EDCs can have effects at low doses that are not predicted by effects at higher doses
Abstract: For decades, studies of endocrine-disrupting chemicals (EDCs) have challenged traditional concepts in toxicology, in particular the dogma of “the dose makes the poison,” because EDCs can have effects at low doses that are not predicted by effects at higher doses. Here, we review two major concepts in EDC studies: low dose and nonmonotonicity. Low-dose effects were defined by the National Toxicology Program as those that occur in the range of human exposures or effects observed at doses below those used for traditional toxicological studies. We review the mechanistic data for low-dose effects and use a weight-of-evidence approach to analyze five examples from the EDC literature. Additionally, we explore nonmonotonic dose-response curves, defined as a nonlinear relationship between dose and effect where the slope of the curve changes sign somewhere within the range of doses examined. We provide a detailed discussion of the mechanisms responsible for generating these phenomena, plus hundreds of examples from the cell culture, animal, and epidemiology literature. We illustrate that nonmonotonic responses and low-dose effects are remarkably common in studies of natural hormones and EDCs. Whether low doses of EDCs influence certain human disorders is no longer conjecture, because epidemiological studies show that environmental exposures to EDCs are associated with human diseases and disabilities. We conclude that when nonmonotonic dose-response curves occur, the effects of low doses cannot be predicted by the effects observed at high doses. Thus, fundamental changes in chemical testing and safety determination are needed to protect human health.
Do the data on the drugs we call antidepressants justify the label of “antidepressant”?
Abstract: This paper raises the question about whether the data on the medications we call antidepressants justify the label of antidepressant. The authors argue that a true antidepressant should be clearly superior to placebo, should offer a risk/benefit balance that exceeds that of alternative treatments, should not increase suicidality, should not increase anxiety and agitation, should not interfere with sexual functioning, and should not increase depression chronicity. Unfortunately, these medications appear to fall short on all of these dimensions. Many of the “side effects” of these medications have larger effect sizes than the antidepressant effect size. To call these medications antidepressants may make sense from a marketing standpoint but may be misleading from a scientific perspective. Consumers deserve a label that more accurately reflects the data on the largest effects and helps them understand the range of effects from these medications. In other words, it may make just as much sense to call these medications antiaphrodisiacs as antidepressants because the negative effects on libido and sexual functioning are so common. It can be argued that a misleading label may interfere with our commitment to informed consent. Therefore, it may be time to stop calling these medications antidepressants.
Sources: NCBI, by Dr David Healy, PMID: 24278764, 4 June 2012
Full Article: Scientifica, by Dr David Healy Volume 2012 (2012), Article ID 965908, 6 pages, 28 May 2012
FACSaware aims to raising global awareness of Fetal Anti Convulsant Syndromes and other teratogen-related syndromes. The Fetal AntiConvulsant Trust (F.A.C.T.) was set up in 2011 to campaign for responsibility from the government and drug company.
Obama Signs Drug Compounding, Tracking Bill Into Law
President Barack Obama signed the The Drug Quality and Security Act on Wednesday that gives U.S. FDA health regulators greater oversight of bulk pharmaceutical compounding and strengthens the Food and Drug Administration ability to track pharmaceuticals drugs through the distribution chain.
Vitamins in a box: Can damage the body’s own defences
Vitamin supplements are a massive money-making industry. Each year, we spend billion of dollars on dietary supplements. We want to stay healthy and fit and help our bodies with this. But perhaps we are achieving precisely the opposite?
A new research, lead by Hilde Nilsen, head researcher at the Biotechnology Centre, University of Oslo, indicates that vitamin pills may upset the fragile balance in our cells and thus cause more harm than good.
… The so-called War on Drugs, it turns out, is a very selective war that targets only those drugs that don’t make money for Big Pharma. Street drug chemicals, when packaged as medications, are openly allowed to be consumed by infants as young as six months old (under doctor’s orders, no less!), and there’s even an effort underway now to drug expectant mothers with antidepressant drugs just to ensure their children aren’t born with depression. That’s called “preventive medicine”.
The War on Drugs completely ignores the drug companies, even when teen abuse of prescription drugs is widespread and highly dangerous. Doped up on Ritalin, Oxycontin, SSRIs and other dangerous mind-altering drugs, millions of teens are becoming prescription drug addicts… Continue reading: Partnership for a Drug-Free America
Too much Tylenol in pregnancy could affect development
Expectant mothers often take Tylenol, with the active ingredient acetaminophen, to deal with back pain, headaches or mild fevers during pregnancy. Is it safe to take Tylenol during pregnancy? This question has been asked by millions of pregnant women. Typically, they hear from their doctor that Tylenol during pregnancy is completely safe for both the mother and her developing baby.
However, a new Norwegian study has found symptoms aligned with autism spectrum disorder (ASD) in Tylenol-exposed children. Children exposed to long-term use of paracetamol during pregnancy had substantially adverse developmental outcomes at three years of age.
HRT: Estrogen Won’t Make Women Sharper After Menopause
Low levels of the hormone estrogen are not to blame for mood swings and poor memory after menopause, a new study suggests.
Based on this finding, the researchers believe there’s no reason to use hormone replacement therapy to boost mental well-being after periods stop.
Variations in the hormonal milieu after menopause may influence neural processes concerned with cognition, cognitive aging, and mood, but findings are inconsistent. In particular, cognitive effects of estradiol may vary with time since menopause, but this prediction has not been assessed directly using serum hormone concentrations. We studied 643 healthy postmenopausal women not using hormone therapy who were recruited into early (-6 y after menopause) and late (10+ y after menopause) groups. Women were administered a comprehensive neuropsychological battery and assessed with the Center for Epidemiologic Studies Depression Scale. They provided serum for free estradiol, estrone, progesterone, free testosterone, and sex hormone binding globulin measurements. Cognitive outcomes were standardized composite measures of verbal episodic memory, executive functions, and global cognition. Covariate-adjusted linear regression analyses were conducted for each hormone separately and after adjustment for other hormone levels. Endogenous sex steroid levels were unassociated with cognitive composites, but sex hormone binding globulin was positively associated with verbal memory. Results for early and late groups did not differ significantly, although progesterone concentrations were significantly positively associated with verbal memory and global cognition in early group women. Hormone concentrations were not significantly related to mood. Results fail to support the hypothesis that temporal proximity to menopause modifies the relation between endogenous serum levels of estradiol and verbal memory, executive functions, or global cognition. Physiological variations in endogenous postmenopausal levels of sex steroid hormones are not substantially related to these aspects of cognition or mood; positive associations for progesterone and sex hormone binding globulin merit additional study.
UK Rare Diseases Strategy launched by Health Minister Lord Howe
The UK’s first strategy to help build understanding of rare diseases and boost research to find effective treatments and therapies was launched by Health Minister Lord Howe today.
The UK Rare Diseases Strategy aims to ensure that none of the three million people in the UK who are affected by rare diseases are left behind.
For the first time, it sets out a UK-wide vision for building on our reputation as a world leader in rare disease research, including revolutionary genomic research to help transform diagnosis and treatment.
Key elements of the strategy include:
a clear personal care plan for every patient that brings together health and care services, with more support for them and their families
support for specialised clinical centres to offer the best care and support
better education and training for health and social care professionals to help ensure earlier diagnosis and access to treatment
promoting the UK as a world leader in research and development to improve the understanding and treatment of rare diseases