Soutenez Daniel Cueff, maire courageux, contre les pesticides à proximité des habitations

Paradoxalement, un maire a pris un risque juridique en protégeant ses administrés

“Ne doutez jamais qu’un petit groupe de personnes peuvent changer le monde. En fait, c’est toujours ainsi que le monde a changé.”

~Margaret Mead~

Le 18 mai dernier, Daniel Cueff, maire de Langouët en Bretagne a signé un arrêté interdisant l’épandage de pesticides “à une distance inférieure à 150 m de toute parcelle cadastrale comprenant un bâtiment à usage d’habitation ou professionnel“. Un mois plus tard, la préfecture de Bretagne a fait savoir qu’elle souhaitait casser cette décision.
Vidéo publiée le 08.08.2019 par agir pour l’environnement.

  • Soutenez le maire de Langouët sur agirpourlenvironnement, sur change. ou sur mes opinions.
  • Pesticides. En Ille-et-Vilaine, le maire de Langouët tient tête à la préfète de Bretagne, ouest-france, 25/06/2019. Lire la réponse du maire.
  • Daniel Cueff, le maire breton qui invente le village de l’après-pétrole, Le Monde, 19 juin 2019.
  • Arrêté contre les pesticides en Bretagne. C’est le tribunal administratif qui devra trancher, ouest-france, 11/06/2019.
  • Bretagne. La préfecture demande au maire de Langouët de retirer son arrêté contre les pesticides, ouest-france, 11/06/2019.
  • Pesticides à Langouët : un arrêté discutable mais une opportunité, selon la Conf’paysanne, ouest-france, 04/06/2019.
  • Langouët, village breton 100 % écolo, veut interdire les pesticides, ouest-france, 23/05/2019.
  • Ille-et-Vilaine. Le maire de Langouët interdit les pesticides près des habitations, ouest-france, 18/05/2019.

Identification of Spin in Clinical Studies Evaluating Biomarkers in Ovarian Cancer

Medical research publications : how to modify (abstracts) perception of results

Mona Ghannad presents a systematic review which documents and classifies spin or overinterpretation, as well as facilitators of spin, in recent clinical studies evaluating performance of biomarkers in ovarian cancer. Video published on 11 Oct 2017. Reference.

The objective of this systematic review was to document and classify spin or overinterpretation, as well as facilitators of spin, in recent clinical studies evaluating performance of biomarkers in ovarian cancer.

We searched PubMed systematically for all studies published in 2015. Studies eligible for inclusion described 1 or more trial designs for identification and/or validation of prognostic, predictive, or diagnostic biomarkers in ovarian cancer. Reviews, animal studies, and cell line studies were excluded. All studies were screened by 2 reviewers. To document and characterize spin, we collected information on the quality of evidence supporting the study conclusions, linking the performance of the marker to outcomes claimed.

In total, 1026 potentially eligible articles were retrieved by our search strategy, and 345 studies met all eligibility criteria and were included. The first 200 studies, when ranked according to publication date, will be included in our final analysis. Data extraction was done by one researcher and validated by a second. Specific information extracted and analyzed on study and journal characteristics, key information on the relevant evidence in methods, and reporting of conclusions claimed for the first 50 studies is provided here. Actual forms of spin and facilitators of spin were identified in studies trying to establish the performance of the discovered biomarker.

Actual forms of spin identified as shown (Table) were:

  1. other purposes of biomarker claimed not investigated (18 of 50 studies [36%]);
  2. incorrect presentation of results (15 of 50 studies [30%]);
  3. mismatch between the biomarker’s intended clinical application and population recruited (11 of 50 studies [22%]);
  4. mismatch between intended aim and conclusion (7 of 50 studies [14%]);
  5. and mismatch between abstract conclusion and results presented in the main text (6 of 50 studies [12%]).

Frequently observed facilitators of spin were:

  1. not clearly prespecifying a formal test of hypothesis (50 of 50 studies [100%]);
  2. not stating sample size calculations (50 of 50 studies [100%]);
  3. not prespecifying a positivity threshold of continuous biomarker (17 of 43 studies [40%]);
  4. not reporting imprecision or statistical test for data shown (ie, confidence intervals, P values) (12 of 50 studies [24%]);
  5. and selective reporting of significant findings between results for primary outcome reported in abstract and results reported in main text (9 of 50 studies [18%]).

