Obesity and ... Chemicals

[nadinbrzezinski]

Let the articles do the talking (and crow will be at the end for those who want it)

These data suggest a role for toxicology in the etiology of obesity. This role has received additional support from a recent review (Baillei-Hamilton, 2002) that presents a provocative hypothesis to explain the global obesity epidemic: chemical toxins. This article presents data showing that the current epidemic in obesity cannot be explained solely by alterations in food intake and/or decrease in exercise. There is a genetic predisposition component of obesity; however, genetics could not have changed over the past few decades, suggesting that environmental changes might be responsible for at least part of the current obesity epidemic. Indeed, the level of chemicals in the environment is purported to coincide with the incidence of obesity, and examples of chemicals that appear to cause weight gain by interfering with elements of the human weight control system—such as alterations in weight-controlling hormones, altered sensitivity to neurotransmitters, or altered activity of the sympathetic nervous system—are noted. 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. These chemicals included heavy metals, solvents, polychlorinated biphenols, organophosphates, phthalates, and bisphenol A. This is an aspect of the data that has generally been overlooked.

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Thus, the data on the fetal basis of adult disease, along with the above-referenced chemical hypothesis of obesity, add significance to examination of exposure to environmental chemicals as likely candidates to be tested for an effect on obesity. Chemicals having endocrine-disrupting activity rise to the top of the list as most act via receptors linked to activation of transcriptional activity. The state of the science in the area of endocrine disruptors, including data on their mechanism of action has recently been reviewed (Damstra et al., 2002). This World Health Organization- (WHO-)sanctioned review clearly shows that endocrine disruptors, especially those with estrogenic activity, act via alterations in gene expression and that many of these changes are imprinted and remain even into the next generation. The focus of endocrine-disruptor research around the world has been on the reproductive, immune, and nervous systems as evidenced by the WHO review. There has been little information of the possible direct effect of endocrine-disrupting chemicals on fat cell differentiation or physiology. Neither has there been an attempt to link effects of endocrine-disrupting chemicals on the immune or nervous system with effects on fat cell metabolism via alterations in hormonal or nervous system control of adipose tissue.

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As with any article, this one also asks more questions than it answers. For example, why are the effects of NP only partially inhibited by the estrogen receptor antagonist ICI182,780? It would have been helpful if the effects of estrogen were measured in this system and the effects of ICI182,780 tested on the estrogen response. Measurement of the estrogen receptor in these cells across the differentiation process would also be helpful. Since these analyses were not done, it is not clear if the effect of NP and OP in this article or that of BPA in a previous article (Masuno et al., 2002), in which ICI182,780 was not tested, mediated their effects via an estrogen receptor. In light of the potential impact of this research, answers to these questions must be forthcoming. Other questions relevant to this article include consideration of the use of serum that contains steroids in the cultures and the use of plastic culture dishes and their impact on the data.

There are also other, more global questions that need answers: Will these results extrapolate to the in vivo situation in rodents and other animal models? Will the results shown with high concentrations in vitro be replicated in vivo with low environmentally relevant concentrations? Will humans be sensitive to the in utero exposure to environmental estrogens with regard to the development of adipocytes? Will toxicology and environmental health sciences play a major role in addressing the obesity epidemic via reduction in exposures to environmental chemicals in utero and throughout life? Will this area of research be a fruitful area for intervention and prevention studies of obesity? Only time and more research will tell, but the door has been opened by the novel work being highlighted.



http://toxsci.oxfordjournals.org/cgi/content/full/76/2/247

Abstract

Xenobiotic and dietary compounds with hormone-like activity can disrupt endocrine signaling pathways that play important roles during perinatal differentiation and result in alterations that are not apparent until later in life. Evidence implicates developmental exposure to environmental hormone-mimics with a growing list of health problems. Obesity is currently receiving needed attention since it has potential to overwhelm health systems worldwide with associated illnesses such as diabetes and cardiovascular disease. Here, we review the literature that proposes an association of exposure to environmental endocrine disrupting chemicals with the development of obesity. We describe an animal model of developmental exposure to diethylstilbestrol (DES), a potent perinatal endocrine disruptor with estrogenic activity, to study mechanisms involved in programming an organism for obesity. This experimental animal model provides an example of the growing scientific field termed “the developmental origins of adult disease” and suggests new targets of abnormal programming by endocrine disrupting chemicals.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TC0-4MV750S-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1099965918&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=70ce8ca18d2f699c3a3dd5c86f054684

Obesity continues to rise in the United States and throughout the world. Both leptin from fat cells and insulin from pancreatic B cells are created in direct proportion to body fat. Obese persons have higher levels of these two hormones than lean individuals. Recent studies show that another hormone, estrogen, also has a similar affect.

When estrogen receptors in the hypothalamus of rats were destroyed, female rats ate more food, burnt less energy and became obese. Research suggests a link between estrogen and obesity, especially the dangerous accumulation of abdominal fat linked to cardiovascular disease, type-2 diabetes mellitus, and certain cancers. The abstract was submitted by Deborah J. Clegg, PhD, Assistant Professor of Psychiatry, Obesity Research Center, at the University of Cincinnati Academic Health Center, to the 234th national meeting of the American Chemical Society on August 20, 2007. Her findings will assist scientists in developing new hormone replacement therapies.

http://ezinearticles.com/?Estrogen-Link-to-Obesity&id=1668125

And I do not expect most of you to read this either... that is the truth...

Now back to my hidey hole and waiting for the expected sniping and the it is just calories in calories out... easy mantra to repeat and believe... and yes ghosts are real and so are UFOs...Carl Sagan was so right, and we now live in an age of warlocks and witches...