Recharging the batteries with refurbished eggs, or just many unknowns?

Can You Really Freshen Up Women’s ‘Aging’ Eggs?

Every medical treatment has risks and benefits and no outcome can ever be guaranteed says OvaScience… Image of team at at ESHRE 2015.

A fertility treatment company called OvaScience, claims it can “increase IVF success rates by improving egg health, increasing egg reserve and developing the next generation of IVF“. They say their AUGMENTSM treatment method aims to improve the health of an egg’s mitochondria, which are the tiny powerhouses that give cells the energy to divide and grow.

But experts advise caution over those claims. Although some early evidence suggests aging mitochondria could reduce a woman’s fertility, expert say, there are no studies that prove the new method will work. In addition, the company isn’t forthcoming with details of its process…

Read Can You Really Freshen Up Women’s ‘Aging’ Eggs? livescience, March 20, 2015.

Santé : la loi du marché

France 2, Cash investigation 2015 avec Elise Lucet

Cash investigation, Saison 3 Episode 5,
Elise Lucet, France 2, vidéo publiée le 15 septembre 2015

Plus d’information
  • Longtemps érigé en modèle, le système de santé français est aujourd’hui au bord de l’asphyxie. En 2014, le trou de la sécurité sociale a atteint plus de onze milliards d’euros, deux milliards de plus que prévu. En quinze ans, la dette des hôpitaux publics a été multipliée par trois. Pour sortir de cette situation catastrophique, une dangereuse course à la rentabilité s’est engagée. Multiplication des actes inutiles mais rémunérateurs, recours aux sociétés d’optimisation, médicaments à l’efficacité contestée : pendant un an, Elise Lucet et l’équipe de “Cash investigation” ont mené l’enquête. Plusieurs reportages mettent en lumière des pratiques effarantes, qui plombent le système de santé.
  • Regardez cette liste de vidéos sur l’industrie pharmaceutique sur notre chaîneYouTube.

FDA Hearings…

If off-label marketing is “speech”, why even have the FDA?

FDA-Hearings cartoon
If off-label marketing is ‘speech,’ why even have the FDA?

Exposure to Bovine Leukemia Virus Is Associated with Breast Cancer

Virus in cattle linked to human breast cancer

bovine image
University of California Berkeley researchers have linked bovine leukemia virus, a cancer-causing virus prevalent in cattle, with human breast cancer.

2015 Study Abstract

Background
Age, reproductive history, hormones, genetics, and lifestyle are known risk factors for breast cancer, but the agents that initiate cellular changes from normal to malignant are not understood. We previously detected bovine leukemia virus (BLV), a common oncogenic virus of cattle, in the breast epithelium of humans. The objective of this study was to determine whether the presence of BLV DNA in human mammary epithelium is associated with breast cancer.

Methods
This was a case-control study of archival formalin fixed paraffin embedded breast tissues from 239 donors, received 2002–2008 from the Cooperative Human Tissue Network. Case definition as breast cancer versus normal (women with no history of breast cancer) was established through medical records and examination of tissues by an anatomical pathologist. Breast exposure to BLV was determined by in situ-PCR detection of a biomarker, BLV DNA, localized within mammary epithelium.

Results
The frequency of BLV DNA in mammary epithelium from women with breast cancer (59%) was significantly higher than in normal controls (29%) (multiply- adjusted odds ratio = 3.07, confidence interval = 1.66–5.69, p = .0004, attributable risk = 37%). In women with premalignant breast changes the frequency of BLV DNA was intermediate (38%) between that of women with breast cancer and normal controls (p for trend < .001).

Conclusions
Among the specimens in this study, the presence of amplified BLV DNA was significantly associated with breast cancer. The odds ratio magnitude was comparable to those of well-established breast cancer risk factors related to reproductive history, hormones, and lifestyle and was exceeded only by risk factors related to genetics (familial breast cancer), high dose ionizing radiation, and age. These findings have the potential for primary and secondary prevention of breast cancer.

