Programmed For Obesity: Early Exposure To Common Chemicals Can Permanently Alter Metabolic System
Science Daily
Obesity is generally discussed in terms of caloric intake (how much a person eats) and energy output (how much a person exercises). However, according to a University of Missouri-Columbia scientist, environmental chemicals found in everyday plastics and pesticides also may influence obesity. Frederick vom Saal, professor of biological sciences in MU's College of Arts and Science, has found that when fetuses are exposed to these chemicals, the way their genes function may be altered to make them more prone to obesity and disease.
"Certain environmental substances called endocrine-disrupting chemicals can change the functioning of a fetus's genes, altering a baby's metabolic system and predisposing him or her to obesity. This individual could eat the same thing and exercise the same amount as someone with a normal metabolic system, but he or she would become obese, while the other person remained thin. This is a serious problem because obesity puts people at risk for other problems, including cancer, diabetes, cardiovascular disease and hypertension," vom Saal said.
Using lab mice, vom Saal has studied the effects of endocrine-disrupting chemicals, including bisphenol-A, which recently made news in San Francisco, where controversy has ensued over an ordinance that seeks to ban its use in children's products. In vom Saal's recent study, which he will present at the 2007 Annual Meeting of the American Association for the Advancement of Science (AAAS), he found that endocrine-disrupting chemicals cause mice to be born at very low birth weights and then gain abnormally large amounts of weight in a short period of time, more than doubling their body weight in just seven days. Vom Saal followed the mice as they got older and found that these mice were obese throughout their lives. He said studies of low-birth-weight children have shown a similar overcompensation after birth, resulting in lifelong obesity.
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"You inherit genes, but how those genes develop during your very early life also plays an important role in your propensity for obesity and disease. People who have abnormal metabolic systems have to live extremely different lifestyles in order to not be obese because their systems are malfunctioning," vom Saal said. "We need to figure out what we can do to understand and prevent this."
http://www.sciencedaily.com/releases/2007/02/070218140845.htmDevelopmental Effects of
Endocrine-Disrupting Chemicals
in Wildlife and Humans
THEO COLBORN et al. Environmental Health Perspectives v.101, n.5, 1oct1993
Theo Colborn,1 Frederick S. vom Saal,2 and Ana M. Soto3
1W. Alton Jones Foundation and World Wildlife Fund, Washington, DC, 20037 USA; 2Division of Biological Sciences and John M. Dalton Research Center, University of Missouri, Columbia, MO 65211 USA; 3Department of Anatomy and Cellular Biology, Tufts University, Boston, MA 02111 USA
Abstract
Large numbers and large quantities of endocrine-disrupting chemicals have been released into the environment since World War II. Many of these chemicals can disturb development of the endocrine system and of the organs that respond to endocrine signals in organisms indirectly exposed during prenatal and/or early postnatal life; effects of exposure during development are permanent and irreversible. The risk to the developing organism can also stem from direct exposure of the offspring after birth or hatching. In addition, transgenerational exposure can result from the exposure of the mother to a chemical at any time throughout her life before producing offspring due to persistence of endocrine-disrupting chemicals in body fat, which is mobilized during egg laying or pregnancy and lactation. Mechanisms underlying the disruption of the development of vital systems, such as the endocrine, reproductive, and immune systems, are discussed with reference to wildlife, laboratory animals, and humans. Key words: developmental effects, diethylstilbestrol, differentiation, endocrine function, estrogen, fertility, hormones, organochlorines, pesticides, phenolics, reproductive function. Environ Health Perspect 101: 378-384(1993)
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It is now recognized that numerous endocrine-disrupting chemicals have been released into the environment in large quantities since World War II (Table 1). Some of these chemicals bind to intracellular receptor proteins for steroid hormones (4) and evoke hormonal effects in animals (5), humans (6), and cell culture (7,8). They thus interfere with the functioning of receptors whose normal role is to mediate the effects of the endogenous steroid hormones (9). Laboratory experiments have demonstrated that exposure of fetuses to endocrine-disrupting chemicals can profoundly disturb organ differentiation (10,11) because they can act as hormone agonists or antagonists. Organs that appear to be at particular risk for developmental abnormalities in offspring because of maternal exposure are those with receptors for gonadal hormones: in female fetuses this includes the mammary glands, fallopian tubes, uterus, cervix, and vagina, and in male fetuses it includes the prostate, seminal vesicles, epididymides, and testes. In both sexes the external genitalia, brain, skeleton, thyroid, liver, kidney, and immune system are also targets for steroid hormone action and are thus potential targets for endocrine-disrupting chemicals, although these chemicals may have multiple modes of action, in addition to acting as hormone agonists and antagonists, in different target tissues (11-15).
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http://www.mindfully.org/Pesticide/EDs-Developmental-Effects-Colborn1oct93.htm