Pour la Protection des Lanceurs d’Alerte

Des ONG et 60K citoyens demandent une réécriture de l’article définissant le lanceur d’alerte

En savoir plus

  • 17 ONG & 55K citoyens appellent les députés à protéger les #lanceursdalerte, Transparency France.
  • Irène Frachon, une colère toujours alerte, liberation, 20 mai 2016.
  • Protection des lanceurs d’alerte : les ONG demandent une réécriture de l’article définissant le lanceur d’alerte, transparency-france, 10 juin 2016.
  • Protégeons nos lanceurs d’alerte, PowerFoule.

Diethyl-Stilbestrol prescription tablets 1 mg

DES prescription tablets manufactured by Eli Lilly & Co, Indianapolis, USA

image of diethyl-stilbestrol
Diethyl-Stilbestrol prescription tablets manufactured by Eli Lilly & Co, Indianapolis, USA.

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 Diethyl-Stilbestrol prescription drugs – 100 tablets of 1 mg – were manufactured by: Eli Lilly & Co, Indianapolis, USA.

DES Drug Pictures
More DES DiEthylStilbestrol resources

Les perturbateurs endocriniens et la Commission Européenne

Perturbateurs endocriniens : ultimes manœuvres à Bruxelles des scientifiques liés à l’industrie

Pour limiter la réglementation, les géants de la chimie et des pesticides tentent d’imposer une critère de “puissance” des polluants chimiques.

Substance Abuse in Schools

School Counselor’s Role With Students At Risk for Substance Abuse

School Counselor’s Role With Students At Risk for Substance Abuse

This infographic by Bradley University’s Online Master of Arts in Counseling program discusses prevention strategies and also the various treatments that are available for the students that are at risk to substance abuse.

Stress exposure during pregnancy observed in mothers of children with autism

Stress in pregnancy and autism: New gene-stress interaction uncovered

Stress during pregnancy has been linked to several conditions, including some instances of autism spectrum disorder. Now, researchers at the University of Missouri School of Medicine have observed a variant of a stress-sensitive gene and exposure to stress during pregnancy among two groups of mothers of children with autism. The researchers believe the finding could be a step toward helping identify women who have greater risks for having children with autism when exposed to stressors during a specific time window during pregnancy.


Maternal serotonin transporter genotype affects risk for ASD with exposure to prenatal stress, International Society for Autism Research, 19 APR 2016

Stress exposure during gestation is implicated in several neuropsychiatric conditions, including autism spectrum disorder (ASD). Previous research showed that prenatal stress increases risk for ASD with peak exposure during the end of the second and the beginning of the third trimester. However, exposures to prenatal stress do not always result in ASD, suggesting that other factors may interact with environmental stressors to increase ASD risk. The present study examined a maternal genetic variation in the promoter region of the serotonin transporter gene (5-HTTLPR) affecting stress tolerance and its interaction with the effect of environmental stressors on risk for ASD. Two independent cohorts of mothers of ASD children recruited by the University of Missouri and Queen’s University were surveyed regarding the prenatal environment and genotyping on 5-HTTLPR was performed to explore this relationship. In both samples, mothers of children with ASD carrying the stress susceptible short allele variant of 5-HTTLPR experienced a greater number of stressors and greater stress severity when compared to mothers carrying the long allele variant. The temporal peak of stressors during gestation in these mothers was consistent with previous findings. Additionally, increased exposure to prenatal stress was not reported in the pregnancies of typically developing siblings from the same mothers, regardless of maternal genotype, suggesting against the possibility that the short allele might increase the recall of stress during pregnancy. The present study provides further evidence of a specific maternal polymorphism that may affect the risk for ASD with exposure to prenatal stress.

Nonbinary: now a legal gender in the United States

US Court Allows a Person to Choose Neither Sex

On June 10, 2016, a Multnomah County Circuit Court Judge for the State of Oregon granted Jamie Shupe’s petition to change the legal sex/gender marker from female to nonbinary. This is understood to be the first order from a United States state court to recognize “non-binary” as a legal gender/sex identifier as part of a legal sex change procedure.

Oregon Court Allows a Person to Choose Neither Sex, nytimes, JUNE 13, 2016.

Oregon law does not specifically limit gender choices to male or female. Instead, the law allows a judge to order a legal change of sex and enter a judgment indicating the change of sex of a person if the court determines that the individual has undergone surgical, hormonal or other treatment appropriate for that individual for the purpose of gender transition and that sexual reassignment has been completed.

Other countries already federally recognize genders other than male and female—including Australia, Denmark, Nepal, and New Zealand.

A Generation in Jeopardy

How pesticides are undermining our children’s health and intelligence

A-Generation-in-Jeopardy book cover image
Read and download the full report, A Generation in Jeopardy, How pesticides are undermining our children’s health & intelligence, October 2012 Pesticide Action Network North America.

Children today are sicker than they were a generation ago. From childhood cancers to autism, birth defects and asthma, a wide range of childhood diseases and disorders are on the rise. Our assessment of the latest science leaves little room for doubt: pesticides are one key driver of this sobering trend.