Sources and more information

Atypical vaginal adenosis and cervical ectropion, Association with CCAC in DES-exposed offspring

Atypical vaginal adenosis and atypical cervical ectropion of the tuboendometrial type are precursors of clear cell adenocarcinoma

Cervical-Ectropion-Analysis image
The frequency with which atypical tuboendometrial glands in the vagina and cervix were associated with the carcinomas and the proximity of the former to the latter provide strong evidence that atypical vaginal adenosis and atypical cervical ectropion of the tuboendometrial type are precursors of clear cell adenocarcinoma.

1984 Study Abstract

Knowledge of the evolution of clear cell adenocarcinomas of the vagina and cervix in diethylstilbestrol-exposed progeny has remained elusive despite the known topographical association of these tumors with the tuboendometrial form of vaginal adenosis and cervical ectropion.

Twenty radical hysterectomy or radical hysterectomy and vaginectomy specimens of clear cell adenocarcinoma of the vagina or cervix were serially blocked in toto;

  • tuboendometrial epithelium was found in the vagina in 19 (95%) of the cases, usually in greatest concentration at the margin of the tumor, particularly inferiorly.
  • Foci of atypical tuboendometrial epithelium were identified in 16 (80%) of the cases, almost always immediately adjacent to the tumor.

Twenty-five of a second group of 47 specimens in which only substantial portions of the vagina or cervix adjacent to a clear cell adenocarcinoma were available for examination also had foci of atypical tuboendometrial epithelium.

The frequency with which atypical tuboendometrial glands in the vagina and cervix were associated with the carcinomas and the proximity of the former to the latter provide strong evidence that atypical vaginal adenosis and atypical cervical ectropion of the tuboendometrial type are precursors of clear cell adenocarcinoma.

Sources and more information
  • Atypical vaginal adenosis and cervical ectropion. Association with clear cell adenocarcinoma in diethylstilbestrol-exposed offspring, Cancer. 1984, Sep 1, ;54(5):869-75. Robboy SJ, Young RH, Welch WR, Truslow GY, Prat J, Herbst AL, Scully RE, NCBI PMID: 6537153.
  • Full paper: Cancer Volume 54, Issue 5, Article first published online: 29 JUN 2006, PDF.
More DES DiEthylStilbestrol Resources

The contribution of outdoor air pollution sources to premature mortality on a global scale

More people die from air pollution than Malaria and HIV/Aids

Mortality-air-pollution image
Units of mortality, deaths per area of 100 km × 100 km (colour coded). In the white areas, annual mean PM2.5 and O3 are below the concentration–response thresholds where no excess mortality is expected. More than 3 million people die prematurely each year from outdoor pollution and without action deaths will double by 2050. Image credit nature.

Assessment of the global burden of disease is based on epidemiological cohort studies that connect premature mortality to a wide range of causes including the long-term health impacts of ozone and fine particulate matter with a diameter smaller than 2.5 micrometres (PM2.5). It has proved difficult to quantify premature mortality related to air pollution, notably in regions where air quality is not monitored, and also because the toxicity of particles from various sources may vary. Here we use a global atmospheric chemistry model to investigate the link between premature mortality and seven emission source categories in urban and rural environments. In accord with the global burden of disease for 2010, we calculate that outdoor air pollution, mostly by PM2.5, leads to 3.3 (95 per cent confidence interval 1.61–4.81) million premature deaths per year worldwide, predominantly in Asia. We primarily assume that all particles are equally toxic, but also include a sensitivity study that accounts for differential toxicity. We find that emissions from residential energy use such as heating and cooking, prevalent in India and China, have the largest impact on premature mortality globally, being even more dominant if carbonaceous particles are assumed to be most toxic. Whereas in much of the USA and in a few other countries emissions from traffic and power generation are important, in eastern USA, Europe, Russia and East Asia agricultural emissions make the largest relative contribution to PM2.5, with the estimate of overall health impact depending on assumptions regarding particle toxicity. Model projections based on a business-as-usual emission scenario indicate that the contribution of outdoor air pollution to premature mortality could double by 2050.

