Breast cancer risks: consumer concerns about hormones in food

Today’s modern food: it’s not what you think

food-in-my-fridge image
Synthetic steroid hormones used as pharmaceutical drugs, have been found to affect cancer risk. Lifetime exposure to natural steroid hormone estrogen is associated with an increased risk for breast cancer. Hence, consumers are concerned about whether they are being exposed to hormones used to treat animals, and whether these hormones affect human health. Day75 image by J.J. Merrick.
  • What are hormones?
  • Why are hormones used in food production?
  • Why are consumers concerned about hormones in foods?
  • History of hormone use in food production
  • What are the different hormones used now by the meat and dairy industries?
  • How are the hormones introduced into the animals?
  • Do federal agencies monitor for the presence of these hormones in food?
  • Do hormones remain in the milk or meat of treated animals?
  • Can steroid hormones in meat affect the age of puberty for girls?
  • Can eating meat from hormone-treated animals affect breast cancer risk?
  • Can drinking milk, or eating dairy products from hormone-treated animals affect breast cancer risk?
  • Can hormones that remain in milk affect human health?
  • What do we know about growth factors in milk of treated animals?
  • Concern about milk-related allergies
  • Are hormone-treated animals healthy?
  • Are growth hormones used elsewhere in the world?
  • Some healthy diet tips that also help reduce exposure to hormones used in food production

Read Consumer Concerns About Hormones in Food, Cornell University,
Fact Sheet #37, June 2000.
Read How did You get your Dose of DES? with Chicken, Turkey, Beef or Vitamin Supplement? See also all posts tagged Stilbosol.

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A Social History of Medicines in the Twentieth Century

To Be Taken Three Times a Day.

Get a fresh perspective on the day-to-day use of medicine!

To Be Taken Three Times a Day

A Social History of Medicines in the Twentieth Century explores the most perplexing issues concerning the uses of prescriptions and other medicines on both sides of the Atlantic. The book equips you with a thorough understanding of the everyday use of medicine in the United States, Canada, and Britain, concentrating on its recent past. Dr. John K. Crellin, author of several influential books on the history of medicine and pharmacy, addresses vital topics such as: the emergence of prescription-only medicines; gate-keeping roles for pharmacists; the role of the drugstore; and the rise of alternative medicines.

A Social History of Medicines in the Twentieth Century adds the historical perspective missing from most medical and pharmaceutical literature about trends in the day-to-day use of medicines in society. The book is essential reading for anyone taking regular medication, either as self-care or by a physician’s prescription. Topics discussed include the non-scientific factors that validate medicines, the relevance of the control of narcotics, marketing strategies used by the pharmaceutical industry, the changing authority of physicians and pharmacists, over-the-counter medicines, tonics and sedatives, and patient compliance—and non-compliance.

A Social History of Medicines in the Twentieth Century also addresses:
– medicines for weakness (“health” foods, fortifiers, digestives/laxatives)
– poison and pharmacy legislation
– placebos
– tranquilizers and antidepressants
– hormones
– side-effects
– psychoactive medications
– herbal medicines
– a brief history of the use of medicines from the 17th to 19th centuries
– suggestions for future policies
– and much more!

A Social History of Medicines in the Twentieth Century is equally vital as a professional resource for physicians, pharmacists, and health care administrators, as a classroom guide for academics working in the medical and pharmaceutical fields, and as a resource for patients.

Pregnant? Many everyday products contain pollutants that can be harmful to your baby

Protect your child from Endocrine Disrupting Chemicals (EDCs)

This film published on 13 May 2015 by WECF Women in Europe provides information on how you can protect yourself and your child from Endocrine Disrupting Chemicals (EDCs).

More information

  • You are pregnant and looking forward to meeting your child! You want to make sure you do everything possible to give your child a great start in life. You know that it is important to avoid alcohol, nicotine and certain foods. However, what is less well known is that many everyday products contain pollutants that can also be harmful to your baby.
  • Watch more BPA chemicals videos on our YouTube channel.