As the recent President’s Cancer Panel reports, we have been “grossly underestimating” the contribution of environmental contamination to disease, and the policies meant to protect us have fallen far short. Nearly 20 years ago, scientists at the National Research Council called for swift action to protect young and growing bodies from pesticides. Yet today, U.S. children continue to be exposed to pesticides that are known to be harmful in places they live, learn and play.

Report Overview

1. Brainpower at Risk
Studies find pesticides can compromise intelligence
• ADHD rates continue to rise
• Autism rates jump 250% in one decade
• Derailed brain development means falling IQs
2. Cancer, Birth Defects & Early Puberty
Latest science links many health harms to pesticides
• Some childhood cancers linked to pesticides
• Birth defects rise with seasonal or occupational exposures
• Changes in puberty timing linked to low-level exposures
3. Emerging Science
Obesity, diabetes & asthma
• Childhood obesity, diabetes & disrupted metabolism
• Asthma epidemicaffects more than 7 million children
4. Critical Junctures
Prenatal & early childhood exposures most harmful
• Fetal exposure can have life long effects
• Pesticide exposures common at home,daycare & school
• Pesticide residues, from breastmilk to the school lunch tray
• Children’s developing minds & bodies particularly vulnerable
5. Case Studies
Communities win protections for children
• Pesticideuse now 1.1 billion poundsyearly
• Saferpest control in daycare & at school
• Pesticide-freeschool lunches
• Parks & playgrounds without pesticides
6. Investing in Healthy Futures
A solid start for children must be a national priority
• Pesticide industry well servedbycurrentpolicies
• Prioritizing children’s health requires real change
• Effective policies urgently needed: Our recommendations
Appendix A: More Science: Key study descriptions
Appendix B: Top Pesticides Used in Agriculture & at Home
Appendix C: Online Resources & Tools

Read and download the full reportA Generation in Jeopardy, How pesticides are undermining our children’s health & intelligence, October 2012 Pesticide Action Network North America.

The Evidence of the EDCs Effect on Gender: the DES Situation

Are EDCs blurring issues of gender?


Although scientists have postulated a wide range of adverse human health effects of exposure to endocrine-disrupting chemicals (EDCs), the nexus of the debate is the concern that prenatal and childhood exposure to EDCs may be responsible for a variety of abnormalities in human sexuality, gender development and behaviors, reproductive capabilities, and sex ratios. Scientists today are asking hard questions about potential human effects: Do EDC exposures impair fertility in men or women? Can they cause sexual organ malformations, stunted reproductive development, or testicular or breast cancer? Do fetal exposures to EDCs alter sex phenotypes? Do they change later gender-related neurobiological characteristics and behaviors such as play activity and spatial ability? Could such exposures even be involved in the etiology of children born with ambiguous gender?

Are EDCs Blurring Issues of Gender?, Environnement Health Perspectives, NCBI PubMed PMC1281309, 2005 Oct.

EDCs include a spectrum of substances that can be loosely classified according to their known or suspected activity in relation to sex hormone receptors and pathways. The most-studied and best known are the environmental estrogens, which mimic estradiol and bind to estrogen receptors (ERs). ER agonists include the pesticide methoxychlor, certain polychlorinated biphenyls (PCBs), bisphenol A (BPA; a high production volume chemical used to make polycarbonate plastic), pharmaceutical estrogens such as diethylstilbestrol (DES) and ethinyl estradiol, and phytoestrogens, which occur naturally in many plants, most notably in soybeans in the form of genistein and related substances. There are a few known ER antagonists, or antiestrogens. Antiandrogens, or androgen receptor (AR) antagonists, include the fungicide vinclozolin, the DDT metabolite p,p′-DDE, certain phthalates (a group of chemicals used to soften polyvinyl chloride plastics), and certain other PCBs. And there are other types of EDCs that affect particular endocrine targets. The various EDCs differ greatly in their potencies relative to natural hormones, and in their affinity for target receptors. Some have been shown to act via non–receptor-mediated mechanisms, for example by interfering with hormone synthesis.

In many well-documented cases of high-level fetal exposures to known EDCs such as DES, certain PCBs, and DDT, the answer to the question of whether exposure is associated with gender-related effects is clearly yes. But high-level exposures such as these are relatively rare and isolated. The debate today centers on low-dose exposures—generally defined as doses that approximate environmentally relevant levels—and the idea that low-dose intrauterine exposure to some EDCs during certain critical windows of development can have profound, permanent impacts on subsequent fetal development and adult outcomes.

Critics of this idea maintain that thus far there is no credible evidence to suggest that low-dose exposures cause any adverse human health effects. But if low-dose exposures were confirmed to be the threat that proponents of the concept insist they are, public health would clearly be at risk, regulatory agencies’ risk assessment approach would need to be revised, and certain common chemicals—including some that are massively produced and economically important—would likely disappear from the marketplace.