Sources and more information

  • More people die from air pollution than Malaria and HIV/Aids, new study shows, the guardian, 16 September 2015.
  • The contribution of outdoor air pollution sources to premature mortality on a global scale, nature, doi:10.1038/nature15371, 17 September 2015.

Aneuploidy Induction and Cell Transformation by DES: Possible Chromosomal Mechanism in Carcinogenesis

aneuploidy image
This 1983 study talks about DES-induced aneuploidy, and how it can cause cancer. This is something that appears to be the result of its particular chemical structure, not because it acts as an estrogen.
Image credit Iain M Porter, Univ. of Dundee.

Hugh Easton, DES Son, said:

In 1983, researchers “ identified the way DES causes cancer as being through it inducing aneuploidy, or abnormal numbers of chromosomes in cells. It interferes with the process of allocating chromosomes during cell division, so that some cells end up with too many or too few chromosomes. These cells can later become cancerous.

This is something that appears to be related to it’s chemical structure rather than it acting as an estrogen, since tamoxifen, a drug which is an antiestrogen, but whose chemical structure shares some similarities with DES, causes similar changes to cells and is also a carcinogen.

This book appears to confirm that DES induces cancer through inducing aneuploidy, not by acting as a hormone. ”

1983 Study Abstract

Diethylstilbestrol (DES) has been demonstrated previously to induce morphological and neoplastic transformation of Syrian hamster embryo cells in the absence of any measurable induction of gene mutation. To determine if DES induces cell transformation by a genetic mechanism at the chromosomal level, the effect of DES on structural aberrations and numerical chromosome changes was examined in asynchronous and synchronized cells. Over the concentration range which is optimal for cell transformation, DES failed to induce any increase in chromosome aberrations in the cells. In contrast, significant numerical chromosome changes were observed in DES-treated cultures. The percentage of metaphases with a near diploid chromosome number increased to 19% at 48 hr after treatment. By comparison, cells from control cultures contained only 1 to 2% aneuploid metaphases with a near diploid chromosome number. No significant increase in the number of metaphases with a near tetraploid number (>70) of chromosomes was observed in the DES-treated cultures. DES induced both chromosome loss and gain, and no significant difference was detected between the number of hyperdiploid and hypodiploid cells. Chromosome loss or gain was observed for chromosomes in each karyotype group. These findings suggest that DES induces chromosome nondisjunction. Synchronized cell cultures were obtained by first growing the cells in 1% serum and then in 10% serum with hydroxyurea which blocked the cells at the G1-S border. Upon release of the hydroxyurea block, the cells entered into S phase in a very synchronous manner. The cells were treated for 3 hr during one of four time periods after hydroxyurea release. During the first period, the cells were primarily in early S phase, while the second period included cells in late S phase. During the third period most of the cells were undergoing mitosis, while in the fourth period most of the cells were in G1 phase, although some mitotic cells were observed. Treatment of the synchronized cells with DES during early or late S phase resulted in little morphological transformation. However, treatment during the third period, when the majority of the cells were in mitosis, resulted in a peak of transformation which was 15 times the level observed in cultures treated in early or late S phase. Treatment during the fourth time period resulted in a reduced level of cell transformation. Treatment of synchronized cultures with DES resulted also in a cell cycle-dependent induction of aneuploid cells which paralleled the induction of cell transformation, with the greatest level observed following treatment during mitosis. No increase in the percentage of polyploid metaphases or chromosome aberrations was observed in the DES-treated synchronized cells. Parallel dose-response curves for cell transformation and aneuploidy induction by DES were observed when the synchronized cultures were treated during the mitotic phase of the cell cycle. Possible mechanisms for DES-induced aneuploidy and the evidence supporting a role for nonrandom numerical chromosome changes in neoplastic development, as well as significance of aneuploidy in cancer, are discussed.

