Forum d’Information et d’Aide aux Personnes Infertiles

Joignez la Journée Nationale de l’Infertilité, cet Automne !

5ème Journée Nationale de l’Infertilité

La 5ème journée Nationale de l’Infertilité aura lieu VENDREDI 9 NOVEMBRE 2018 et sous un nouveau format 100% média.

4ème Journée Nationale de l’Infertilité

Le 10 novembre 2017 à Paris 12ème, et en duplex à Lyon et Marseille

Au programme : 5 conférences pour informer et échanger avec les plus grands experts de l’infertilité (Pr Grynberg, Pr Olivennes, Dr Harvey etc…)

INFORMATIONS PRATIQUES
De 8H00 à 18h00 à Paris, Lyon et Marseille

Paris : Espace Charenton :5 rue Théodore Hamont, Paris 12
Lyon : en duplex live – adresse à venir
Marseille : en duplex live – adresse à venir

ENTRÉE GRATUITE
Préinscription obligatoire sur magicmaman.com/journeeinfertilite
et maia-asso.org.

Lors de la 4ème journée nationale de l’infertilité, le Pr Michel Tournaire et le Dr Anne Wautier de l’association Réseau D.E.S. France :

  • présenteront de nouveaux résultats de l’étude Distilbène 3 générations : fertilité et grossesses des “petites-filles DES“.
  • aborderont des notions telles que :
    • épigénétique,
    • perturbateurs endocriniens
    • effets transgénérationnels

2ème Journée Nationale de l’Infertilité

Le 25 septembre 2015, à Paris 6ème

journe-infertilit-2015
La 2ème journée nationale de l’infertilité 2015, événement ouvert à tous, aura lieu de 9 h à 18 h le 25 septembre 2015 à l’université de médecine Paris-Descartes ,15, rue de l ‘école de médecine PARIS 6 éme (Métro Odéon ou Cluny-Sorbonne).

Programme

OUVERTURE DE la JOURNEE 9h00
Discours d’accueil :
Famili ; Association MAIA ; Imany Marraine de cette journée ; Dr Thierry Harvey (Diaconesses)

PREVENIR ET COMBATTRE L’INFERTILITE 10h
possibilités & moyens, facteurs environnementaux
facteurs psy : le poids des histoires perso dans l’infertilité,
grossesse tardive et cryo …

Dr Christophe Siffer (Jean-Verdier) ; Dre Silvia Alvarez (Eylau-La Muette) ;
Dre DAVY (La Muette) ; Dre Laurence Levy Dutel (Tenon)
Dre Joelle Desjardin (psy) ; Dr Bernard Jegou (environnement et fertilité)
Associations Fertilité Europe et Lydia Sophrologue de MAIA

ENDOMETRIOSE, DISTILBENE, SYNDROME MRKH ET CANCERS 11h30

Imany représentera EndoMind Marraine de cette journée
Pr Grynberg (Jean-Verdier Bondy) ; Pf Paniel /MRKH (Creteil)
Pf Tournaire /DES (SVP) ; Réseau DES
Assoc LiliH contre l’endométriose ; MRKH Amélie VICTOR

Discussion avec les associations et pause déjeuner 12h30 à 14h15

PARENTALITE ET GENETIQUE 14h30

Chromosomes, épigénétique dans l’infertilité et la parentalité
Dons d’ovocytes : est-ce que mon enfant me ressemblera ?
être parent sans génétique, qu’est-ce qui fait que l’on est parent ?
Dr HARVEY Thierry (Diaconesses) ; Dr Marie-Charlotte DUMARGNE (Institut PASTEUR)
Dr Laurence FRANCOIS (psychiatre assoc MAIA) ; ADEDD
Jérôme COURDURIES Maître de conférences Anthropologue ;
Pf Lansac (Collège national des gynécologues) ; Dr Rassoulzadegan, (Nice)

TRAITEMENT DE L’INFERTILITE 16h30

Où la FRANCE en est elle ? Accès au remboursement ? au traitement ? au diagnostic ?
Qualité des protocoles ? des centres FIV, de la recherche ? Se tourner vers l’étranger ?
Pf RAVEL (CECOS RENNES) ; Pf Olivennes (La Muette) ; Dre GALLO (IVI Barcelonne)
Pf Jean-Marc Ayoubi (Foch) ; Dr Philippe Durand (spermato in vitro)
Irène Thery Sociologue (Directrice d’études à l’EHESS) ; Association MAIA Isabelle Chandler
Dr Debbie Montjean (spécialiste ICSI)

