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Are Chemicals in the Environment Making Us Fat?

Kimbra Hoehn

October 5, 2009

Introduction

        Obesity rates have risen worldwide in the past several decades and is becoming so widespread that it has been declared an epidemic (Jefferson, 2007). Until recently, weight gain and obesity have been attributed to a combination of genetics, over consumption of calories and lack of exercise. However, there is some speculation that exposure to certain chemicals, known as obesogens may also have an impact on weight gain (Jefferson, 2007). The idea arose from the observation that over the past thirty years, obesity has increased in infants under six months of age by 73% . Since their diets are the same as they have always been and they are not exercising any less, scientists have began to speculate that there may be more to the obesity equation than diet, exercise and genetics. Exposure to toxic chemicals found in everyday products and the environment may be interfering with human endocrine systems and contributing to the larger than ever number of obesity cases (http://www.newsweek.com/id/215179/page/1 ).

 

Obesity is a growing problem... literally

        Obesity is the state of having an excess of body fat, more than 30% for women and 25% for men. (Jefferson, 2007) It can be determined by a body mass index, BMI, that is a ratio of height to weight. A BMI over twenty five is considered overweight and a BMI over thirty is considered obese.

        In the past thirty years, obesity rates have doubled in adults and tripled in children in America (Centers for Disease Control and Prevention, 2009). As of 2008, about 34% of adults and 16% of children are obese while another 32.7% of adults and 32% of children are overweight. In the past several years, obesity growth rates have declined, but the governments wants to bring the population of obese Americans down to 15% (http://www.cdc.gov/obesity/causes/index.html).

       

Consequences of Obesity

        Obesity increases the risks for developing many diseases such as hypertension, type 2 diabetes, heart disease, stroke, insulin resistance, hyperinsulinemia, high blood pressure, asthma, gall bladder diseases and even some types of cancer (Jefferson 2007). These and many more obesity related illnesses result in over 300,000 preventable premature deaths annually. Not only are obese individuals estimated to have a 50%-100% increased risk of death, but being overweight is also emotionally damaging. Obese individuals are stereotyped as lazy and often discriminated against. As a result they often experience depression, anxiety and other psychological disorders causing a decreased quality of life. Additionally, obesity costs Americans roughly $117 billion dollars annually in obesity related health care (http://www.cdc.gov/obesity/causes/index.html).

 

 

What are obesogens and where are they found?

        Obesogens are chemicals we are exposed to in everyday life that interfere with our endocrine systems and metabolic pathways that may be causing us to gain more weight. Examples include chemicals such as insecticides, herbicides, fumigants and fungicides that are found in plastics, pesticides, paints, as well as other places in the environment (Allison, 2008). Exposure to these chemicals may be direct or due to consumption of contaminated food, water and even air. The most common obesogens are phthalates, the industrial chemicals in plastics, lubricants, and solvents (Hatch, 2008). These chemicals are used in the production of children’s toys, medical equipment, medications, food packaging, and water bottles.

                 

 

        Sources                                             Types                                     Examples

          Incineration                       Industrial by-products                   PCB’s, dioxins

          Atmospheric transport                  Organochlorine pesticides              DDT, lindane,dieldrin

          Agricultural runoff              Pesticides                          Atrazine

          Harbors                                      Anitifoulants (paint used on ships)   TBT

          Industrial/municipal effluents          Alkylphenols, natural estrogens       Nonlyphenol, estradiol

          Pulp mill effluents               Plant estrogens                            Geinstin

          Consumer products             Flame retardants                         PBDEs

          Consumer products             Platicizers                         Dibutyl phthalate

(Allison, 2008)

 

What does the web say the connection is?

        According to the Centers for Disease Control, some people are genetically predisposed to be heavier than others. However, weight gain is most directly a function of calorie intake and energy expenditure. A calorie is a unit of energy found in food and beverages. The human body uses calories to perform everyday functions. When a person consumes more calories than he or she burns, the body stores the extra calories as fat. Weight gain is caused by an excess of energy whether from over consumption or under expenditure of calories (http://www.cdc.gov/obesity/causes/index.html).

