Endocrine disrupters, microRNAs, and primordial germ cells: a dangerous cocktail

Endocrine disrupting chemicals: female and male reproduction


Endocrine-disrupting chemicals (EDCs) are environmental pollutants that may change the homeostasis of the endocrine system, altering the differentiation of germ cells with consequences for reproduction.

In mammals, germ cell differentiation begins with primordial germ cells (PGCs) during embryogenesis.

Primordial germ cell development and gametogenesis are genetically regulated processes, in which the posttranscriptional gene regulation could be mediated by small noncoding RNAs (sncRNAs) such as microRNAs (miRNAs).

Endocrine disrupters, microRNAs, and primordial germ cells: a dangerous cocktail, Fertility and Sterility, Volume 106, Issue 4, Pages 871–879, September 15, 2016.

An Early Fall, light_seeker.

Here, we review the deleterious effects of exposure during fetal life to EDCs mediated by deregulation of ncRNAs, and specifically miRNAs on PGC differentiation.

Moreover, the environmental stress induced by exposure to some EDCs during the embryonic window of development could trigger reproductive dysfunctions transgenerationally transmitted by epigenetic mechanisms with the involvement of miRNAs expressed in germ line cells.


Diethylstilbestrol Injection, Veterinary Products, TradeIndia

image of diethylstilbestrol-injection
DES is still sold under different names.

DES was sold under many names including Distilbène®, Stilbetin®, Stilboestrol-Borne®, Benzestrol®, Chlorotrianisene®, Estrobene® and Estrosyn® to name just a few.

Many different companies manufactured and marketed this drug under more than 200 different brand names.

This Diethylstilbestrol Injection – DIBESTROL Inj.- is marketed by TradeIndia, Haryana, India.

DES Drugs Pictures
More DES DiEthylStilbestrol Resources

Effects of BPA on male and couple reproductive health

Endocrine disrupting chemicals: female and male reproduction


Bisphenol A (BPA) is a ubiquitous environmental toxicant with endocrine-disrupting properties and is suspected to affect human reproduction.

The objective of this review was to summarize the potential effects of male exposure to BPA on markers of testicular function and couple reproductive outcomes.

  • Five epidemiologic studies on BPA and reproductive hormones all found significant associations with at least one reproductive hormone; however, no consistent relationships were observed across studies.
  • Six epidemiologic studies evaluated the relation between BPA and semen parameters, and although the majority reported negative associations with various parameters, there were few consistent trends across studies.
  • Finally, three epidemiologic studies examined BPA and couple reproductive outcomes, and only one found an association.

Effects of bisphenol A on male and couple reproductive health: a review, Fertility and Sterility, Volume 106, Issue 4, Pages 864–870, September 15, 2016.

Scenes from around Thompson Research Center, cafnr.

Overall, the evidence supporting an association between BPA exposure and adverse male reproductive health outcomes in humans remains limited and inconclusive. Reasons for the discrepancies in results could include, but are not limited to, differences in study populations (e.g., fertile vs. subfertile men), BPA urinary concentrations (occupationally vs. nonoccupationally exposed), misclassification of BPA exposure (e.g., using one urine sample to characterize exposure vs. multiple samples), sample sizes, study design (e.g., cross-sectional vs. prospective), and residual confounding (e.g., due to diet and lifestyle factors). It is also possible that some of the statistically significant findings were due to chance alone.

Clearly, further studies are needed to further clarify the role of this ubiquitous endocrine-disrupting chemical on male reproductive health.

How did Doctors Not Know about the Risks of Hormone Therapy?

Via NutritionFacts.org, Dr. Greger, 21 September 2016

Read our posts tagged HRT, watch our video playlist on meds: prescription drugs side effects.

Bisphenol A and Ovarian Steroidogenesis

Endocrine disrupting chemicals: female reproduction, 2016


Bisphenol A is widely used as a component in polycarbonate plastics for food and beverage packaging, epoxy linings for canned foods, and dental sealants, among other applications.

Experimental literature demonstrates BPA‘s affinity for estrogen receptors and downstream effects on estrogen-responsive genes. Additional data suggest that BPA reduces endogenous estrogen synthesis, likely by antagonizing ovarian enzyme activities involved in sex-steroid hormone synthesis. More specifically, evidence indicates BPA-mediated disruption of STAR, CYP450scc, and HSD-3β in theca cells and CYP450 aromatase activity in granulosa cells.

Bisphenol A and ovarian steroidogenesis, Fertility and Sterility, Volume 106, Issue 4, Pages 857–863, September 15, 2016.

Piedras en el mar, chechipe.

Yet the results of the few human studies reported to date are equivocal. It also remains in question the extent to which BPA penetrates developing ovarian follicles. Uncertainty as to the relevance of experimental BPA doses and administration routes for common human exposure levels limits extrapolation of experimental results.

To more definitively address the potential risk of BPA on human ovarian steroidogenesis, additional experimental studies using biologically active BPA doses likely to reflect those within the ovarian follicle will be necessary, as will additional prospective investigations in human populations with the use of standardized assay methodology.

Children’s rights violation by toxic chemical exposure

Our duty to prevent childhood exposure

The best interests of the child should be at the heart of decision making when it comes to protecting children’s rights to life, survival and development, health, freedom from the worst forms of child labour, and also to safe food, water and housing. The UN Convention on the Rights of the Child explicitly links children’s right to health with pollution and contamination, but there are still systemic failures to realizing children’s rights in the context of toxic chemicals.