Logistique

La 2ème journée nationale de l’infertilité 2015, événement ouvert à tous, organisée par l’association Maia et le magazine Famili. aura lieu de 9 h à 18 h le 25 septembre 2015 à l’université de médecine Paris-Descartes ,15, rue de l ‘école de médecine PARIS 6 éme (Métro Odéon ou Cluny-Sorbonne). Voir la 1ère journée 2014.


Le Distilbène DES, en savoir plus

Cytology of 575 young women with prenatal exposure to diethylstilbestrol

Obstetrics and gynecology, Dr Arthur Herbst, 1976

cytology lab image
This 1976 study indicates that the presence of mucinous columnar or metaplastic squamous cells in vaginal scrapes is suggestive of vaginal adenosis but that vaginal cytology cannot be considered a uniformly reliable screening technic for detecting the presence of this disorder.

1976 Study Abstract

The vaginal and cervical cellular changes encountered in 575 postpubertal females exposed prenatally to diethylstilbestrol (DES) were compared with those of an unexposed population with particular reference to the role of cytology in the detection of vaginal adenosis and cervical ectropion (erosion).

Several methods of obtaining specimens were utilized, the most effcacious of which was scraping of the vagina, especially the fornices, and the portio vaginalis of the cervix.
With this technic, columnar cells of the mucinous type and metaplastic squamous cells were observed in 34% of the vaginal scrapes and 54% of the scrapes of the cervical portio.
A higher incidence was apparent among those patients in whom iodine staining of the vaginal mucosa was abnormal or vaginal adenosis was proven by biopsy.
Moderate to severe dysplasia of the squamous cells or atypical glandular cells were found in 1% of the exposed subjects.

This study indicates that the presence of mucinous columnar or metaplastic squamous cells in vaginal scrapes is suggestive of vaginal adenosis but that vaginal cytology cannot be considered a uniformly reliable screening technique for detecting the presence of this disorder.

Sources and more information
  • Cytology of 575 young women with prenatal exposure to diethylstilbestrol, Robboy SJ, Friedlander LM, Welch WR, Keh PC, Taft PD, Barnes AB, Scully RE, Herbst AL., Obstet Gynecol. 1976 Nov;48(5):511-5. NCBI PMID: 980279.
More DES DiEthylStilbestrol Resources

Fetal exposure to dietary carcinogens and risk of childhood cancer

What the NewGeneris project tells us

foetus image
The development of childhood cancer seems to be affected by both genetic and environmental factors.

2015 Study Abstract

Cancer in childhood is rare. Globally, there are around 175 000 new cancer cases a year among children aged 0-14 years.

However, in Europe, since the 1950s the incidence of cancer in this age group has increased by about 1% a year, with leukaemia, brain tumours, and lymphomas accounting for most cases. The increases in incidence of lymphoid leukaemia, in particular, are more apparent in European than in Asian or African children.

The development of childhood cancer thus seems to be affected by both genetic and environmental factors. Given that the highest incidences of childhood leukaemia are reported in children younger than 6-7 years, that the latency period of leukaemia in children is relatively short, and that adverse genetic events in utero have been shown to give rise to leukaemia in childhood, we hypothesised that fetal exposure to environmental carcinogens may be an underlying cause.

Diet is an important source of carcinogenic compounds because of the accumulation of environmental carcinogens within the food chain (dioxins, polychlorinated biphenyls (PCBs), polycyclic aromatic hydrocarbons (PAHs)), as well as of formation of carcinogens such as PAHs, heterocyclic amines, and acrylamide during baking, frying, and grilling of food.

The New Generis (Newborns and Genotoxic Exposure Risks) project therefore set out to investigate whether intake of dietary carcinogens by the pregnant mother leads to exposures of the fetus and initiates adverse biological responses that can induce cancer in later childhood.

Sources and more information

Fetal exposure to dietary carcinogens and risk of childhood cancer: what the NewGeneris project tells us, BMJ 2015;351:h4501, 28 August 2015.

