DES, Epigenetics and Gene Expression, DNA Function, and various Aspects of Inheritance

EpigeneticsDES Diethylstilbestrol, Journal of a DES Daughter logo is cited as one example showing what is happening in our world today when we are exposed to certain chemicals:

” … Like with so many other medical drugs, DES was a horror story of unimaginable proportions and did not stop with the mother. Besides causing … “. Read Epigenetics by Dr. Anderson

More DES DiEthylStilbestrol Resources

Pregnancy Exposure to High-Fat and Estrogen increases Breast Cancer Inheritance in Three Generations of Offspring

High-fat or ethinyl-oestradiol intake during pregnancy increases mammary cancer risk in several generations of offspring

Pregnancy Exposure Increases Breast Cancer Inheritance in OffspringA study by researchers from Georgetown Lombardi Comprehensive Cancer Center and Virginia Tech shows that exposure to diets high in fat or a large amount of estrogen during pregnancy can heighten the risk of breast cancer for numerous subsequent generations of female offspring, including daughters, granddaughters and great-granddaughters. ”

Abstract

Maternal exposures to environmental factors during pregnancy influence the risk of many chronic adult-onset diseases in the offspring. Here we investigate whether feeding pregnant rats a high-fat (HF)- or ethinyl-oestradiol (EE2)-supplemented diet affects carcinogen-induced mammary cancer risk in daughters, granddaughters and great-granddaughters. We show that mammary tumourigenesis is higher in daughters and granddaughters of HF rat dams and in daughters and great-granddaughters of EE2 rat dams. Outcross experiments suggest that the increase in mammary cancer risk is transmitted to HF granddaughters equally through the female or male germ lines, but it is only transmitted to EE2 granddaughters through the female germ line. The effects of maternal EE2 exposure on offspring’s mammary cancer risk are associated with changes in the DNA methylation machinery and methylation patterns in mammary tissue of all three EE2 generations. We conclude that dietary and oestrogenic exposures in pregnancy increase breast cancer risk in multiple generations of offspring, possibly through epigenetic means.

  • Read Pregnancy Exposure Increases Breast Cancer Inheritance in Offspringredorbit, September 2012..
  • High-fat or ethinyl-oestradiol intake during pregnancy increases mammary cancer risk in several generations of offspring, nature, 11 September 2012.
  • Pregnancy exposures determine risk of breast cancer in multiple generations of offspring, eurekalert, 11-SEP-2012.
  • DES studies on epigenetics and transgenerational effects.

Poisoned by every Day Life: PLOS One Landmark Study

Plastics Derived Endocrine Disruptors (BPA, DEHP and DBP) Induce Epigenetic Transgenerational Inheritance of Obesity, Reproductive Disease and Sperm Epimutations

Chemicals found in every home may cause breast cancer, asthma, infertility and birth defects, global health chiefs said yesterday

Poisoned by every day life: Landmark study warns gender bending chemicals in your home, food and car ARE linked to a huge range of diseases  Read more: http://www.dailymail.co.uk/news/article-2281394/Poisoned-day-life-Landmark-study-warns-gender-bending-chemicals-home-food-car-ARE-linked-huge-range-diseases.html#ixzz2LfOpgG2J  Follow us: @MailOnline on Twitter | DailyMail on Facebook

  • Phthalates is used to soften plastic and improve consistency of cosmetics
  • Chemical commonly found in children’s toys, make up, cars and PVC flooring
  • Could cause breast cancer, asthma, infertility and birth defects, WHO says

Read Poisoned by every day life: Landmark study warns gender bending chemicals in your home, food and car ARE linked to a huge range of diseases.

PLOS One Study Abstract

Environmental compounds are known to promote epigenetic transgenerational inheritance of adult onset disease in subsequent generations (F1–F3) following ancestral exposure during fetal gonadal sex determination. The current study was designed to determine if a mixture of plastic derived endocrine disruptor compounds bisphenol-A (BPA), bis(2-ethylhexyl)phthalate (DEHP) and dibutyl phthalate (DBP) at two different doses promoted epigenetic transgenerational inheritance of adult onset disease and associated DNA methylation epimutations in sperm. Gestating F0 generation females were exposed to either the “plastics” or “lower dose plastics” mixture during embryonic days 8 to 14 of gonadal sex determination and the incidence of adult onset disease was evaluated in F1 and F3 generation rats. There were significant increases in the incidence of total disease/abnormalities in F1 and F3 generation male and female animals from plastics lineages. Pubertal abnormalities, testis disease, obesity, and ovarian disease (primary ovarian insufficiency and polycystic ovaries) were increased in the F3 generation animals. Kidney and prostate disease were only observed in the direct fetally exposed F1 generation plastic lineage animals. Analysis of the plastics lineage F3 generation sperm epigenome previously identified 197 differential DNA methylation regions (DMR) in gene promoters, termed epimutations. A number of these transgenerational DMR form a unique direct connection gene network and have previously been shown to correlate with the pathologies identified. Observations demonstrate that a mixture of plastic derived compounds, BPA and phthalates, can promote epigenetic transgenerational inheritance of adult onset disease. The sperm DMR provide potential epigenetic biomarkers for transgenerational disease and/or ancestral environmental exposures.

Read Plastics Derived Endocrine Disruptors (BPA, DEHP and DBP) Induce Epigenetic Transgenerational Inheritance of Obesity, Reproductive Disease and Sperm Epimutations, PLOS one, January 24, 2013.

Could you blame your Ancestors for your Fertility Problems?

Toxic Environmental Exposures Could Cause Reproductive Harm Across Generations

Could you blame your Ancestors for your Fertility Problems?

Industry likes to say that the risk isn’t so big or the exposures are not so high. But, in fact, these exposures can have far-reaching effects. Unfortunately, regulators are having difficulty even coming to sensible conclusions on direct effects, let alone transgenerational ones.

Why are they not drawing any lessons from the DES drug disaster? … !!!

Abstract

The actions of environmental toxicants and relevant mixtures in promoting the epigenetic transgenerational inheritance of ovarian disease was investigated with the use of a fungicide, a pesticide mixture, a plastic mixture, dioxin and a hydrocarbon mixture. After transient exposure of an F0 gestating female rat during embryonic gonadal sex determination, the F1 and F3 generation progeny adult onset ovarian disease was assessed. Transgenerational disease phenotypes observed included an increase in cysts resembling human polycystic ovarian disease (PCO) and a decrease in the ovarian primordial follicle pool size resembling primary ovarian insufficiency (POI). The F3 generation granulosa cells were isolated and found to have a transgenerational effect on the transcriptome and epigenome (differential DNA methylation). Epigenetic biomarkers for environmental exposure and associated gene networks were identified. Epigenetic transgenerational inheritance of ovarian disease states was induced by all the different classes of environmental compounds, suggesting a role of environmental epigenetics in ovarian disease etiology.