Childhood exposure to toxic substances in every part of the world has created a “silent pandemic” of disease and disability affecting millions of children and adults. Rates of disease and disability linked to childhood exposure to toxic chemicals have increased around the world at rates that can not be explained by genetics or lifestyle choices, leaving toxic chemicals and pollution as a major contributing factor. Recent cases have called into question how effectively States are protecting human rights when it comes to toxics, and children’s rights are arguably the most at risk. The World Health Organisation estimates that more than 1,700,000 children under the age of five died prematurely from modifiable environmental factors; but these figures are only the tip of the iceberg when it comes to death, disease and disability linked to toxics and pollution.

Duty to prevent childhood exposure, srtoxics, September 15, 2016.

Report of the Special Rapporteur on the implications for human rights of the environmentally sound management and disposal of hazardous substances and wastes, A/HRC/33/41, August 2016 .

Childhood exposure, See-ming Lee.

My new report, to be presented to the Human Rights Council in Sept. 2016, offers an examination of how children’s rights are violated by both State and non-state entities by exposure of under-18s to toxic chemicals and pollution. It argues that States have a duty, and businesses a corresponding responsibility, to prevent childhood exposure. Today, the laws, policies and practices of States and businesses are inconsistent with this obligation.

Emissions from manufacturing and extractive industries, the use of hazardous pesticides and industrial chemicals in consumer products and food incessantly expose children to hundreds of chemicals that are unquestionably hazardous and countless others with unknown risks. These exposures can all drastically affect the health and quality of life of children when exposed during critical periods of development, affecting their rights to life, health and physical integrity.

When exposure does occur, children are too often left without access to an effective remedy or justice for harms related to toxics and pollution. The deadly, lifelong impacts of this assault on children’s bodies frequently remain invisible until later in their lives, making it difficult to prove how and when the damage was done, and enabling impunity for perpetrators.

Solutions to the challenge of toxics and their impacts on children are available, but they must be rooted in human rights to be effective, including the obligation on States to prevent childhood exposure to toxic chemicals.”

Baskut, UN SPECIAL RAPPORTEUR On Human Rights & Toxics.

Stilbetin 25mg

DES Manufacturer: ER Squibb & Sons, New-York

image of stilbetin
DES was sold under many different names.

DES was sold under many names including Distilbène®, Stilbetin®, Stilboestrol-Borne®, Benzestrol®, Chlorotrianisene®, Estrobene® and Estrosyn® to name just a few.

Many different companies manufactured and marketed this drug under more than 200 different brand names.

These DES tablets – Stilbetin 25 mg Squibb Diethylstilbestrol- were manufactured by ER Squibb & Sons, New-York.

DES Drugs Pictures
Some Squibb & Sons DES Cases
More DES DiEthylStilbestrol Resources

La vaccination inutile et le racket des laboratoires pharmaceutiques

Invité du jour: Serge Rader, lanceur d’alerte

Vidéo publiée le 18 janvier 2016 par TV Libertés.

Aujourd’hui le calendrier vaccinal pose des soucis, et la balance bénéfices/risques semble peser très lourd sur le plateau des risques…

  • Auteur du livre “Le racket des laboratoires pharmaceutiques : et comment s’en sortir” Serge Rader, pharmacien durant de très nombreuses années et depuis peu lanceur d’alertes met en lumière, au travers de cas concrets, les dangers de la vaccination.
  • Nos liste de vidéos sur les médicaments et labos.

Environmental toxicants: hidden players on the reproductive stage

Endocrine disrupting chemicals: female and male reproduction


A growing body of evidence suggests that environmental contaminants, including natural gas, endocrine-disrupting chemicals, and air pollution, are posing major threats to human reproductive health.

Many chemicals are in commonly used personal care products, linings of food containers, pesticides, and toys, as well as in discarded electronic waste, textile treatments, and indoor and outdoor air and soil. They travel across borders through trade, food, wind, and water.

Reproductive and other health effects can be incurred by exposures in utero, in the neonatal or adolescent periods, or in adulthood and can have transgenerational effects.

Environmental toxicants: hidden players on the reproductive stage, Fertility and Sterility, Volume 106, Issue 4, Pages 791–794, September 15, 2016.

Most chemicals do not undergo the level of evaluation for harm that pharmaceuticals, e.g., do, and they are rarely seen or seriously considered as a danger to human health.

Herein, the burden of exposures, challenges in assessing data and populations at risk, models for evaluating harm, and mechanisms of effects are briefly reviewed, ending with a call to action for reproductive health care professionals to advocate for further research, education, and chemical policy reform for the health of this and future generations.

BPA may be associated with infertility in women

Endocrine disrupting chemicals: female reproduction


We summarized the scientific literature published from 2007 to 2016 on the potential effects of bisphenol A (BPA) on female fertility. We focused on overall fertility outcomes (e.g., ability to become pregnant, number of offspring), organs that are important for female reproduction (i.e., oviduct, uterus, ovary, hypothalamus, and pituitary), and reproductive-related processes (i.e., estrous cyclicity, implantation, and hormonal secretion).

The reviewed literature indicates that BPA may be associated with infertility in women. Potential explanations for this association can be generated from experimental studies.

Evidence for bisphenol A-induced female infertility: a review (2007–2016), Fertility and Sterility, Volume 106, Issue 4, Pages 827–856, September 15, 2016.

Infertility by adrianos_evangelidis.

Specifically, BPA may alter overall female reproductive capacity by affecting the morphology and function of the oviduct, uterus, ovary, and hypothalamus-pituitary-ovarian axis in animal models.

In addition, BPA may disrupt estrous cyclicity and implantation. Nevertheless, further studies are needed to better understand the exact mechanisms of action and to detect potential reproductive toxicity at earlier stages.