Mortality among fetuses: preventable spina bifida and anencephaly in Europe

Lack of folic acid enrichment in Europe causes mortality among fetuses

cot image
Europe has an epidemic of spina bifida and anencephaly compared with countries with mandatory folic acid fortification policy. Primary prevention through mandatory folic acid fortification would considerably reduce the number of affected pregnancies, and associated additional costs.

A new international study shows that 5,000 foetuses in Europe annually are affected by spina bifida and other severe defects on the central nervous system. Seventy per cent of these pregnancies are terminated, while increased mortality and serious diseases affect the children who are born. At least half of the cases can be avoided by adding folic acid to staple foods as is already being done in seventy non-European countries.

Sources and more information
  • Lack of folic acid enrichment in Europe causes mortality among fetuses, medicalxpress, August 28, 2015.
  • Preventable spina bifida and anencephaly in Europe, Birth Defects Research Part A: Clinical and Molecular Teratology, 14 JUL 2015, DOI: 10.1002/bdra.23400.

Rates and risks of DES-related clear-cell adenocarcinoma of the vagina and cervix

CCAC update, Dr Arthur Herbst, 1987

clear_cell_carcinoma image
DiEthylStilbestrol usage review buttress the need for adequate and rigorous research into the use of drugs in pregnancy and ensure that they do more good than harm before being introduced for consumption.

1987 Study Abstract

We reviewed 519 cases of clear-cell adenocarcinoma of the vagina and cervix identified by the Registry for Research on Hormonal Transplacental Carcinogenesis of the University of Chicago through June 30, 1985. In 60 percent of all cases the patient’s mother had received diethylstilbestrol during pregnancy. An additional 12 percent of all mothers had been treated with another hormone or with an unidentified medication. Ninety-one percent of the cases in diethylstilbestrol-exposed women were diagnosed when the patient was between the ages of 15 and 27. The median age at diagnosis was 19.0 years. The risk that clear-cell adenocarcinoma will develop in an exposed female from birth through age 34 is 1 case per 1000 women. The temporal pattern of occurrence of clear-cell adenocarcinoma corresponds closely with that of the use of diethylstilbestrol for pregnancy support in the United States. The rarity of this tumor among exposed women suggests that diethylstilbestrol is not a complete carcinogen and that some other factor is also involved in the pathogenesis of clear-cell adenocarcinoma of the vagina and cervix.

Sources and more information
  • Rates and risks of diethylstilbestrol-related clear-cell adenocarcinoma of the vagina and cervix. An update., Melnick S, Cole P, Anderson D, Herbst A., N Engl J Med. 1987 Feb 26;316(9):514-6, NCBI Pubmed PMID: 3807995.
More DES DiEthylStilbestrol Resources

“Feeds with Stilbosol keep us in the cattle busine$$ today”

DES advert, FFA National Future Farmer, 1956

stilbosol-ad mage
Stilbosol patenting turned the cattle feed industry upside down in the mid 50s with its phenomenal use by farmers.
Image sources
Related posts
Related books
More DES DiEthylStilbestrol Resources

Glyphosate-based herbicides link to kidney, liver damage at ultra-low doses

More evidence of Roundup’s link to kidney, liver damage

roundup image
Long-term exposure to tiny amounts of Roundup—thousands of times lower than what is permitted in U.S. drinking water—may lead to serious problems in the liver and kidneys, according to a new study.

2015 Study Abstract

Background
Glyphosate-based herbicides (GBH) are the major pesticides used worldwide. Converging evidence suggests that GBH, such as Roundup, pose a particular health risk to liver and kidneys although low environmentally relevant doses have not been examined. To address this issue, a 2-year study in rats administering 0.1 ppb Roundup (50 ng/L glyphosate equivalent) via drinking water (giving a daily intake of 4 ng/kg bw/day of glyphosate) was conducted. A marked increased incidence of anatomorphological and blood/urine biochemical changes was indicative of liver and kidney structure and functional pathology. In order to confirm these findings we have conducted a transcriptome microarray analysis of the liver and kidneys from these same animals.

