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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

2010 March « Our Health and Environment Blog - 0 views

  • n addition to these issues, the prestigious international Endocrine Society published a seminal report last year stating that, “scientific research implies the impact of environmental substances in the generative roots of obesity.”
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    This is a letter addressing the "obesogen theory" and how the government could play a role in the prevention of obesity through the implementation of beter food regulations. I thought it was interesting to see a current letter addressing my topic and maybe it's a type source other people can look for that they may not have initially thought of.
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    A link in this article led me to another useful source. I didn't know that the White House was involved with this and that obesogens were brought to their attention until I read this letter. Bruce Blumberg signed the letter and since many of my sources are about his studies I thought it was neat how this letter tied together some of my research.
Vanessa Ward

Endocrine Disruptors and the Obesity Epidemic -- Heindel 76 (2): 247 -- Toxicological S... - 1 views

  • "We are faced with the seeming paradox of increased adiposity at both ends of the birth weight spectrum—higher BMI with higher birth weight and increased central obesity with lower birth weight" (Oken and Gillman, 2003). Thus prevention of childhood and adult obesity must start in utero.
  • Indeed, many synthetic chemicals are actually used to increase weight in animals.
  • This article provides fascinating examples of chemicals that have been tested for toxicity by standard tests that resulted in weight gain in the animals at lower doses than those that caused any obvious toxicity.
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  • Chemicals having endocrine-disrupting activity rise to the top of the list as most act via receptors linked to activation of transcriptional activity.
  • In the adult, loss of circulating estrogen due to ovariectomy leads to increased body and adipose tissue weights. Estrogen receptor alpha knockout mice have a significantly increased body fat content, and estrogen decreases the activity of lipoprotein lipase
  • estrogenic endocrine-disrupting chemical bisphenol A at concentrations as low as 2 µg/ml, in the presence of insulin, stimulated differentiation of the 3T3L1 cells into adipocytes
  • he fact that an environmental chemical has the potential to stimulate growth of "preadipocytes" has enormous implications for the area of obesity and its control.
  • Differentiation could be inhibited and more potential fat cells could be formed, as seems to be the case with NP, or differentiation could be stimulated, as appears to be the case with BPA
  • Will these results extrapolate to the in vivo situation in rodents and other animal models?
  • Only time and more research will tell, but the door has been opened by the novel work being highlighted.
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    An article discussing how the area of research of obesity as a result of endocrine disrupting chemical exposure could be a beneficial area for intervention and prevention studies of obesity. This was one of the first articles I found directly addressing how endocrine disrupting chemical exposure can lead to a predisposition to obesity
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