There is growing interest in the possible health threat posed by endocrine-disrupting chemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction.
In this first Scientific Statement of The Endocrine Society , we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology.
Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs as a significant concern to public health. The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, antiandrogenic, thyroid, peroxisome proliferator-activated receptor γ, retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans, and which can be modeled in laboratory in vitro and in vivo models. Furthermore, EDCs represent a broad class of molecules such as organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals that are present in the environment or are in widespread use.
We make a number of recommendations to increase understanding of effects of EDCs, including enhancing increased basic and clinical research, invoking the precautionary principle, and advocating involvement of individual and scientific society stakeholders in communicating and implementing changes in public policy and awareness.
Accepted: April 17, 2009 – First Published Online: July 01, 2013.
A Prescription for Sticker Shock Caused by Drug Costs
2015 Paper Abstract
Escalating drug prices have alarmed physicians and the American public and led to calls for government price controls. Less visibly, they have also spawned a flurry of private-sector initiatives designed to help physicians, payers, and patients understand the value of new therapies and thus make better choices about their use. Programs recently introduced or advanced by nonprofit organizations, including leading medical professional societies, represent an important innovation in the United States, but they have also revealed numerous analytic and implementation challenges.
Sources and more information
Measuring the Value of Prescription Drugs, The New England Journal of Medicine, DOI: 10.1056/NEJMp1512009, November 25, 2015.
A Prescription for Sticker Shock Caused by Drug Costs, New-York Times, NOVEMBER 23, 2015.
Genes and the wider environment are inextricably intertwined, each affecting the other
Evidence has been mounting about the importance of interactions between people’s genetics and their environment, especially in pregnancy and childhood. Knowledge about how wider environmental factors can turn genes on and off—the new science of environmental epigenomics—is gaining wider coverage and influence. Research has shown that genes and the wider environment are inextricably intertwined, each affecting the other. These gene markers can be passed on to future generations in mammals, and they can also be reversed.
Continue reading Children are the guardians of our genome,
thebmj, 2015;351:h6265, 23 November 2015.
The full moon that appears in November is usually called the Beavers Moon, stemming from when traps were set for beavers who are busily preparing for winter. Traps are set before swamps freeze. November full moon is also referred to as the Full Frost Moon as, by this time of year, there has been a hard frost.
The Full Pink Moonsaw some extravaganza – such as special achievements, moon pies, and daily drawings… so let’s see what happens this time! Recent joiners can expect to receive some extra support during the five days.
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Apocalypse Pig: The Last Antibiotic Begins to Fail
2015 Study abstract
Until now, polymyxin resistance has involved chromosomal mutations but has never been reported via horizontal gene transfer. During a routine surveillance project on antimicrobial resistance in commensal Escherichia coli from food animals in China, a major increase of colistin resistance was observed. When an E coli strain, SHP45, possessing colistin resistance that could be transferred to another strain, was isolated from a pig, we conducted further analysis of possible plasmid-mediated polymyxin resistance. Herein, we report the emergence of the first plasmid-mediated polymyxin resistance mechanism, MCR-1, in Enterobacteriaceae.
The mcr-1 gene in E coli strain SHP45 was identified by whole plasmid sequencing and subcloning. MCR-1 mechanistic studies were done with sequence comparisons, homology modelling, and electrospray ionisation mass spectrometry. The prevalence of mcr-1 was investigated in E coli and Klebsiella pneumoniae strains collected from five provinces between April, 2011, and November, 2014. The ability of MCR-1 to confer polymyxin resistance in vivo was examined in a murine thigh model.
Polymyxin resistance was shown to be singularly due to the plasmid-mediated mcr-1 gene. The plasmid carrying mcr-1 was mobilised to an E coli recipient at a frequency of 10−1 to 10−3 cells per recipient cell by conjugation, and maintained in K pneumoniae and Pseudomonas aeruginosa. In an in-vivo model, production of MCR-1 negated the efficacy of colistin. MCR-1 is a member of the phosphoethanolamine transferase enzyme family, with expression in E coli resulting in the addition of phosphoethanolamine to lipid A. We observed mcr-1 carriage in E coli isolates collected from 78 (15%) of 523 samples of raw meat and 166 (21%) of 804 animals during 2011–14, and 16 (1%) of 1322 samples from inpatients with infection.
