all subjects. These findings show that there is a strong relationship between serum BPA and androgen concentrations, speculatively due to the effect of androgen on the metabolism of BPA.

Is there proof that our bodies are 'infected' with these toxins?
Biomonitoring studies have identified these compounds in adults, children, pregnant women, and fetuses. Among the diseases of the female reproductive tract associated with EDCs exposure are the following: precocious puberty, polycystic ovary syndrome, and premature ovarian failure.
Is anyone not affected?
The different populations of the world are exposed to a great number of chemicals through different routes of infection; despite the various available studies, there is still much doubt regarding the additive effect of a mixture of EDCs with similar mechanisms of action.

What have we learned from animal studies?
"Importantly, the effects of BPA were evident at levels, which approximated twice the highest levels found in human maternal circulation of industrialized nations. These findings provide evidence in support of developmental origin of adult reproductive and metabolic diseases and highlight the risk posed by exposure to environmental endocrine disrupting chemicals."

Environmental Toxins by producing abnormal proteins cause 'oxidative stress'. The following documents the parameters of oxidative stress that were very significantly affected.

Clinical Picture:
RESULTS: Independently of body weight, higher bisphenol A levels in PCOS women were associated with higher grades of insulin resistance, HS, FAI and inflammation, spleen size showing the best correlation. At multivariate analysis, spleen size and FAI were the best predictors of bisphenol A (β coefficients 0.379, P = 0.007 and 0.343, P = 0.014, respectively).

Another author states "DES, genistein, bisphenol A, organotins (TBT, TPT), and phthalates. The first three groups of substances mainly act upon estrogen receptors, while organotins and phthalates activate PPARγ".
Yet the One Chinese study does not confirm it, but a second and the JCEM journal articles does.

Hypothyroidism: In a review of 33 patients with PCOS and being treated with levothyroine, "These results indicate that metformin treatment has a TSH-lowering effect in hypothyroid patients with PCOS, both treated with l-thyroxine and untreated."

Males and PCOS higher levels of BPA?
To investigate human exposure to bisphenol A (BPA), a widely used endocrine disruptor, we measured serum BPA concentrations and analyzed the interrelation of BPA with sex-related hormones. BPA was detected in all human sera by a novel enzyme-linked immunosorbent assay. Serum BPA concentrations were significantly higher in normal men (1.49 +/- 0.11 ng/ml; P < 0.01) and in women with polycystic ovary syndrome (1.04 +/- 0.10 ng/ml; P < 0.05) compared with normal women (0.64 +/- 0.10 ng/ml). There were significant positive correlations between serum BPA and total testosterone (r = 0.595, P < 0.001) and free testosterone (r = 0.609, P < 0.001) concentrations in all subjects and likewise between serum BPA and total testosterone (r = 0.559, P < 0.01) and free testosterone (r = 0.598, P < 0.001) concentrations in all female subjects, but not between serum BPA and other sex-related hormone concentrations in any group. These findings showed that there are gender differences in serum BPA concentrations, possibly due to differences in the androgen-related metabolism of BPA.

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