Spin was frequently documented in abstracts, results, and conclusions of clinical studies evaluating performance of biomarkers in ovarian cancer. Inflated and selective reporting of biomarker performance may account for a considerable amount of waste in the biomarker discovery process. Strategies to curb exaggerated reporting are needed to improve the quality and credibility of published biomarker studies.

Toxic Soup Flooding Through Consumer Products and Toys Made of Recycled Plastics

High Levels of Dioxins Found in Children’s Toys and Other Products Made of Recycled Plastics Found in Argentina, Brazil, Cambodia, Canada, the EU, India, Japan and Nigeria

Despite being largely phased out a decade ago because of their adverse health effects, PBDEs continue to show up in everyday products made from recycled plastics, ensia reports.

Alarming levels of some of the most toxic chemicals, including brominated dioxins and brominated flame retardants, were found in consumer products made of recycled plastics sold in Argentina, Brazil, Cambodia, Canada, the EU, India, Japan and Nigeria, ipen says. Dioxins were measured in children’s toys and hair accessories at levels comparable to those found in hazardous wastes, including the ash from waste incinerators, ipen reports.

Systematic reviews with financial conflicts of interest linked to favourable conclusions and lower methodological quality

Financial conflicts of interest in systematic reviews: associations with results, conclusions, and methodological quality


Financial conflicts of interest in systematic reviews (e.g. funding by drug or device companies or authors’ collaboration with such companies) may impact on how the reviews are conducted and reported.

To investigate the degree to which financial conflicts of interest related to drug and device companies are associated with results, conclusions, and methodological quality of systematic reviews.

Search methods
We searched PubMed, Embase, and the Cochrane Methodology Register for studies published up to November 2016. We also read reference lists of included studies, searched grey literature sources, and Web of Science for studies citing the included studies.

Selection criteria
Eligible studies were studies that compared systematic reviews with and without financial conflicts of interest in order to investigate differences in results (estimated treatment effect and frequency of statistically favourable results), frequency of favourable conclusions, or measures of methodological quality of the review (e.g. as evaluated on the Oxman and Guyatt index).

Data collection and analysis
Two review authors independently determined the eligibility of studies, extracted data, and assessed risk of bias. We synthesised the results of each study relevant to each of our outcomes. For meta‐analyses, we used Mantel‐Haenszel random‐effects models to estimate risk ratios (RR) with 95% confidence intervals (CIs), with RR > 1 indicating that systematic reviews with financial conflicts of interest more frequently had statistically favourable results or favourable conclusions, and had lower methodological quality. When a quantitative synthesis was considered not meaningful, results from individual studies were summarised qualitatively.

Main results
Ten studies with a total of 995 systematic reviews of drug studies and 15 systematic reviews of device studies were included. We assessed two studies as low risk of bias and eight as high risk, primarily because of risk of confounding. The estimated treatment effect was not statistically significantly different for systematic reviews with and without financial conflicts of interest (Z‐score: 0.46, P value: 0.64; based on one study of 14 systematic reviews which had a matched design, comparing otherwise similar systematic reviews). We found no statistically significant difference in frequency of statistically favourable results for systematic reviews with and without financial conflicts of interest (RR: 0.84, 95% CI: 0.62 to 1.14; based on one study of 124 systematic reviews). An analysis adjusting for confounding due to methodological quality (i.e. score on the Oxman and Guyatt index) provided a similar result. Systematic reviews with financial conflicts of interest more often had favourable conclusions compared with systematic reviews without (RR: 1.98, 95% CI: 1.26 to 3.11; based on seven studies of 411 systematic reviews). Similar results were found in two studies with a matched design, which therefore had a reduced risk of confounding. Systematic reviews with financial conflicts of interest tended to have lower methodological quality compared with systematic reviews without financial conflicts of interest (RR for 11 dimensions of methodological quality spanned from 1.00 to 1.83). Similar results were found in analyses based on two studies with matched designs.

Authors’ conclusions
Systematic reviews with financial conflicts of interest more often have favourable conclusions and tend to have lower methodological quality than systematic reviews without financial conflicts of interest. However, it is uncertain whether financial conflicts of interest are associated with the results of systematic reviews. We suggest that patients, clinicians, developers of clinical guidelines, and planners of further research could primarily use systematic reviews without financial conflicts of interest. If only systematic reviews with financial conflicts of interest are available, we suggest that users read the review conclusions with skepticism, critically appraise the methods applied, and interpret the review results with caution.

