J. SmithCarr, A. PerfettiThomas, Hayes A Wallace, B. Colin
Background: Obesity is a worldwide epidemic with approximately two billion adults classifiable as overweight and over 600 million as obese. In the US, approximately two-thirds of adults over age 20 are overweight with about 35% currently obese with the obesity percentage steadily rising. Aim: Obesity is a complex disease wherein an excessive amount of body fat accumulates from ingesting more calories than are burned. Obesity usually results from a combination of factors including genetics, ready availability of inexpensive high caloric foods, low exercise levels or sedentary lifestyles, and poor dietary choices. Methods: This paper provides an overview of the available information on synthetic endocrine disrupter chemicals and reasons why these chemicals are not a significant cause of obesity. Results: Prenatal effects of exposure to synthetic endocrine disrupting chemicals (EDCs) have been proposed as a causative factor in the obesity epidemic. Population effects from prenatal EDCs would be expected to be very minor as exposures to EDCs are very low; and humans are routinely exposed to a huge number and high concentration of naturally occurring chemicals with potential endocrine effects. Further reducing exposures to the trace amounts of EDCs in the environment would not be expected to measurably ameliorate the obesity epidemic which is mainly being driven by excessive caloric intake of high carbohydrate and high sugar content foods. Conclusions: While exposure to synthetic EDCs is not a major factor in developing obesity, the converse is true; adipose tissue is an important source of estrogens, testosterone, thyroid stimulating hormone, leptin and approximately 500 biologically active compounds termed adipokines. The hormonal and pro-inflammatory effects of adipose tissue underlie the association between obesity and increased risk of a number of chronic diseases.
{"title":"Synthetic Endocrine Disrupting Chemicals are not a Significant Cause of Obesity","authors":"J. SmithCarr, A. PerfettiThomas, Hayes A Wallace, B. Colin","doi":"10.36959/736/637","DOIUrl":"https://doi.org/10.36959/736/637","url":null,"abstract":"Background: Obesity is a worldwide epidemic with approximately two billion adults classifiable as overweight and over 600 million as obese. In the US, approximately two-thirds of adults over age 20 are overweight with about 35% currently obese with the obesity percentage steadily rising. Aim: Obesity is a complex disease wherein an excessive amount of body fat accumulates from ingesting more calories than are burned. Obesity usually results from a combination of factors including genetics, ready availability of inexpensive high caloric foods, low exercise levels or sedentary lifestyles, and poor dietary choices. Methods: This paper provides an overview of the available information on synthetic endocrine disrupter chemicals and reasons why these chemicals are not a significant cause of obesity. Results: Prenatal effects of exposure to synthetic endocrine disrupting chemicals (EDCs) have been proposed as a causative factor in the obesity epidemic. Population effects from prenatal EDCs would be expected to be very minor as exposures to EDCs are very low; and humans are routinely exposed to a huge number and high concentration of naturally occurring chemicals with potential endocrine effects. Further reducing exposures to the trace amounts of EDCs in the environment would not be expected to measurably ameliorate the obesity epidemic which is mainly being driven by excessive caloric intake of high carbohydrate and high sugar content foods. Conclusions: While exposure to synthetic EDCs is not a major factor in developing obesity, the converse is true; adipose tissue is an important source of estrogens, testosterone, thyroid stimulating hormone, leptin and approximately 500 biologically active compounds termed adipokines. The hormonal and pro-inflammatory effects of adipose tissue underlie the association between obesity and increased risk of a number of chronic diseases.","PeriodicalId":339470,"journal":{"name":"Annals of Toxicology","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130140163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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