Results
The expression of 4224 and 4447 transcript clusters (a group of probes corresponding to a known or putative gene) were found to be altered respectively in liver and kidney (p < 0.01, q < 0.08). Changes in gene expression varied from −3.5 to 3.7 fold in liver and from −4.3 to 5.3 in kidneys. Among the 1319 transcript clusters whose expression was altered in both tissues, ontological enrichment in 3 functional categories among 868 genes were found. First, genes involved in mRNA splicing and small nucleolar RNA were mostly upregulated, suggesting disruption of normal spliceosome activity. Electron microscopic analysis of hepatocytes confirmed nucleolar structural disruption. Second, genes controlling chromatin structure (especially histone-lysine N-methyltransferases) were mostly upregulated. Third, genes related to respiratory chain complex I and the tricarboxylic acid cycle were mostly downregulated. Pathway analysis suggests a modulation of the mTOR and phosphatidylinositol signalling pathways. Gene disturbances associated with the chronic administration of ultra-low dose Roundup reflect a liver and kidney lipotoxic condition and increased cellular growth that may be linked with regeneration in response to toxic effects causing damage to tissues. Observed alterations in gene expression were consistent with fibrosis, necrosis, phospholipidosis, mitochondrial membrane dysfunction and ischemia, which correlate with and thus confirm observations of pathology made at an anatomical, histological and biochemical level.

Conclusion
Our results suggest that chronic exposure to a GBH in an established laboratory animal toxicity model system at an ultra-low, environmental dose can result in liver and kidney damage with potential significant health implications for animal and human populations.

Sources and More Information
  • More evidence of Roundup’s link to kidney, liver damage, environmentalhealthnews, August 28, 2015.
  • Transcriptome profile analysis reflects rat liver and kidney damage following chronic ultra-low dose Roundup exposure, BioMed Central Ltd, Environmental Health, 2015, 14:70 doi:10.1186/s12940-015-0056-1.

Environmental Exposures in Girls increase Breast Cancer Risks

Adolescent Window of Breast Cancer Risk Explained

Girls may be vulnerable to environmental exposures that contribute to breast cancer decades later.

More info and videos
  • In this short video published 29 August 2011 by UC San Francisco (UCSF), Zena Werb – PhD, founding member of the Bay Area Breast Cancer and the Environment Research Center (BABCERC) – and breast cancer advocates discuss research goals and an award winning, 15-minute animated video, called the “The Breast Biologues,” which helps explain to a general audience what researchers want to know about breast development, environmental exposures and breast cancer. Werb was a scientific consultant for the video project.
  • Watch more research videos on our YouTube channel.

No Gazaran, les gaz de schiste dans le Sud-Est et le Bassin Parisien

Le gaz de schiste arrive dans nos villages, nos paysages, nos vies

No-Gazaran image
L’alerte est lancée dans le sud est de la France début 2011 : le gaz de schiste arrive dans nos villages, nos paysages, nos vies. Carnet de route d’une mobilisation citoyenne imprévue, le film témoigne des soubresauts d’une société prise au piège d’un modèle économique en crise.

En savoir plus

Autism pathway from gene to brain found by UNC scientists

Researchers discover a potential cause of autism

Key enzymes are found to have a ‘profound effect’ across dozens of genes linked to autism. The insight could help illuminate environmental factors behind autism spectrum disorder and contribute to a unified theory of how the disorder develops.

… “Mark Zylka, a professor at the UNC School of Medicine, and his team believe they have figured out the rough outlines of one such pathway, from the tiny genetic glitch on the gene to the physical changes that the glitch causes in the brain. Like many discoveries, it piggybacked on the work of others, involved a little luck and has raised more questions for researchers. ” …

… “Both Zylka and Birnbaum of the National Institute of Environmental Health Sciences believe that in many cases, genetic mutations and outside factors probably work together to trigger autism. As Birnbaum puts it, people whose DNA puts them at risk may be “kind of pushed over the edge” when exposed to one or more of these triggers. With more and more people living with autism, it is becoming increasingly urgent to solve this question.” …

Sources and more information

  • UNC scientists pinpoint how a single genetic mutation increases autism risk,
    newsobserver, AUGUST 6, 2015.
  • UNC scientists trace autism ‘pathway’ from gene to brain,
    newsobserver, AUGUST 19, 2015.
  • Researchers discover a potential cause of autism,
    news.unchealthcare, August 28, 2013.