In a June 2000 EHP review article on human health problems associated with EDCs, Stephen Safe, director of the Center for Environmental and Genetic Medicine at Texas A&M University, concluded that

“the role of endocrine disruptors in human disease has not been fully resolved; however, at present the evidence is not compelling.”

Frederick vom Saal, a developmental biologist at the University of Missouri–Columbia, disagrees, particularly in light of the research that’s been presented in the years since that review. He says

“The jury is not out on human effects. In terms of the amount of information we have in animals and the amount of information we have in humans, clearly there is a huge difference, but that’s a lot different than saying the jury is out on whether EDCs influence humans.”

One thing both scientists might agree on, though, is that right now there are still more questions than answers.

Evidence of Effects: the DES situation

The Global Assessment further states that the only evidence showing that humans are susceptible to EDCs is currently provided by studies of high exposure levels. There is, in fact, clear evidence that intrauterine EDC exposures can alter human reproductive tract development and physiology. The most thoroughly characterized example is DES, the synthetic estrogen prescribed to millions of pregnant women in the United States and elsewhere from the 1940s to the 1970s to prevent miscarriage. The drug is known to have caused a rare form of vaginal cancer in thousands of daughters of women who took DES, as well as a variety of adverse reproductive tract effects in both the daughters and sons of those women.

The DES situation could be seen as a worst-case scenario for prenatal EDC exposure—the deliberate delivery of a potent estrogenic chemical in high doses. Viewed another way, it has provided researchers a rare opportunity to study the effects of prenatal EDC exposure in a relatively controlled fashion, with a well-defined population and well-characterized exposure to a single potent agent.

Over the course of her research, Newbold has developed a mouse model of DES exposure that has proven extremely useful in studying the effects of DES and other environmental estrogens, particularly those outcomes that may be manifested only later in life. She says

“With the experimental model, there are a lot of questions we can ask with DES that will tell us about the weaker environmental estrogens. We can change the timing of exposure and the amount of exposure, and we can look at different target tissues.”

The animal model has replicated numerous abnormalities reported in DES-exposed humans, and has also predicted some human outcomes.

“We have published documentation [see, for example, the October 1985 issue of Cancer Research and volume 5, issue 6 (1985) of Teratogenesis, Carcinogenesis, and Mutagenesis] that a number of the reproductive anomalies seen in DES-exposed mice, such as retained testes and abnormalities in the oviduct in females, were also later reported in DES-exposed humans,”

says Newbold.

More DES DiEthylStilbestrol resources

How Cancer Screening Is Portrayed in the U.K. National Press

Annals of Graphic Medicine : Living on Benefits

Annals of Graphic Medicine : Living on Benefits

Written by Jack W. Bedeman, BM, BSc, MSc; Susanne F. Meisel, PhD; and Nora Pashayan, MD, PhD, and illustrated by Jack W. Bedeman, BM, BSc, MSc., 3 May 2016.

Ann Intern Med. 2016;164(9):W13-W14. doi:10.7326/G15-0019
© 2016 American College of Physicians.

Health comics

Most terminal cancer patients are not aware they are approaching the end

Two third of terminal illness patients do not discuss their treatment goals, prognosis/life expectancy with their oncologists


Discussions of Life Expectancy and Changes in Illness Understanding in Patients With Advanced Cancer, American Society of Clinical Oncology, May 23, 2016.

Image “Blowing in the wind” by Benn Berrigan.

Accurate illness understanding enables patients to make informed decisions. Evidence of the influence of prognostic discussions on the accuracy of illness understanding by patients would demonstrate the value of discussions.

Recent and past oncology provider-patient discussions about prognosis/life expectancy were examined for their association with changes in illness understanding by patients. Patients (N = 178) with advanced cancers refractory to prior chemotherapy whom oncologists expected to die within 6 months were interviewed before and after a visit in which cancer restaging scan results were discussed. Illness understanding scores were the sum of four indicator variables: patient terminal illness acknowledgment, recognition of incurable disease status, knowledge of the advanced stage of the disease, and expectation to live months as opposed to years.

Before the restaging scan visit, nine (5%) of 178 patients had completely accurate illness understanding (ie, correctly answered each of the four illness understanding questions). Eighteen patients (10%) reported only recent discussions of prognosis/life expectancy with their oncologists; 68 (38%) reported only past discussions; 24 (13%) reported both recent and past discussions; and 68 (38%) reported that they never had discussions of prognosis/life expectancy with their oncologists. After adjustment for potential confounders (ie, education and race/ethnicity), analysis identified significant, positive changes in illness understanding scores for patients in groups that reported recent only (least-squares mean change score, 0.62; 95% CI, 0.23 to 1.01; P = .002) and both recent and past (least-squares mean change score, 0.37; 95% CI, 0.04 to 0.70; P = 0.028) discussions of prognosis/life expectancy with their oncologists.

Patients with advanced cancer who acknowledge recent or ongoing discussions of prognosis/life expectancy with their oncology providers come to have a better understanding of the terminal nature of their illnesses and, thus, may be better prepared to make informed end-of-life care decisions.