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Vanessa Ward

Maternal levels of dichlorodiphenyl-dichloroethylene (DDE) may increase weight and body... - 0 views

oem.bmj.com/143.full

obesity epidemiological study exposure DDE BMI fish consupmption Great Lakes

shared by Vanessa Ward on 04 Jun 10 - Cached
  • Objectives: To investigate the effect of prenatal exposure to polychlorinated biphenyls (PCBs) and dichlorodiphenyl-dichloroethylene (DDE) on weight, height and body mass index (BMI) in adult female offspring of the Michigan fisheater cohort examined between 1973 and 1991
  • Maternal height and BMI were significant predictors of the daughters’ height, weight and BMI.
  • The weight and BMI of adult offspring were statistically significantly associated with the extrapolated prenatal DDE levels of their mothers.
  • ...4 more annotations...
  • ncreasingly, however, prenatal exposure to toxicants is suspected of contributing to obesity.
  • Previous studies have shown that Michigan anglers and fisheaters have higher serum levels of PCBs and DDE than population controls.
  • A total of 176 (82.6%) daughters participated in at least one of two repeated investigations
  • Our results suggest that higher prenatal exposure to DDE, but not to PCBs, is statistically significantly associated with increased weight and BMI in adult female offspring.
  • Vanessa Ward on 04 Jun 10
     
    Liz, this article was already in my library and you might want to look at it. I feel as though the study isn't completely controlled since it deals with people who chose to participate in the study over the course of many years but there are some concepts that can be gathered that may be beneficial to you.
  • Vanessa Ward on 11 Jun 10
     
    This is another epidemiological study similar to the study present by Suphada on sport fish consumption. There were many outside variables, leading to only a small sample size that could be used.
Vanessa Ward

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

toxsci.oxfordjournals.org/...247

obesity endocrine disruption

shared by Vanessa Ward on 25 May 10 - Cached
  • "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.
  • Vanessa Ward on 25 May 10
     
    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
Vanessa Ward

Endocrine Disruptors IV: Cancer in Our Foods - 1 views

www.nativeshop.org/...8-endocrine-disruptors-iv.html

shared by Vanessa Ward on 22 May 10 - Cached
  • Polycyclic aromatic hydrocarbons (PAHs) are a group of compounds that include over one hundred different contaminants
  • PAHs are persistent compounds. They are not easily broken down, so they can last for a long time. Also, they bioaccumulate—the higher up in the food chain you go, the higher the concentration of PAHs within the organism.
  • To be safe, there are several ways of reducing exposure to PAHs
  • Vanessa Ward on 22 May 10
     
    I thought this was an interesting introductory site to PAH's and how they relate to endocrine disruption. The main focus is on PAH's, which are the result of incompletely burned material such as coal, wood, oil, or gas. Eating grilled foods could increase the exposure to PAH's as well as cigarette smoke, exhaust and even natural sources such as forest fires. Exposure to PAH's could lead to the development of cancer.
Anna McLean

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

ehp.niehs.nih.gov/...semenza-full.html

shared by Anna McLean on 24 May 10 - Cached
  • 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
      Anna McLean on 24 May 10
       
      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
      Anna McLean on 24 May 10
       
      Emphasizes the difficultly scientists have in proving the causes of the observed problems in many species, such as the Lake Apopka alligators.
Vanessa Ward

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

www.sfms.org/...Template.cfm

SFMS Blumberg Grun obesity epidemic endocrine disruption EDCs obesity

shared by Vanessa Ward on 11 Jun 10 - Cached
  • “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.
  • Vanessa Ward on 11 Jun 10
     
    San Francisco Medical Society discusses the possible relationship between chemical exposure and the obesity epidemic.
srom88

Pesticide Mixtures, Endocrine Disruption, and Amphibian Declines: Are We Underestimatin... - 1 views

www.ncbi.nlm.nih.gov/...PMC1874187

shared by srom88 on 24 May 10 - Cached
  • In addition to having highly permeable skin (which makes amphibians particularly vulnerable to chemical contaminants), amphibians also typically reproduce and pass through critical hormone-regulated developmental stages while in the aquatic environment
    • srom88
      srom88 on 24 May 10
       