         The body breaks down calories in a system of metabolic pathways .All of these pathways must work together to maintain a balance of energy. Malfunction of these systems may cause an imbalance or abnormal energy flow which could lead to weight gain and obesity. The obesity epidemic corresponds with the exponentially increased amount of toxic chemicals in our environment (Allison, 2008). Many of these chemicals may be responsible for the malfunctioning of metabolic pathways in the human body and are thus know as obesogens (http://endo.endojournals.org/cgi/content/full/147/6/s50).

 

Web Overview

        The web pages on obesogens did little more than present the claim that these toxic chemicals may be a contributing factor to obesity. This may be because it is a fairly new concept and there is little research on the topic, but it  also may be an effort to suppress the information so as not to alarm citizens. The websites may want to be informative and warn people of the possible dangers of toxic chemicals. However, they do not want to make the situation seem so urgent that companies using these chemicals loose their consumer bases.

 

Research

          Study One: Chemicals in Paint, Plastics and Fish Nets

        Tributlytin or TBT is a potentially endocrine disrupting chemical that is used in boat paint and fish nets contaminating the marine environment (Baker, 2008). TBT is broken down in the liver to another potentially harmful chemical dibutylin. or DBT. DBT is used in the production of plastic pipes and bottles and through consumption of water stored in these bottles or pipes, we are directly exposed to DBT.

                        

        According to Baker (2008) a study was done to determine if TBT, DBT, TPT or DPT would interfere with the human metabolic process. Scientists tested the exposure of DBT, TPT, TBT, DPT on HEK-293 cells to measure the inhibition of GR mediated transactivation in humans (Baker, 2008). The inhibition of the transactivation process would hinder the production of the two key enzymes in the metabolic process and would slow the body’s metabolic rate, increasing the amount of calories stored as fat.

        The cells were incubated with varying amounts of each of these chemicals and a control of 100 nM cortical for twenty hours. Afterwards, the inhibition of GR mediated transactivation was measured and compared. The amounts of TPT, TBT and DPT the cells were exposed to had little to no correlation with the transactivation percentage. However, greater amounts of exposure to DBT had a strong positive correlation with the inhibition of GR mediated transactivation. The cells that were exposed to higher doses of DBT had significantly lower transactivation percentages. The cortisol control allowed for 100% transactivation, an exposure of 1000 nM of DBT only allowed for 20% transactivation, or 80% inhibition of the key metabolic enzymes. This study concluded that amount of exposure to DBT proportionately effects the inhibition of the production of the two key enzymes in the human metabolic process. This is significant because human consumption of DBT from water bottles or PVC pipes could lead to slower metabolisms and increased fat storage (Baker 2008).

(Baker, 2008)

 

 

 

          Study Two: Phthalates in Toys, Cosmetics, Food Packaging, and Medications

                              

 

        In the past twenty years, researchers have also been investigating the connections between various chemicals found in plastics, known as phthalates, and obesity. The National Health and Nutrition Examination Survey, performed a cross section of 5,149 participants ages six and above to examine possible correlations between the amounts and types of phthalates in their urine, waist circumference and BMI (Hatch, 2008). The urine samples were tested for mono-ethyl (MEP), mono-2-ethylhexyl (MEHP), mono-n-butyl (MBP), mono-benzyl phthalate (MBzP).

        For subjects age 20-59, there were strong positive correlations between males’ BMIs and traces of MBzP, MEHHP and MEOHP, but females had more diverse results. They showed a positive correlation between increased BMI and increased levels of MEP, but showed inverse relationships with MEHP and MBzP. This suggests that there could be different effects of varying obesogens on males and females due to the different effects and presence of hormones in male and female bodies. There was little to no correlation between the levels of any of these chemicals and the BMI’s and waist circumferences of children 6-11 years of age. This could be partially because the weights of children are highly inconsistent based on their varying stages of  development. There was also a reverse correlation in subjects 60-80 years of age which could be contributed to the general weight loss trend of the elderly. Although the study did suggest that there could be an impact of these specific obesogens in increasing BMI’s and waist circumferences, the study concluded that the results called for further research to be done and prospective studies to be conducted to be able to support positive correlation (Hatch, 2008).

