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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.
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
Liz Richardson

Environmental Signaling: What Embryos and Evolution Teach Us About Endocrine Disrupting... - 0 views

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    An overview of many endocrine disrupting chemicals, useful to anyone looking into the effects of environmental chemicals on organisms. Reference made to a book titled "Hormonal Chaos", by Sheldon Krimsky, describing how industrial and agricultural chemicals contact organisms and disrupt hormone function. Specifics on effects of environmental estrogens and fetal development.
Liz Richardson

Interview with Fredrick Vom Saal by Frontline PBS - 0 views

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    Related to the estrogen video viewed in class, plastics are feminizing males of mostly all species.
Vanessa Ward

Prenatal Genistein In Soy Reduces Obesity In Offspring - DukeHealth.org - 8 views

  • The agouti methylation consistently occurred throughout several germ layers of embryonic tissue, indicating that genistein acted during early embryonic development. Moreover, the methylation changes persisted into adulthood, providing the first evidence that in utero dietary genistein alters epigenetic gene regulation, coat color, and susceptibility to adult obesity in animals.
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    Vanessa - This pertains to both my study and yours. Is lack of soy consumption linked to obesity? Is it worth it to consume soy while pregnant if your child will lose risk of being fat but gain risk of being infertile?
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    This is awesome, thanks Liz.
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    This addresses the controversy of the role of estrogenics and the role they play in predispostion to obesity. DDE studies were positive for resulting in obesity but genistein studies show that in utero exposure results in a lower adult body weight. Both are estrogenics.
Liz Richardson

Cellular and Physiological Effects of Soy Flavonoids - 0 views

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    Abstract describes how phytoestrogens can be estrogen receptor modulators. Recent studies suggest beneficial health effects of soy and recommend increasing the intake of isoflavone-rich soy protein to the level of intake commonly used in Asian countries. Must try to open this article at the library to gain access to the free full version of the article. Vanessa - Once I access the full version I will be better able to tell you whether this is related to the other article concerning cultural differences in soy consumption and its effects on obesity.
Matthew Ragan

Estrogen Receptor Interacting with DNA - 0 views

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    Nuclear hormone receptor proteins form a class of ligand activated proteins that, when bound to specific sequences of DNA serve as on-off switches for transcription within the cell nucleus. These switches control the development and differentiation of skin, bone and behavioral centers in the brain, as well as the continual regulation of reproductive tissues.
suwhitte

Welcome to CDC's DES Update Homepage - 0 views

shared by suwhitte on 16 May 10 - Cached
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    Background on diethylstilbesterol, a synthetic estrogen, that has caused transgenerational effects.
Liz Richardson

Cellular and Physiological Effects of Soy Flavonoids - 1 views

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    Vanessa- you may not be able to open this from home, but it is the full text version of the link I provided earlier. Soy isoflavones are felt to protect against different cancers, cardiovascular disease, and bone loss, and possibly weight gain.
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.
Liz Richardson

Soy Alert -- Tragedy and Hype - 0 views

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    Anti-soy campaign: what information can be trusted? Soy crops cover 72 million acres of American farmland. Much of this harvest will be used to feed chickens, turkeys, pigs, cows and salmon. Another large fraction will be squeezed to produce oil for margarine, shortenings and salad dressings. Do we ever really know how much soy we are ingesting? Many of these products are not listed as including soy.
Vanessa Ward

The Toxic Origins of Disease - 1 views

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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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    This source is probably the biggest contribution to my paper. I accidentally shared it twice because I couldn't figure out how to edit the tags on this one since it didn't come from my library. I shared it before I figured out how to share the sources from my library to the group, I thought I had to do it separately.
Anna McLean

Our Stolen Future: New science on the impacts of endocrine disruptors on brain and beha... - 0 views