      What about human skin and its permeability to these pesticides?
  • atrazine is of special concern because it is a ubiquitous, persistent contaminant of ground-water and surface water that is active at low, ecologically relevant concentrations
    • srom88
      srom88 on 24 May 10
       
      Atrazine is common pesticide used; definite possibility for a focus.
  • realistic pesticide mixture composed of chemicals applied to cornfields in York County, Nebraska.
    • srom88
      srom88 on 24 May 10
       
      Can also find different experiments in different locations in the US or even out of the country.
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  • Radioimmunoassay
    • srom88
      srom88 on 24 May 10
       
      very sensitive technique used to measure concentrations of antigens (for example, hormone levels in the blood) without the need to use a bioassay.
  • With the exception of metalaxyl, no single compound affected mortality
  • mortality was 4% for animals exposed to single pesticides (range = 0–7.8%), with the highest mortality (7.8%)
  • Propiconizole significantly delayed time to initiate metamorphosis (FLE; F = 2.72, df = 10, p = 0.003) and time to complete metamorphosis (TR; F = 2.81, df = 10, p = 0.002) relative to controls (Figure 1).
  • Animals exposed to pesticide mixtures at 0.1 ppb had significantly longer larval periods: initiation of metamorphosis (days to FLE) was delayed
  • there was a significant effect on SVL at metamorphosis (F = 2.1, df = 10, p < 0.05; Figure 3). The smallest animals to metamorphose were those exposed to cyfluthrin, tebupirimphos, or atrazine
  • All the mixtures (0.1 ppb each pesticide) retarded growth
  • For the pesticide mixtures, 0.1 and 10 ppb atrazine + S-metolachlor resulted in a negative but nonsignificant relationship between TR and SVL, whereas 0.1 and 10 ppb Bicep II Magnum exposure resulted in maintenance of the positive relationship between TR and SVL, but the relationship was significant for the 0.1 ppb concentration only
    • srom88
      srom88 on 24 May 10
       
      Different combinations of pesticides will affect the organism differently.
  • Histologically, presumptive males maintained both a cortex and a medulla separated by connective tissue without clear formation of testicular lobules (e.g., undifferentiated), whereas females showed regression of the gonadal medulla and an ovarian vesicle but lacked significant numbers of developing oocytes in the cortical regions of the gonad
  • Seventy percent of the animals exposed to the nine-compound mixture were unable to sit upright. Exposure to the nine-compound pesticide mixture was associated with meningitis, otitis interna, and septicemia due to the gram-negative, water-borne bacteria Chryseobacterium (Flavobacterium) menigosepticum
  • Morbidity and mortality rates in animals treated with the nine-pesticide mixture were significant (G = 100.12, df = 4, p < 0.001) compared with those in controls or the other mixtures (all of which showed a 0% incidence) and reached 70% of the 59 animals that survived to complete metamorphosis in animals exposed to the pesticide mixture.
  • After noting that animals exposed to the nine-compound mixture contracted flavobacterial meningitis (see above “Flavobacterial response”), we examined the condition of the thymus as an estimate of immune function.
  • Although a sizable database examining the toxicological effects of pesticides on amphibians exists (Pauli 2004), most of these studies examine acute toxicity, morbidity, and mortality only
  • We demonstrated that a realistic pesticide mixture (based on a mixture applied to an actual field) at low ecologically relevant concentrations can have dramatic effects on amphibian development and growth, and ultimately (we predict) survivorship
  • one of these compounds (propiconizole) retards larval development and delays metamorphosis, and two others (tebupirimphos and cyfluthrin) retard larval growth. In addition to these new data, the present study confirms the retardation of amphibian development
  • Atrazine has a number of well-documented adverse effects on amphibian larvae. It is a potent endocrine disruptor that both chemically castrates and feminizes exposed male amphibian larvae and also retards larval development and growth
  • It also induces edema (Carr et al. 2003), erratic swimming (Carr et al. 2003), and irregular behavioral activity (Rohr and Palmer 2005) and is an immunosuppressant (Christin et al. 2003; Gendron et al. 2003; Kiesecker 2002) in amphibians.
  • As one of the world’s most commonly applied pesticides, it is the most common contaminant of groundwater and surface water
  • effects of atrazine on the gonads were not detectable because individuals from the present population do not complete sexual differentiation of the gonads before metamorphosis
  • retardation of growth and development was more severe when atrazine was combined with other pesticides (e.g., S-metolachlor), and the nine-pesticide mixture had the most severe impact.
  • amphibians (including leopard frogs) often breed in temporary water sources
  • Retardation of growth is also detrimental. Smaller size at metamorphosis limits food availability for newly metamorphosed frogs, which are gape-limited predators (Figure 12A). Further, smaller individuals are more susceptible to predators, which may also themselves be gape-limited predators
  • esticide mixtures retard growth and size at metamorphosis, exposed amphibians are less likely to find food and more likely to be preyed upon. Also, decreased size at metamorphosis combined with subsequent decreased postmetamorphic growth decreases the chances that amphibians will survive overwintering
  • alteration of the relationship between time to metamorphosis and size at metamorphosis is even more significant than either measured alone. In amphibians, the larval stage is a period of growth. A
  • pesticides that produce no effects alone may act as “enhancers” that worsen the effects of pesticides that act as “effectors” when the two groups of chemicals are combined.
  • characterize pesticide interactions as concentration additive or response additive
  • Pesticide-induced declines in populations as a result of decreased prey availability and increased susceptibility to predators (as a result of decreased size and the negation or reversal of the relationship between time to metamorphosis and size at metamorphosis) may be difficult to discern in the wild. Perhaps more important, emergent diseases caused by agents such as ranavirus
  • and chytrid
  • are considered major contributors to amphibian declines
  • the effects of atrazine on sex differentiation can negatively affect amphibian population
  • trazine has been shown to increase disease rates and parasite loads in amphibians by several pathogens
  • including the trematode associated with development of limb deformities
Vanessa Ward