 

 

          Study Three: Prenatal Vulnerability, Specifically Medication

         Obesogen exposure before birth could also have damaging effects on an individuals BMI’s later in life. From 1940-1970 a drug called diethylstilbestrol, DES, was commonly used to prevent miscarriages and once thought to be safe (Jefferson, 2007). After linking the drug to development of several types of cancer and infertility, the drug is no longer used, but the influence of DES on prenatal development shows that exposure to even small amounts of particular chemicals in the womb may have resulted in predisposition to obesity in many individuals whose mothers took the drug.

        A study was done to investigate the effects of the exposure of  DES during prenatal development on the fetuses’ adult weight. (Jefferson, 2007) The study injected CD-1 mice with DES on days 9-16 of gestation and 1-5 of neonatal life. The injected mice, on average, weighted slightly less at birth, but by two months began to outweigh the control mice. By four months the DES exposed mice weighed significantly more than the controls weighing on average 7 grams more than the controls and had significantly more belly fat. The experiment supported the connection between exposure to DES in early life and increased body weight with age. Although scientists cannot be positive that the results of this experiment are applicable to human patterns of development, it does suggest that exposure to DES and other environmental obesogens during prenatal and neonatal development could be playing a role in the obesity epidemic (Jefferson, 2007).

 

                    

(Jefferson, 2007)                                 (Jefferson, 2007)

 

 

Conclusion

        Based on the available research, it can be concluded that the toxic chemicals known as obesogens are contributing to the obesity epidemic. The various chemicals effect different aspects of the human metabolic process and endocrine system and have varying effects on individuals depending on factors like age and gender. The interferences slow down the body’s ability to break down energy and causes more energy to be stored as fat. Exposure to these obesogens, even in small amounts, during development can have a significant effect on an individual’s weight later in life. 

        In a society with such a vast portion of its population suffering from obesity, it is a very important factor and needs further investigation. If research continues to support the theory of obesogens, the use of these toxic chemicals should be kept to a minimum, if not eliminated. In the meantime it is wise to attempt to minimize contact with these chemicals. Try to buy organic foods, read labels, and avoid plastics to avoid exposure to obesogens.

 

 

References

Allison D. B., Elobeid M. A. (2008). Putative Environmental-Endocrine Disruptors and         Obesity: A Review. Curr Opin Endocrinol Diabetes Obes, 15(5), 403-408. dio:         10.1097/MED.0b013e32830ce95c.

 

Baker M. E., Chandsawangbhuwana C., Dzyakanchuk A. A., Gumy C., Kratschmar D.    V., Odermatt A., (2008). Dibutylin Disrupts Glucocorticoid Receptor Function     and Impairs Glucocorticoid-Induced Suppression of Cytokine Production. PloS        ONE, 3(10), e3545. doi: 10.1371/journal.pone/0003545

 

Begley, Sharon. (2009). Born to Be Big. Retrieved September 30, 2009, from Newsweek         Web site: http://www.newsweek.com/id/215179/page/1

 

Blumberg B., Grun F. (2006). Environmental Obesogens: Organotins and Endocrine         Disruption via Nuclear Receptor Signaling. Retrieved September 30, 2009, from         Endocrinology Web site: http://endo.endojournals.org/cgi/content/full/147/6/s50

 

Centers for Disease Control and Prevention. (2009). Overweight and Obesity. Retrieved:         September 30, 2009, from CDC Home. Web site:         http://www.cdc.gov/obesity/causes/index.html

 

Hatch E. E., Moore L. L., Nelson J. W., Qureshi M. M., Singer M., Webster T. F., et al.         (2008). Association of urinary phthalate metabolite concentrations with body         mass index and waist circumference: a cross-sectional study of NHANES data,         1999-2002. Environmental Health, 7, 27. doi:10.1186/1476-069X-7-27

 

Jefferson W. N., Newbold R. R., Padilla-Banks E., Phillips T. M., Snyder R. J. (2007).         Developmental Exposure to Endocrine Disruptors and the Obesity Epidemic.         Reprod Toxicol, 23(3), 290-296. doi: 10.1016/j.reprotox.2006.12.010.

 

 

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