Is our effect on the environment and the environments, in turn, effect on us politics or science? It is science that is manipulated by politicians for political gain/power. In this study of male small/large mouth bass in NE America are found to have significant female characteristics i.e. eggs where testes should exist...where none should exist. The numbers were as high as 85% in the small mouth base compared to 27% for the large mouth bass. Is there any wonder we have a low T epidemic in men? The most likely cause are endocrine disruptors. It is a concern that the authors did not look for endocrine disruptors in the water at the time of this study of the fish.
Endocrine Disrupting Chemicals from 1970 still disrupting hormones today. Three fold increase in DHEA in 3 year old children via saliva and androstenedione in mothers compared to controls.
Endocrine Disrupting chemicals, xenoestrogens, alter the hormone receptors very early. Increased estrogenic load with the change in ER increase prostate cancer.
Review finds endocrine disruption from Organocholrides, also called persistent organohalogen pollutants. Common POP, would be DDE, DDT...
This is a review of several cohorts, but this follows the rest of the literature that these environmental toxicants are endocrine disruptors.
There is growing evidence that some parabens have endocrine disrupting effects. IN this study, they found that butyl paraben acted as an endocrine disruptor.
Great review article on the endocrine disrupting role of Cadmium. Cadmium binds to the ER-alpha inducing an estrogen signal. Cadmium also binds to the androgen receptor as well. This study proposes a similar activation of ER-alpha and AR by Cadmium.
Most recently, obesity has been proposed to be yet another adverse health effect of exposure to endocrine disrupting chemicals (EDCs) during critical stages of development. Obesity is quickly becoming a significant human health crisis
The emerging idea of an association of EDCs and obesity expands the focus on obesity from intervention and treatment to include prevention and avoidance of these chemical modifiers.
Prenatal exposure to BPA has been shown to alter a variety of reproductive endocrine parameters, such as testosterone and luteinizing hormone levels
arly onset of sexual maturation of female mice
imbalanced T-helper (TH)1/TH2 immune responses have been demonstrated on exposure to BPA
indicating that BPA exerted its effects by reducing the number of Treg cells.
Exposure to BPA by subcutaneous injection in adulthood significantly promoted antigen-stimulated production of IL-4, IL-10, and IL-13 in TH2-skewed
BPA can leak from the placenta and accumulate in the fetus
We showed that prenatal exposure to BPA increased the production of a TH1 cytokine, IFN-γ, and a TH2 cytokine, IL-4, after the offspring developed, suggesting that prenatal exposure to BPA can induce persistent immunologic effects lasting into adulthood.
These results are consistent with a previous report that fetal exposure to BPA augmented TH1 and TH2 immune responses
our results clearly demonstrate that the production of TH2 cytokines is promoted by BPA in adult mice and in offspring during developmental exposure.
The decrease of Treg cells would predispose to immune dysfunction in aged individuals, explaining their higher risk of immune-mediated diseases, cancer, and infections.
BPA might cause these diseases. Thus, avoiding exposure to or promoting the excretion of BPA and other EDCs would help in preventing diseases and adverse health effects.
Glyphosate, component of Roundup is well known to be an endocrine disruptor. This rat study describes the mechanism of disruption of the Sertoli cells resulting in male infertility. In addition to the disruption of spermatogenesis, Glyphosate was shown to deplete glutathione levels compromising detoxification. If that is not enough, oxidative damage marker TBARS was elevated.
Animal study finds that Cadmium is estrogenic. This study found that not only was Cadmium an endocrine disruptor for the pregnant animals, but was also estrogenic in the mammary glands of the offspring.