Chemotherapy for near-death cancer patients does not improve “quality of life”

Chemotherapy Use, Performance Status, and Quality of Life at the End of Life

chemotherapy-drug image
Many patients with terminal cancer are offered chemotherapy in order to improve their quality of life. But according to a new study, the treatment does not improve quality of life for cancer patients who are near death – and may even worsen it for those who have good performance status. Chemotherapy drug by Nicki Dugan Pogue.

2015 Study Abstract

Although many patients with end-stage cancer are offered chemotherapy to improve quality of life (QOL), the association between chemotherapy and QOL amid progressive metastatic disease has not been well-studied. American Society for Clinical Oncology guidelines recommend palliative chemotherapy only for solid tumor patients with good performance status.

To evaluate the association between chemotherapy use and QOL near death (QOD) as a function of patients’ performance status.

Design, Setting, and Participants
A multi-institutional, longitudinal cohort study of patients with end-stage cancer recruited between September 2002 and February 2008. Chemotherapy use (n = 158 [50.6%]) and Eastern Cooperative Oncology Group (ECOG) performance status were assessed at baseline (median = 3.8 months before death) and patients with progressive metastatic cancer (N = 312) following at least 1 chemotherapy regimen were followed prospectively until death at 6 outpatient oncology clinics in the United States.

Main Outcomes and Measures Patient QOD was determined using validated caregiver ratings of patients’ physical and mental distress in their final week.

Chemotherapy use was not associated with patient survival controlling for clinical setting and patients’ performance status. Among patients with good (ECOG score = 1) baseline performance status, chemotherapy use compared with nonuse was associated with worse QOD (odds ratio [OR], 0.35; 95% CI, 0.17-0.75; P = .01). Baseline chemotherapy use was not associated with QOD among patients with moderate (ECOG score = 2) baseline performance status (OR, 1.06; 95% CI, 0.51-2.21; P = .87) or poor (ECOG score = 3) baseline performance status (OR, 1.34; 95% CI, 0.46-3.89; P = .59).

Conclusions and Relevance
Although palliative chemotherapy is used to improve QOL for patients with end-stage cancer, its use did not improve QOD for patients with moderate or poor performance status and worsened QOD for patients with good performance status. The QOD in patients with end-stage cancer is not improved, and can be harmed, by chemotherapy use near death, even in patients with good performance status.

Sources and more information
  • Chemotherapy Use, Performance Status, and Quality of Life at the End of Life, JAMA Oncology Published online July 23, 2015. doi:10.1001/jamaoncol.2015.2378, July 23, 2015.
  • Chemotherapy for near-death cancer patients ‘does not improve quality of life’, MedicalNewsToday, 24 July 2015.

His scales proved it pays to feed Stilbosol full time

Stilbosol patenting turned the cattle feed industry upside down in the mid fifties with its phenomenal use by the farmers and feeders

stilbosol-1957 advert image
Stilbosol patenting turned the cattle feed industry upside down in the mid fifties with its phenomenal use by the farmers.
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Positive reinforcement plays key role in cognitive task performance in ADHD children

Evaluating cognitive and motivational accounts of greater reinforcement effects among children with attention-deficit/hyperactivity disorder

A little recognition for a job well done means a lot to children with Attention Deficit/Hyperactivity Disorder (ADHD) – more so than it would for typically developing kids. Effort image by Tom Woodward

2015 Study Abstract

Attention Deficit/Hyperactivity Disorder is associated with cognitive deficits and dysregulated motivation. Reinforcement improves cognitive performance, often to a greater degree among children with ADHD compared to typically-developing controls. The current study tests the degree to which cognitive (individual differences in baseline cognition) and/or motivational (individual differences in Sensitivity to Reward; SR) processes can account for diagnostic group differences in reinforcement effects.

Participants were 58 children (25 ADHD, 33 control) ages 9-12. Children completed measures of inhibitory control (Stop Signal Task), working memory (n-back), and sustained attention (Continuous Performance Task) during a baseline week and again one week later under reinforcement and no-reinforcement conditions; composites were computed across cognitive domains. Parent-and child-reported trait SR (SPSRQ; BIS/BAS) were combined to index a child’s response towards appetitive, rewarding stimuli.