Sources and more information
  • Aneuploidy Induction and Cell Transformation by Diethylstilbestrol: A Possible Chromosomal Mechanism in Carcinogenesis, Cancer Research August 1983 43; 3814.
More DES DiEthylStilbestrol Resources

Why off-label marketing is irresistible to Big Pharma

If off-label marketing is ‘speech,’ why even have the FDA?

This post content is written by Martha Rosenberg and published by Reporting on Health, a nonprofit, nonpartisan and educational offering resources & community for journalists covering health

off-label-marketing
It has always been legal for U.S. doctors to prescribe drugs for off-label uses but marketing of off-label uses has been illegal. Image via pharmamkting.blogspot.

It has always been legal for U.S. doctors to prescribe drugs for off-label uses but marketing of off-label uses has been illegal. In August, U.S. District Judge Paul A. Engelmayer ruled that the First Amendment allows a drug company to “engage in truthful and non-misleading speech promoting the off-label use” of drugs and that the FDA cannot bar such “speech.” The ruling, pertaining to the drug Amarin, which targets high triglyceride levels, is likely to be appealed and only applies to the 2nd U.S. Circuit Court of Appeals, which includes New York, Connecticut and Vermont. But patients had better beware.

Off-label marketing is irresistible to Big Pharma because it saves years and millions spent on clinical trials which may not assure FDA approval anyway. It allows drug companies to circumvent the pesky and slow FDA altogether and get on with the business of making money– bringing their sales pitch to doctors and patients directly. Almost all major drug companies—GSK, Eli Lilly, Abbott, AstraZeneca, Pfizer, Johnson & Johnson, Amgen, Allergen, Bristol-Myers Squibb, Cephalon, Novartis and Purdue (which makes Oxycontin)––have agreed to huge settlements which include charges of off-label marketing.

In court-released confidential memos, Pfizer (then Parke-Davis) admits why it chose to off-label market Neurontin (only approved for postherpetic neuralgia and adjunctive seizure therapy) for the unapproved indication of bipolar disorder. “The U.S. market for Bipolar Disorders is an attractive commercial opportunity that warrants clinical development of Neurontin. Based on the current patent situation, an investment in full clinical development is not recommended at this time since completion of two pivotal trials and regulatory filing and approval would occur close to patent expiration,” says the memo. Translation: It would take too long to get legal approval—our patent would expire. Instead, says the memo, “it is recommended to implement only an exploratory study in outpatients with bipolar disorders with the results highlighted through a peer reviewed publication.” Translation: Let’s not do the studies and plant some info in medical journals that looks like we did.

Pfizer paid a $430 million fine and signed a corporate integrity agreement for off-label marketing of Neurontin which was linked to wrongful deaths and suicides. But that did not stop Pfizer from off-label marketing Lyrica, sometimes called “son of Neurontin,” soon afterward. Who can say incorrigible?

Nor did Eli Lilly’s guilty plea in 2009 to the off-label promotion of the antipsychotic Zyprexa deter it from requesting permission from the FDA to market Zyprexa to children three months later. The FDA said—yes! At the same time, Pfizer and AstraZeneca also requested permission to market their antipsychotics, Geodon and Seroquel respectively, to kids though both agreed to off-label marketing those exact drugs months later.

Another off-label marketing scheme centered around the selective estrogen receptor modulator Evista. Eli Lilly, its manufacturer, had noted fewer incidences of breast cancer in an Evista trial and wanted to market it not just for its approved treatment of prevention of osteoporosis but for prevention of breast cancer. A group of doctors told Lilly the anticancer marketing claims were “an egregious stretch” and that Evista’s high risk of stroke canceled out any anticancer benefits.

Undaunted, Lilly armed 1000 of its drug reps with an off-label Evista sales plan to sell the unapproved use of breast cancer prevention. Drug reps were told to hide a disclosure page that said, “The effectiveness of [Evista] in reducing the risk of breast cancer has not yet been established,” and “All of the authors were either employees or paid consultants of Eli Lilly at the time this article was written,” according to the Department of Justice.