  • The sex steroids (testosterone, estrogen, etc.) contribute to, among other things, sexual differentiate of brain centers, and thereby, to the development of sexual identity and sexual behaviors
  • A rapidly increasing body of scientific research is revealing mechanisms of action, demonstrating impacts of disrupted development, and exploring links between intelligence, behavior and contamination experienced in the womb. What is emerging from this research is that brain and behavior are likely to be the most sensitive endpoints vulnerable to endocrine disruption. Many synthesized compounds in commercial use today, moreover, can derail neurological development.
  • April 2003. Exposure in the womb to extremely low levels of bisphenol A alters sexual differentiation of the brain and behavior in rats. More...
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  • September 2002. Dutch scientists report that boys exposed prenatally to higher levels of PCBs and dioxin are more likely to show demasculinized play behaviors. Girls and boys exposed to modestly elevated dioxin levels demonstrate more feminized play behaviors. The scientists suggest that that these alterations in play result from endocrine disruption of the development of sex-specific behaviors. More...
  • disturbed sexual differentiation of reproductive behavior, potentiating the expression of feminine sexual behavior and reducing masculine behavior."
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    This document is the web site for the book titled Our Stolen Future. There are numerous sections with "more..." links to full pages on the summarized topic. This is a great tool for my project.
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    Highlighted text indicates areas applicable to my topic.
Vanessa Ward

Epigenetics, Evolution, Endocrine Disruption, Health, and Disease -- Crews and McLachla... - 1 views

  • Endocrine-disrupting chemicals (EDCs) in the environment have been linked to human health and disease. This is particularly evident in compounds that mimic the effects of estrogens.
  • information recently uncovered, regarding mechanisms of endocrine and environmental signaling, to explore the role of the environment in health and disease.
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    This a good article that gives a general overview of EDC's and the role they play in the compromise of physical and mental health. One particularly interesting thing is how a discussion of EDC's and evolution is presented.
Anna McLean

Human Health: Fish consumption -- Critical contaminants - 1 views

  • DDT and DDE are probable human carcinogens and endocrine disrupters.
  • Mercury is not known to be a carcinogen, but it is toxic to the fetuses of humans and animals.
  • ercury in Lake Huron fish has caused fish consumption advisories and has been detected in Lake Huron water, sediment and wildlife.
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    Although the use of DDT was banned a long time ago, it is still negatively affecting wild life. This page adds more detail to what we saw in the film, "The Estrogen Effect: Assault on the Male."
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    Under the metals section, there is a short description of heavy metals. These metals are known to damage organisms, and as shown in some of our mini-presentations, can act as EEDs. For example, erythropoietin's functions are inhibited by lead as an EED.
Anna McLean

Reproductive Toxins and Alligator Abnormalities at Lake Apopka, Florida - 0 views

  • it has been shown that many of the environmental chemicals found in alligator plasma or eggs bind the alligator estrogen and/or progesterone receptors in vitro
  • Guillette et al. ( 1 ) suggested that the reproductive failure at Lake Apopka could have been related to general agricultural pollution and to a spill from a nearby pesticide manufacturing facility. From 1957 to 1981, the facility (Tower Chemical Co.) manufactured and stored both chlorinated and organophosphate insecticides as well as a copper-salt-based fungicide at a site 1.5 miles from Lake Apopka. Wastewater from the manufacturing process was discharged into an unlined pond, and chemicals were burned or buried on site. During a heavy rain in 1980, the percolation pond overflowed and acidic wastewater discharged into a marsh that drains into Lake Apopka. DDT and other chemicals contaminated the lake during this extensive spill.
  • ecause of the endocrine-disruptive potential of DDT's degradation products DDE and DDD, they have been the prime suspects in the reproductive abnormalities of the alligators
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  • The route of exposure for the alligators living in this environment might have occurred through both oral and dermal exposure
  • he testicular abnormalities in alligators from Lake Apopka are similar to those in pesticide workers exposed to DBCP in that the seminiferous tubules are the affected target tissues.
    • Anna McLean
       
      Similar abnormalities act as evidence for the negative effects of DBCP. Evidence such as this help to support the cause, and disable individuals from referring to the alligators' issues as coincidence. Or that they have nothing to do with chemical spills, pesticides, and other pollutants.
  • given the levels found in the remaining pond, it is almost certain that DBCP entered Lake Apopka during the 1980 spill.
  • The findings discussed above indicate a complex exposure scenario in which the etiology of the reproductive failure cannot be reconstructed with certainty due to the historic nature of the event
    • Anna McLean
       
      Emphasizes the difficultly scientists have in proving the causes of the observed problems in many species, such as the Lake Apopka alligators.
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