In separate analyses, diagnostic group, individual differences in baseline cognition, and individual differences in SR all moderated the impact of reinforcement on cognition. When considered together, the Diagnostic Group × Reinforcement and Baseline Cognition × Reinforcement interactions both remained robust. In contrast, neither the Diagnostic Group × Reinforcement nor the SR × Reinforcement interactions accounted for unique variance when evaluated together.

Both baseline cognition and trait SR predict reinforcement effects on cognition, but only SR shares significant variance with diagnostic group. These results suggest that ADHD children’s greater response to reinforcement on cognition is strongly related to their heightened trait sensitivity to rewarding stimuli, consistent with motivational models of ADHD.

Sources and more information
  • Evaluating cognitive and motivational accounts of greater reinforcement effects among children with attention-deficit/hyperactivity disorder, Behavioral and Brain Functions 2015, 11:20 doi:10.1186/s12993-015-0065-9, 29 April 2015.
  • Positive reinforcement plays key role in cognitive task performance in ADHD kids, according to new study, University at Buffalo, July 30, 2015.

The Rising Cost of Autism Spectrum Disorder

Autism costs estimated to reach nearly $500 billion, potentially $1 trillion, by 2025

costs-of-autism infographic
The study senior author Paul Leigh hopes his findings inspire policy changes that emphasize early intervention to reduce ASD symptoms, along with employment and other programs that support the independence of adults with the disorder.

UC Davis health economists have for the first time projected the total costs of caring for all people with autism spectrum disorder (ASD) in the U.S. for the current calendar year and in 10 years if effective interventions and preventive treatments for the condition are not identified and widely available.

Their forecasts for ASD-related medical, nonmedical and productivity losses are $268 billion for 2015 and $461 billion for 2025. The researchers noted that these estimates are conservative and, if ASD prevalence continues to increase as it has in recent years, the costs could reach $1 trillion by 2025.

Read Autism costs estimated to reach nearly $500 billion, potentially $1 trillion, by 2025
ucdmc.ucdavis, July 28, 2015.

Multigenerational Effects of Endocrine-Disrupting Molecules

Emilie Rissman PhD, interviewed by Jill Escher, 2014

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I would stress that our data show that in mice, social interactions, as a class of behaviors, are disrupted by transgenerational exposure to ‘human-like’ levels of BPA. ” Rippled reflections by 57Andrew.

Emilie Rissman, PhD, Professor of Biochemistry & Molecular Genetics, University of Virginia, studies mammalian behavioral genetics. Because many social behaviors are activated only when gonadal steroid hormones are present, the genes for steroid hormone receptors are currently under study in her lab. She has found that androgen receptor is required for normal social affiliative behavior in male mice. In addition, her work shows that several social behaviors are sexually dimorphic, in part, because of differences in sex chromosome genes. Her work in mice is relevant to several sexually dimorphic neurobehavioral diseases including autism spectrum disorder.

  • Dr. Rissman, I’m very pleased to be interviewing you because since you are one of the few researchers to explicitly examine multigenerational effects of endocrine disruption as it relates to abnormal behavior and neurodevelopment in offspring. How did you come to examine this question?
  • How did gestational BPA exposure differentially affect succeeding generations?
  • What epigenetic mechanisms are at play with exposure to EDCs?
  • What do we know about hormone and other receptors on and in germ cells? And somatic cells, if there’s a difference.
  • What role does the steroid hormone receptor play in epigenetic function?
  • Why do hormone-disrupting molecules affect epigenetic activity?
  • Some of the scientists I’ve spoken with differentiated between “strong” exposures and weak ones in terms of likelihood of epigenetic impacts. Some strong ones mentioned included steroid hormones and their mimics, cigarette smoke and psychoactive drugs. Comparatively weak ones were thought to include variability in stress and nutrition. Do you agree with this general distinction?
  • It seems we forget there’s a long and complicated molecular phase of the human life cycle. For example, those who say BPA or pesticides are safe cite studies on adults, children or fetuses. But isn’t the most vulnerable phase gametes and precursor cells? What do you consider to be important windows of vulnerability?
    While nearly all scientists find endocrine disruption a concern, some say “there’s just not enough evidence yet” to be concerned about ambient exposures. How do you respond to that? What would be “enough” evidence?