Reforming disease definitions : a new primary care led, people-centred approach

Drug Companies Shouldn’t Help Decide Who Is Sick, 2019


Expanding disease definitions are causing more and more previously healthy people to be labelled as diseased, contributing to the problem of overdiagnosis and related overtreatment. Often the specialist guideline panels which expand definitions have close ties to industry and do not investigate the harms of defining more people as sick. Responding to growing calls to address these problems, an international group of leading researchers and clinicians is proposing a new way to set diagnostic thresholds and mark the boundaries of condition definitions, to try to tackle a key driver of overdiagnosis and overtreatment. The group proposes new evidence-informed principles, with new process and new people constituting new multi-disciplinary panels, free from financial conflicts of interest. Image wikimedia.


Developing a framework for this long-term reform and facilitating a global collaboration to enact it will involve proactive and reactive efforts that we hope will drive a cultural shift and a practical change in how diseases are defined. Research teams will continue to quantify estimates of overdiagnosis arising from current disease definitions, informing priorities for action. Actions include the constitution of new panels, with new processes and new people, to review and revise existing definitions. Concurrently, primary care organisations will become more reactive to expansions in definitions seen as increasing the risk of overdiagnosis, such as the controversial 2017 hypertension widening, explicitly rejected by the American Academy of Family Physicians, and other groups, and the rejection of the expanded definition of gestational diabetes by the Royal Australian College of General Practitioners. An international meeting to review progress on our proposal and develop more detailed strategies for change will take place at the December 2019 Preventing Overdiagnosis conference in Sydney

There are important limitations, uncertainties and caveats to note as we propose this ambitious reform of disease definitions, which will provoke opposition from those whose markets are directly threatened.

  1. First, we write as a group working across a multitude of influential national and international organisations, but we do not in this instance represent them.
  2. Second, our backgrounds and thinking are largely medical, and there is clearly opportunity for this initiative to be informed by evidence, experience and theories outside medicine, including, for example, from philosophy.
  3. Third, addressing the problem of expanding disease definitions is but one of many potential solutions to overdiagnosis, and much important work is underway already to try and wind back the harms of too much medicine, safely and fairly, such as calls to action within our associations, creation of new medical curricula, scientific discussion at national and international meetings and new information materials for the public.
  4. Fourth, given the novel nature of this proposal, there is not yet a mature evidence-base to support it.
  5. Fifth, there is clear synergy between this proposal and the calls for reform of clinical practice guidelines, which has not been explored in this analysis.
  6. And finally, we acknowledge moves to expand definitions, to detect and treat people earlier, are often driven by the best of intentions, and we see great merit in identifying those who will benefit from a medical label and subsequent care.

However, notwithstanding the good intentions driving a bad system, the human person can no longer be treated as an ever-expanding marketplace of diseases, benefiting professional and commercial interests while bringing great harm to those unnecessarily diagnosed.

Transgenerational BPA exposure may contribute to autism

Transgenerational Bisphenol A Causes Deficits in Social Recognition and Alters Postsynaptic Density Genes in Mice, 2019

According to a recent mouse study, BPA exposure has transgenerational effects on gene linked to autism – social recognition test used for first time in mice showed behavioral deficit – the Endocrine Society reports.

2019 Study Abstract

Bisphenol A (BPA) is a ubiquitous endocrine-disrupting chemical. Developmental exposure produces changes in behavior and gene expression in the brain. Here, we examined social recognition behaviors in mice from the third familial generation (F3) after exposure to gestational BPA. Second-generation mice were bred in one of four mating combinations to reveal whether characteristics in F3 were acquired via maternal or paternal exposures. After repeated habituation to the same mouse, offspring of dams from the BPA lineage failed to display increased investigation of a novel mouse. Genes involved in excitatory postsynaptic densities (PSDs) were examined in F3 brains using quantitative PCR. Differential expression of genes important for function and stability of PSDs were assessed at three developmental ages. Several related PSD genes―SH3 and multiple ankyrin repeat domains 1 (Shank1), Homer scaffolding protein 1c (Homer1c), DLG associated protein 1 (Gkap), and discs large MAGUK scaffold protein 4 (PSD95)―were differentially expressed in control- vs BPA-lineage brains. Using a second strain of F3 inbred mice exposed to BPA, we noted the same differences in Shank1 and PSD95 expression in C57BL/6J mice. In sum, transgenerational BPA exposure disrupted social interactions in mice and dysregulated normal expression of PSD genes during neural development. The fact that the same genetic effects were found in two different mouse strains and in several brain regions increased potential for translation. The genetic and functional relationship between PSD and abnormal neurobehavioral disorders is well established, and our data suggest that BPA may contribute in a transgenerational manner to neurodevelopmental diseases.