Lilly was charged with a violation of the Food, Drug, and Cosmetic Act and ordered to pay a $36 million settlement for the off-label marketing. But Evista did receive approval to reduce the “risk of invasive breast cancer in postmenopausal women with osteoporosis and in postmenopausal women at high risk for invasive breast cancer.” The problem was the drug, marketed so freely for off-label uses, was far from safe. Prescribing information warned “Serious and life-threatening side effects can occur while taking EVISTA” and ads warned about “death due to stroke.” Its effectiveness was also not impressive. Patients were warned that Evista doesn’t “completely prevent breast cancer,” and “Breast examinations and mammograms should be done before starting Evista and regularly thereafter.”

Clearly, forgiveness is cheaper than permission for drug makers who consider such settlements the cost of doing business. But are drug sales pitches really “speech?” Can a “truthful and not misleading” determination really be made by the for-profit company selling the product? If drug companies’ product claims are protected under the First Amendment and they can sell directly to doctors and patients why even have an FDA?

Over 50 years ago, Big Pharma was also annoyed with the slow-paced FDA whose efforts to ensure drugs were safe cut into profits. One company even complained to an FDA official’s bosses that she was a petty bureaucrat. The company made thalidomide.

La campagne “Manger bio et local, c’est l’idéal”

Rendez-vous avec les producteurs BIO du 16 au 24 septembre 2017

 

296 événements sont recensés sur une carte interactive. Des événements sont susceptibles d’être ajoutés jusqu’au dernier moment, n’hésitez donc pas à revenir consulter cette carte!

Le contenu de ce post est publié par bioetlocal, venez rencontrer les producteurs bio près de chez vous!

Nous sommes de plus en plus attentifs aux conséquences de nos actes d’achat.

Le bio et le local ne s’opposent pas, bien au contraire ils se complètent. La consommation de denrées alimentaires produites localement réduit le nombre d’intermédiaires, diminue les transports polluants et contribue activement à renforcer la vitalité économique de nos territoires.

Toutefois les méthodes de production de ces aliments locaux ont également un impact sur l’environnement.

Consommer bio et local est doublement intéressant!

Manger bio c’est faire le choix d’une alimentation de qualité qui garantit des produits sans pesticides, engrais chimiques de synthèse ni OGM.

Les circuits courts qui proposent des produits bio se développent et sont aujourd’hui largement accessibles et diversifiés : vente à la ferme, marchés, magasins de producteurs, AMAP, systèmes de paniers, vente en ligne, restauration collective…

Il existe de nombreuses possibilités de consommer bio et local près de chez soi et de prendre sa part dans la campagne!

Venez les découvrir d’ici à cet automne 2017, et consultez cette carte des événements 20172016 et 2015 pour localiser ceux près de chez vous.

Prenatal exposure to progesterone suppresses reproduction in male mice

P. Sreenivasula Reddy, Harini Challa, Sainath S.B, Sep 2011

Prenatal-exposure-to-proges
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.

Partial recovery of reproduction by testosterone

The role of androgens in development of male reproductive organs is well documented. The role of estrogens in the development of male reproductive organs remains largely unknown; although both estrogen receptors and aromatase enzyme have been identified in the developing penis of a number of species, including humans.

Male offspring of women exposed to diethylstilbestrol during pregnancy have higher incidences of epididymal cysts, cryptorchidism, hypospadiasis, and smaller testes.

Since female hormones were routinely prescribed to treat threatened pregnancy and considering the potential implications of female hormones during prenatal period on the development of male reproductive system, the present book describes the effect of prenatal exposure to progesterone on adult male reproduction.

Significant deterioration in reproduction was observed in mice exposed to progesterone during embryonic development which includes reduction in steroidogenesis and spermatogenesis. Testosterone supplementation during post-natal period partially restored the suppressed reproduction.

More DES DiEthylStilbestrol Resources