The emergence of MCR-1 heralds the breach of the last group of antibiotics, polymyxins, by plasmid-mediated resistance. Although currently confined to China, MCR-1 is likely to emulate other global resistance mechanisms such as NDM-1. Our findings emphasise the urgent need for coordinated global action in the fight against pan-drug-resistant Gram-negative bacteria.
Choosing Wisely Canada is a campaign to help physicians and patients engage in conversations about unnecessary tests, treatments and procedures.
More info and videos
Dr. Mike Evans is a staff physician at St. Michael’s Hospital and an Associate Professor of Family Medicine. He is a Scientist at the Li Ka Shing Knowledge Institute and has an endowed Chair in Patient Engagement in Child Nutrition at the University of Toronto. Check out his new website.
International Federation of Gynecology and Obstetrics opinion on reproductive health impacts of exposure to toxic environmental chemicals
Exposure to toxic environmental chemicals during pregnancy and breastfeeding is ubiquitous and is a threat to healthy human reproduction. There are tens of thousands of chemicals in global commerce, and even small exposures to toxic chemicals during pregnancy can trigger adverse health consequences. Exposure to toxic environmental chemicals and related health outcomes are inequitably distributed within and between countries; universally, the consequences of exposure are disproportionately borne by people with low incomes. Discrimination, other social factors, economic factors, and occupation impact risk of exposure and harm. Documented links between prenatal exposure to environmental chemicals and adverse health outcomes span the life course and include impacts on fertility and pregnancy, neurodevelopment, and cancer. The global health and economic burden related to toxic environmental chemicals is in excess of millions of deaths and billions of dollars every year. On the basis of accumulating robust evidence of exposures and adverse health impacts related to toxic environmental chemicals, the International Federation of Gynecology and Obstetrics (FIGO) joins other leading reproductive health professional societies in calling for timely action to prevent harm. FIGO recommends that reproductive and other health professionals advocate for policies to prevent exposure to toxic environmental chemicals, work to ensure a healthy food system for all, make environmental health part of health care, and champion environmental justice.
Sources and more information
Contaminating Our Bodies With Everyday Products, nytimes, NOV. 28, 2015.
International Federation of Gynecology and Obstetrics opinion on reproductive health impacts of exposure to toxic environmental chemicals, sciencedirect, doi:10.1016/j.ijgo.2015.09.002, 1 October 2015.
Global Obstetrics and Gynaecology group warn of harm to babies from toxic chemicals in consumer products, HEAL, 1 October 2015.
Epigenetic modification might be a potential mechanism of low-dose DES-induced male reproductive toxicity
2015 Study Abstract
Evidence from previous studies suggests that the male reproductive system can be disrupted by fetal or neonatal exposure to diethylstilbestrol (DES). However, the molecular basis for this effect remains unclear. To evaluate the effects of DES on mouse spermatocytes and to explore its potential mechanism of action, the levels of DNA methyltransferases (DNMTs) and DNA methylation induced by DES were detected.
The results showed that low doses of DES inhibited cell proliferation and cell cycle progression and induced apoptosis in GC-2 cells, an immortalized mouse pachytene spermatocyte-derived cell line, which reproduces primary cells responses to E2. Furthermore, global DNA methylation levels were increased and the expression levels of DNMTs were altered in DES-treated GC-2 cells. A total of 141 differentially methylated DNA sites were detected by microarray analysis. Rxra, an important component of the retinoic acid signaling pathway, and mybph, a RhoA pathway-related protein, were found to be hypermethylated, and Prkcd, an apoptosis-related protein, was hypomethylated.
Effects of Low-Dose Diethylstilbestrol Exposure on DNA Methylation in Mouse Spermatocytes, BCBI PubMed PMID: 26588706, PLOS one PMC4654501, Nov 20 2015.
These results showed that low-dose DES was toxic to spermatocytes and that DNMT expression and DNA methylation were altered in DES-exposed cells. Taken together, these data demonstrate that DNA methylation likely plays an important role in mediating DES-induced spermatocyte toxicity in vitro.