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Vanessa Ward

San Francisco Medical Society | The Weight of Evidence - 0 views

  • “leading to neglect of other plausible mechanisms and well-intentioned but potentially ill-founded proposals for reducing obesity rates”
  • Since publication of that review, substantial evidence has emerged that increases the plausibility of one of the alternative mechanisms suggested by Keith et al: disruption of weight regulation by endocrine-disrupting chemicals (EDCs) in the environment.
  • Concerns about the potential contribution of EDCs to childhood obesity build from two considerations, one out of human biology and the other from animal experiments
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  • Prior
  • toxicologists were concerned more with weight loss, which was seen as an adverse outcome.
  • Many of these chemicals alter the behavior of specific genes that are involved in determining the number of fat cells (adipocytes) an individual will have as an adult.
  • he list of contaminants implicated by animal studies is substantial, including several estrogenic EDCs such as DES, bisphenol A, soy phytoestrogens
  • Almost no human data are available to test the obesogen hypothesis in people. No epidemiological evidence exists, because the hypothesis is so new
  • One in vitro experiment, however, has demonstrated that exposure to obesogens increases the rate of conversion of human stem cells to adipocytes (Kirchner et al 2010), confirming the validity of the basic mechanism and the relevance of the animal studies to people.
  • That would be a big win for medicine and public health.
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    San Francisco Medical Society discusses the possible relationship between chemical exposure and the obesity epidemic.
Vanessa Ward

PLoS Biology: The Toxic Origins of Disease - 0 views

  • During embryonic development, steroid hormones like estrogen control gene-expression programs to coordinate cell differentiation, growth, organogenesis, and metabolism.
  • “The moment we published something on bisphenol A, the chemical industry went out and hired a number of corporate laboratories to replicate our research. What was stunning about what they did . . . was they hired people who had no idea how to do the work.”
  • “whole-animal toxicological studies,” which look at different endpoints than the more mechanistic studies do, Hughes says. “That doesn't let you look at changes in gene expression, changes in epigenetic control of gene expression.
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  • “I can tell you simply by the size of the animal which is DES-exposed and which isn't.”
  • “We found out that brain is a target, bone is a target . . . and now the new target is adipocytes.”
  • When he removed all the soy-derived plant estrogens from the mother's diet, he was astonished to see endogenous estradiol levels in the fetus rise, and the offspring become “horrifically obese.
  • Adding the weak plant estrogens back in the diet suppressed the far more potent endogenous estradiol, he discovered, by inhibiting an enzyme required to make it.
  • Recent evidence suggests that a class of ubiquitous environmental pollutants called organotins can also stimulate adipogenesis and interfere with energy balance
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    This was one of the first articles that I looked in depth at and pretty much read all of. It presents some of the original research done on the effects Bisphenol-A on reproductive development and mammary gland formamation and how in the process led to a noticeable pattern between exposure and weight gain. The study of obesogens is a new field that was in a way accidentally discovered. It has been hypothesized that estrogen causes embryonic cells to develop into fat cells through a process called adipogenesis by chemicals called organotins. New research to support this is addressed in this article.
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