The link between pesticides and childhood obesity
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Born to Be Big
Childhood obesity has become an epidemic. According to the Centers for Disease Control and Prevention (CDC), the incidence has more than tripled in the last thirty years. Obese youth are more likely to have risk factors for cardiovascular disease, high blood pressure, bone and joint problems, and sleep apnea. Obese youth are more likely to suffer from social and psychological problems and they are at greater risk than youth of normal weight for becoming overweight or obese adults. Obese adults can suffer from many health problems, including osteoarthritis, heart disease, some types of cancer and Type 2 diabetes (CDC, 2010). Childhood obesity is a very serious matter.
Obesity adds to health care costs. Begley (2009) noted that over sixty percent of Americans are overweight or obese. Their health care costs average approximately $1,500 per year over people of normal weight. Obviously cost is not the most important factor when discussing one's health, but higher costs associated with obesity are still worth consideration.
There are a number of factors potentially contributing to childhood obesity. The biopsychosocial determinates of obesity and overweight exist at biological, behavioral, psychological, family, and societal levels (Lawrence, Hazlett, & Hightower, 2010). There are genetic factors as well. Frances, Ventura, Marini, & Birch (2007) reported that children with two overweight parents are more likely to gain weight even when eating the same food as their peers whose parents are normal weight (in Lawrence et al.). It stands to reason that behaviors with respect to food consumption and physical activity also play a role.
Unfortunately, children who are overweight may also be malnourished, as their diets may rely heavily on fast and processed foods that contain large amounts of sodium, fats and added sugar (Rowe, 2010). These foods are often cheap and filling, making a family's socioeconomic status a factor in childhood obesity as well.
In a 2009 article for Newsweek magazine, Sharon Begley wrote about research that showed a correlation between pesticides and infant obesity. Published in 2002, the work of Scottish doctor Paula Baillie-Hamilton caught the attention of scientists worldwide and provided the basis for further study. The purpose of this paper is to review Baillie-Hamilton's work and other studies that have sought a link between pesticides and childhood obesity.
Chemical Causes of Obesity
Since 1980, the rate of obesity in infants under six months of age has risen by seventy-three percent (Begley, 2009). Endocrinologist Robert Lustig of the University of California, San Francisco, noted that this was remarkable, given that "the conventional explanations of the fattening of America" do not come into play. "Since they're eating only formula or breast milk, and never exactly got a lot of exercise, the obvious explanations for obesity don't work for babies. You have to look beyond the obvious" (Begley). Baillie-Hamilton (2002) also wanted to look beyond the obvious; she found a 2001 study by the Department for Environment, Food, and Rural Affairs (U.K.) that revealed modern caloric consumption has declined modestly, but so have average individual levels of physical activity. However, citing Morris (1995) and Rassvussin (1995), Baillie-Hamilton wrote "hard evidence does not show that levels of physical activity have plummeted sufficiently to cause such a high incidence of obesity (p. 186). Because Baillie-Hamilton noted an increase in the use of pesticides and plastics over the years as well as an increase in obesity rates among children, she wanted to explore a possible causal relationship. She noted that pesticide residues, along with chemical preservatives and are ingested with food and water, inhaled from the air, and absorbed through the skin with the use of personal care products. Citing Jacobson & Jacobson (1996), Alleva et al. (1998), and Bordet et al. (1993), Baille-Hamilton noted that the average person has hundreds of industrial toxins in the body, many of which are transferred across the fetal-maternal blood barrier and through breast milk (p. 187).
Certain chemicals appear to cause weight gain by interfering with the human weight control system by disrupting major weight controlling hormones, including thyroid hormones, estrogens, testosterone, insulin, and growth hormones (Yamagishi et al., 2001, in Baillie Hamilton, 2002). They appear to alter levels of and sensitivity to neurotransmitters, particularly dopamine, adrenaline, and serotonin. They also appear to interfere with many metabolic processes and cause widespread damage to nerve and muscle tissues (Baillie-Hamilton, p. 188).
Japanese scientists found that low levels of certain compounds such as bisphenol a, used to make hard, polycarbonate plastic, could alter cells growing in the lab. They were actually able to change fibroblasts, cells which make up connective tissue, to adipocytes -- fat cells -- with the addition of bisphenol a. They also found that bisphenol a stimulated the proliferation of existing fat cells (Begley, 2009). Since fat cells formed in infancy remain in the body for life, the importance of inhibiting their formation is clear.
It is easy to decry the use of pesticides and food additives and there are indeed measures that individuals can take to reduce their consumption of these chemicals. Crinnion (2010) reviewed a number of studies that show variations in the nutritional value of organic foods from farmer to farmer and from year to year but that, overall, consumption of organic foods by consumers provided better nutrition and reduced exposure to pesticides. These findings would not surprise many people; the results are intuitive and the reason behind the success of organic products, retails stores, and magazines that cater to consumer choices. While it may be easy to avoid fast and processed foods, we may not have as much control over the water we drink and certainly not over the air that we breathe. As well, synthetic chemicals are often found in necessary pharmaceutical products. Baillie-Hamilton noted studies that identified weight gain as an unwanted side effect with the use of pharmaceuticals for treatment in cardiology, oncology, psychiatry, and immunology ((Baptista, 1999; Chrysant et al., 1991; Simpson et al., 2001; Varsano et al., 1993; Wiseman and Adkins, 1998). It would seem that there is no way to avoid these toxins that alter the body and contribute to weight gain.
Baillie-Hamilton was careful not to assume a causal relationship between toxins and weight gain, but cited overwhelming coincidental evidence and suggested further study to investigate which of the many chemicals in the environment are the most likely to cause damage to the human weight-control system.
Researcher Bruce Blumberg of the University of California, Irvine, coined the term "obesogen" to describe the chemical compounds that act as endocrine-disrupters -- they interfere with the body's normal processing of hormones (Economist, 2007). John Peterson Myers, founder and CEO of Environmental Health Sciences heads research on chemicals and fetal development. With co-authors Dr. Theo Colborn and Dianne Dumanowski, he wrote Our Stolen Future (1996) and currently maintains a website and blog through which he synthesizes hundreds of scientific articles about endocrine disruption for the purpose of making them accessible to the media and the general public. Both Blumberg and Myers want people to take seriously warnings about chemicals and their effects on the body, particularly with respect to fetal development.
Conclusion
New evidence suggests that being overweight is not just the result of personal choices about what you eat, combined with inactivity (Newbold, cited in Begley, 2009). It could be blamed on exposure to chemicals in childhood and even in utero. It is thought that the so-named obesogens particularly affect overweight and obese individuals who are fifty years old or younger, since the use of agricultural chemicals has greatly increased over the last half century, therefore increasing individual incidence of exposure. Begley also noted that exposure to chemicals may well account for a phenomenon experienced by many -- they eat the same things as their friends, yet gain weight while their friends do not. Chemical exposure may be a way of explaining the difference in individuals' metabolisms. Scientists have noted that even slight variations in amounts and exposure times change the effects of chemicals on so-called "fat genes" (Begley, 2009).
Scientists also point out that exposure to obesogens does not doom an individual to obesity. Diet and exercise are important, although people predisposed to being overweight may find they have to work harder than their slim counterparts. Perhaps as research shows the mechanisms by which synthetic chemicals alter hormones, further research will shed light on how these effects can be counteracted.
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