The Toxic Origins of Disease - 1 views

www.plosbiology.org/...10.1371%2Fjournal.pbio.0050193

shared by Vanessa Ward on 29 May 10 - Cached
  • Vanessa Ward on 29 May 10
     
    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 on 11 Jun 10
     
    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.
Vanessa Ward

PLoS Biology: The Toxic Origins of Disease - 0 views

www.plosbiology.org/...journal.pbio.0050193

obesity endocrine origins of disease DES Blumberg Grun obesogen

shared by Vanessa Ward on 11 Jun 10 - Cached
  • 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.
  • ...5 more annotations...
  • “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
  • Vanessa Ward on 11 Jun 10
     
    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

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

www.dukehealth.org/...9584

genistein phytoestrogen soy endocrine EED

shared by Vanessa Ward on 04 Jun 10 - Cached
  • 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.
  • Liz Richardson on 04 Jun 10
     
    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?
  • Vanessa Ward on 04 Jun 10
     
    This is awesome, thanks Liz.
  • Vanessa Ward on 13 Jun 10
     
    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.
Anna McLean

Would you like lemon, or BPA with your water? - 0 views

likeafishinwater.com/...e-lemon-or-bpa-with-your-water

shared by Anna McLean on 11 Jun 10 - Cached
  • The only problem was that vinyl products generally contain significant amounts of Bisphenol-A (BPA), a plastic additive, exposure to which causes disruption of endocrine hormones
  • BPA in plastic baby bottles
  • What makes BPA such a problem? It affects everyone, but developing fetuses and small children are particularly vulnerable.
  • ...2 more annotations...
  • It alters the levels of endocrine hormones, which has effects ranging from learning disabilities to diseases and altered sexual development.
  • BPA is currently banned in Chicago, the State of Minnesota and Suffolk County, NY.
Anna McLean

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

www.ourstolenfuture.org/...behav.htm

shared by Anna McLean on 08 Jun 10 - Cached
  • 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...
  • ...2 more annotations...
  • 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."
  • Anna McLean on 11 Jun 10
     
    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.
  • Anna McLean on 11 Jun 10
     
    Highlighted text indicates areas applicable to my topic.
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