DES and the GENES

Disorders of sexual development may be more common in newborns than what we think

Frequency of Ambiguous Genitalia in 14,177 Newborns in Turkey, 2019

According to a recent study, ambiguous genitalia in newborns may be more common than previously thought, the Endocrine Society reports.

“Our research found 18 babies with ambiguous genitalia among 14,177 newborns (1.3 in 1,000 births). This frequency is higher when compared to previous studies (1 in 4,500-5,500),”

“These findings support the hypothesis that early placental dysfunction and androgen deficiency might be important in the etiology of male genital anomalies,”

said the study’s first author, Banu Kucukemre Aydin, M.D., of Istanbul University in Turkey. Image credit Intersex Human Rights Australia.

2019 Study Abstract

Limited data are available on the exact incidence of disorders of sex development (DSD) with genital ambiguity at birth.

To determine frequency of ambiguous genitalia in newborns.

Prospective multicenter study.

Three tertiary care hospitals.

Patients or Other Participants
All 14,177 babies born during the study period were included.

Main Outcome Measures
All newborns were examined at birth; data on weeks of gestation, birth weight, and length were collected. A structured questionnaire was used for data collection. Quigley and Prader scales were used for phenotypic grading. Clinical and genetic investigations were performed.

Eighteen babies with ambiguous genitalia were found among 14,177 newborns (1.3/1000). Fifteen newborns had 46,XY DSD, one had 46,XX congenital adrenal hyperplasia, and one had 45,X/46,XY mixed gonadal dysgenesis. Karyotype analysis was not done in one baby who died in the neonatal period. The ratio of prematurity was higher in the DSD group (44% vs 11%; P < 0.001) and the ratio of small for gestational age was also higher in the DSD group (22% vs 5%; P = 0.007). Eight babies with DSD had mothers who had additional medical conditions, such as preeclampsia, depression, insulin resistance, and gestational diabetes mellitus.

The frequency of ambiguous genitalia was higher than in previous studies, but, as with any experiment, the finding should be met with caution because this study was conducted in tertiary care hospitals. In addition, lower birth weight in the DSD group supports the hypothesis that early placental dysfunction might be important in the etiology of male genital anomalies.

Related DES Studies

House dust can carry hormone-altering chemicals prompting body cells to accumulate fat

Chemicals in household dust may promote fat cell development, 2019

New Orleans, LA – Endocrine-disrupting chemicals present in household dust promote the development of fat cells in a cell model and could contribute to increased growth in children relative to their age, according to research presented Monday, March 25 at ENDO 2019, the Endocrine Society’s annual meeting.

“This is some of the first research investigating links between exposure to chemical mixtures present in the indoor environment and metabolic health of children living in those homes,”

said lead researcher Christopher Kassotis, Ph.D., of Duke University’s Nicholas School of the Environment in Durham, N.C.

Previous research has shown that chemical exposures can promote accumulation of triglycerides—a type of fat found in the blood—and increased obesity in animal models. Many observational studies have found a link between exposure to endocrine-disrupting chemicals believed to contribute to obesity and increased weight in humans.

In this study, Kassotis and colleagues investigated the effect of chemical mixtures isolated from house dust. They collected 194 house dust samples from households in central North Carolina. They then extracted the chemicals from the dust in the lab. These extracts were tested for their ability to promote fat cell development in a cell model.

They found that very low concentrations of dust extracts were able to promote precursor fat cell proliferation and fat cell development. According to the EPA, children are estimated to consume between 60 and 100 milligrams of dust each day.

“We found that two-thirds of dust extracts were able to promote fat cell development and half promote precursor fat cell proliferation at 100 micrograms, or approximately 1,000 times lower levels than what children consume on a daily basis,”

Kassotis said.

The researchers then measured more than 100 different chemicals in the dust and looked at the relationship between their concentrations and the extent of fat cell development. They found that approximately 70 of the chemicals had a significant positive relationship with the development of dust-induced fat cells, and approximately 40 were linked with precursor fat cell development.