Read the full interview on Germline Exposures, by Jill Escher, April 2014

La Grande Invasion, l’enquête 2010 de Stephane Horel

Notre quotidien le plus banal est farci de produits chimiques…

Un livre-enquête de Stéphane Horel sur les produits qui intoxiquent notre quotidien.

Dans nos maisons, à notre insu, des milliers de substances chimiques partagent notre vie quotidienne, nichées dans la nourriture et l’eau, incrustées dans les détergents, les plastiques ou les tissus. Les hommes, les femmes, les enfants et même les ours polaires ont dans le sang des produits chimiques censés se trouver dans les tapis et grille-pains du monde moderne. Quels sont les risques pour la santé ? Tandis que l’industrie défend ses marchés et ses secrets de fabrication, les scientifiques s’inquiètent de l’augmentation de l’asthme, de certains cancers, de troubles du développement et du comportement ou de la chute spectaculaire de la fertilité dans les pays développés. Pour eux, cette pollution invisible et continue empoisonne l’humanité en toute discrétion, et touche en premier lieu les bébés. Souvent ignorée dans le débat environnemental, cette “Grande Invasion” soulève des questions qui dépassent largement le domaine de la médecine et de la science. Elle touche à l’organisation de nos systèmes économiques et politiques, et aux fondements de nos sociétés de profusion.

En dévoilant l’identité chimique des produits de consommation courante, cette enquête de Stephane Horel rend accessible les travaux scientifiques les plus récents et propose des solutions pratiques pour se préserver.

En savoir plus

Intrauterine diethylstilbestrol exposure and increased risk of endometriosis in adulthood

Early-life factors and endometriosis risk

This 2015 study results support the hypothesis that disruption of development during fetal and infant periods may increase the risk of endometriosis in adulthood. Endometriosis Awareness Month image by ALDE Communication.

2015 Study Abstract

To study early-life factors in relation to endometriosis risk in adulthood.

Population-based, case-control study. The Women’s Risk of Endometriosis study was conducted among female enrollees aged 18-49 years of a large, integrated healthcare system in western Washington State.

Cases (n = 310) were women diagnosed for the first time with endometriosis between the years 1996 and 2001, and controls (n = 727) were women without a diagnosis of endometriosis randomly selected from the healthcare system population.

Adjusted odds ratios (aORs) and 95% confidence intervals (CIs) for the associations between intrauterine diethylstibestrol (DES) exposure, maternal smoking, mother’s age at delivery, firstborn status, birth weight, fetal number, prematurity, and regular soy formula feeding during infancy and endometriosis were estimated using unconditional logistic regression, adjusting for frequency matching and confounding variables. Information on early-life factors was ascertained retrospectively by in-person interview, with information on maternal DES use and regular soy formula feeding directly gathered from the participant’s mother or other family member.

We observed that women who were regularly fed soy formula as infants had more than twice the risk of endometriosis compared with unexposed women (aOR 2.4, 95% CI 1.2-4.9). Our data also suggested increased endometriosis risk with prematurity (aOR 1.7, 95% CI 0.9-3.1) and maternal use of DES (OR 2.0, 95% CI 0.8-4.9, adjusting only for frequency matching variables), although these confidence intervals included the null.

Our results support the hypothesis that disruption of development during fetal and infant periods may increase the risk of endometriosis in adulthood.

Sources and more information
  • Early-life factors and endometriosis risk, Upson K, Sathyanarayana S, Scholes D, Holt VL., Fertil Steril. 2015 Jul 23. pii: S0015-0282(15)00469-0. doi: 10.1016/j.fertnstert.2015.06.040, NCBI PMID: 26211883, 2015.
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