“This suggests that mixtures of chemicals occurring in the indoor environment might be driving these effects,”

Kassotis said.

The researchers found several chemicals were significantly elevated in the dust of homes of children who were overweight or obese. They are continuing to study these chemicals—some of which are found in common household products such as laundry detergents, household cleaners, paints and cosmetics—to determine which ones may be linked to obesity.

Reference. Image thecaspiantimes.

Tiny air pollution particles may lead to reduced sperm production

Particulate air pollution linked with reduced sperm production in mice, 2019

New Orleans, LA – Exposure to tiny air pollution particles may lead to reduced sperm production, suggests new research in mice, presented Monday, March 25 at ENDO 2019, the Endocrine Society’s annual meeting.

“Infertility rates are increasing around the world, and air pollution may be one of the main factors,”

said lead researcher Elaine Maria Frade Costa, M.D., Ph.D., of Sao Paulo University in Sao Paulo, Brazil.

The World Health Organization (WHO) estimates that approximately 15 percent of the global population has difficulty with fertility, and male infertility accounts for about half of those problems.

The study looked at the effect of particulate matter (PM) on sperm production. PM is a mixture of solid particles and liquid droplets found in the air. PM2.5 is a fine inhalable particle with diameters that are 2.5 micrometers or smaller. The average human hair is about 70 micrometers in diameters, making it 30 times larger than the biggest fine particle. PM2.5 is known to disrupt the endocrine system in humans and animals. The endocrine system is involved in reproduction, including the production of sperm.

The study included four groups of mice. One was exposed to PM2.5 from Sao Paolo before and after birth, from the day they were weaned from their mother’s milk until adulthood. The second group was exposed only during gestation. The third group was exposed after birth from weaning until adulthood; and the fourth group was exposed only to filtered air during gestation and from the time they were weaned until adulthood.

The researchers analyzed the testes of the mice and their production of sperm. DNA tests were used to evaluate gene expression, the process by which genes in DNA provide instructions for proteins.

The tubes in the testes that produce sperm of all the exposed mice showed signs of deterioration. In comparison with the mice not exposed to PM2.5, the sperm of the first group, which was exposed before and after birth, was of significantly worse quality.

The exposure to PM2.5 led to changes in the levels of genes related to testicular cell function. Exposure to PM2.5 after birth seemed to be the most harmful to testicular function, the study found.

Costa said these changes are epigenetic, which means they are not caused by changes in the DNA sequence. Epigenetic changes can switch genes on or off and determine which proteins a gene expresses.

The research demonstrates for the first time that exposure to air pollution of a large city impairs production of sperm through epigenetics, mainly in exposure after birth, Costa said.

“These findings provide more evidence that governments need to implement public policies to control air pollution in big cities,”

she said. Reference. Featured image.

Endocrine disruptors alter pubertal timing

Endocrine disrupters and possible contribution to pubertal changes

Puberty represents a crucial milestone in one’s reproductive life. For this reason, any effect of the environment on pubertal timing might announce later consequences on reproduction. For the last 20 years, data has accumulated suggesting changes in pubertal timing and a possible role for exposure to endocrine disrupting chemicals (EDCs). This review will summarize the recent data regarding secular trends in age at puberty in boys and girls as well as the likely increase in central precocious puberty incidence in girls. Finally, we will review the epidemiological and animal data suggesting a role for endocrine disrupting chemicals in the reported changes in pubertal timing.


The onset of puberty strongly depends on organizational processes taking place during the fetal and early postnatal life. Therefore, exposure to environmental pollutants such as Endocrine disrupting chemicals (EDCs) during critical periods of development can result in delayed/advanced puberty and long-term reproductive consequences. Human evidence of altered pubertal timing after exposure to endocrine disrupting chemicals is equivocal. However, the age distribution of pubertal signs points to a skewed distribution towards earliness for initial pubertal stages and towards lateness for final pubertal stages. Such distortion of distribution is a recent phenomenon and suggests environmental influences including the possible role of nutrition, stress and endocrine disruptors. Rodent and ovine studies indicate a role of fetal and neonatal exposure to EDCs, along the concept of early origin of health and disease. Such effects involve neuroendocrine mechanisms at the level of the hypothalamus where homeostasis of reproduction is programmed and regulated but also peripheral effects at the level of the gonads or the mammary gland.