Obesity is a medical condition characterised by excess accumulation of body fat, to the degree that it becomes harmful to health.
Obesity reduces life expectancy while increasing the risk of illness and death from a range of other diseases. It is now so common in adults and children that the World Health Organisation characterises the condition as an epidemic.
The health consequences of obesity fall into two broad categories: those attributable to the physical effects of increased weight, including osteoarthritis and sleep apnoea; and those due to the increased size of and metabolic activity of fat cells, including diabetes, cancer and cardiovascular disease (Bray 2004).
Energy imbalance is the immediate cause of obesity, a combination of excess dietary calories and a lack of physical activity. Assuming a well-balanced diet is eaten, only a slight positive energy imbalance, if sustained over several years, can result in obesity. If 0.45kg (1lb) of fat contains 3,500 calories, then to gain 63 kilograms (140 pounds) requires an energy excess of 490,000 calories. This means a mere 134 calorie energy excess per day is sufficient for someone to become substantially overweight over a 10 year period.
The full set of reasons as to why someone might become obese must be more complex than loss of control over energy balance, otherwise treatment of obesity through diet and lifestyle changes alone would be successful more often than in just 2-20% of cases (Wing et al. 2005).
“Thrifty” genes, genetic disorders, endocrine disorders, medications and psychiatric illness are already well-recognised reasons why some people find it relatively easy to maintain a constant weight while others struggle to do so. It is speculated that sleep deficit, stress, viruses, microbes and single mutations in an individual’s genetic code may also be contributing to the incidence of obesity (Keith et al. 2006).
In addition to these, it has been hypothesised that routine exposure to man-made chemicals may also be increasing an individual’s risk of obesity. The obesogen hypothesis “proposes that perturbations in metabolic signalling, resulting from exposure to dietary and environmental chemicals, may further exacerbate the effects of imbalances in diet and exercise, resulting in an increased susceptibility to obesity and obesity-related disorders” (Grun & Blumberg 2009).
The obesogen hypothesis is part of the research programme related to the campaign of US First Lady Michelle Obama to understand and reduce rates of obesity in the US. Not everybody is won over by the concept, however. Writing for the Wall Street Journal, social and political commentator Allysia Finley has said: “By ringing the alarm bells based on insufficient and inconclusive evidence, environmentalists have subverted serious discussion of the issue—and are on track to create another green scare.”
Contrary to what Finley may argue, there is a body of contextual evidence which at least makes the obesogen hypothesis worthy of careful consideration, not least that prenatal exposure to tobacco smoke is strongly associated with obesity (Monasta et al. 2010).
Diabetes drugs also make adults obese, by activating receptors which cause a type of stem cells to become fat cells. The antifouling agent tributyl tin (TBT) has been shown to act on these same receptors in animals at levels detected in a portion of the population (Kirchner et al. 2010). It is therefore plausible that other chemicals could be having the same effect.
Experimental data in animals shows that brief exposure early in development to chemicals with oestrogenic activity can increase weight gain later on. At two months of age, mice treated at birth with the oestrogenic drug diethylstilbestrol (DES) weigh the same as untreated mice. By the time they are six months old, the treated mice have considerably larger fat mass than the untreated controls.
Although they weigh the same at two months of age, the treated mice do show differences in levels of hormones which are produced by adipose (fat) tissue such as leptin, associated with appetite control, and adiponectin.
The altered hormone levels are not associated with changes in feeding habits or physical activity, strongly suggesting that DES induces a range of changes which set a mouse’s metabolism to conserve energy, as if it were living in a low-resource environment, thereby predisposing it towards obesity (Newbold et al. 2009).
Research into obesogens is still very much in its early stages. Little is known about people’s exposure to obesogens or which chemicals are problematic, although there is some evidence that phthalates (Stahlhut et al. 2007), BPA (Somm et al. 2009) and non-stick PFOAs may be obesogenic (Vanden Heuvel et al. 2006).
There is also a lack of human epidemiological evidence, but epidemiology is likely to be ill-suited for any chemical causes of obesity. This would require the detection of effects of exposure to a chemical that acts during a limited time-window of sensitivity to initiate a health problem which only manifests itself later in life and in a limited portion of the population (Grun 2010). Prospective epidemiological studies would take years to produce results, even assuming adequate controls could be defined in such a study so as to allow causation to be proven.
At the very least, however, the fact that prenatal maternal smoking causes obesity ought to provide proof-of-concept: exposure to a chemical cocktail before birth is capable of making people obese who would not otherwise be so. Furthermore, given that small alterations in energy balance can result in relatively drastic weight gain, obesogens themselves may not need to have dramatic effects on metabolism to induce obesity. Combining the effect of obesogens with poor diet and decreased activity could potentially have profound effects on obesity rates.
Given the pronounced effect of obesogens on animals combined with the in-principle plausibility of the obesogen hypothesis and the harm which obesity causes, it seems reasonable that obesogens should at least be a research priority. Given the difficulty of remediating obesity, prevention is vital, especially if some of the ultimate causes of obesity reside in long-term metabolic changes caused by chemical exposures at a young age.
Risk assessors are typically challenged by four questions: What adverse effects result from exposure to a chemical? At what level do these effects occur? Are there populations at special risk? And how sure are we of the answers to the other three questions?
This presentation examines how risk assessment functions when new science presents fresh evidence of potential harm, with case studies of low-dose exposure to arsenic and the health effects of obesogens. It should be useful to anyone looking for an overview of what risk assessment does and tries to achieve, presenting an insider’s view of how risk assessment can incorporate new science.
Related H&E content:
- Is there a better way of assessing the risks which chemicals may pose to human health?
- Association, causation, and the usefulness of epidemiology
This presentation by Dr Ila Cote, a senior science advisor at the US Environmental Protection Agency, was part of a workshop titled Use of In Utero and Post-Natal Indicators to Predict Health Outcomes Later in Life, organised by the US Standing Committee on Emerging Science for Environmental Health Decisions. For more information visit their website; for updates on new workshops and other information, sign up for their newsletter.
The next Standing Committee workshop (27-28 April 2011, Washington DC) will review the significance of the microbiome for human health and how environmental conditions can alter its balance, potentially increasing risk of asthma, autism, obesity and other health problems. Click here for more information about the workshop.
PBDE Disruption of Thyroid Hormone–Induced Purkinje Cell Dendrite Arborization. A technical study which looks at how disruption of the thyroid system may hamper brain development, by changing how nerve cells develop. EHP synopsis here.
Mitochondrial dysfunction in autism spectrum disorders. Systematic review finding that, although many studies suffer from limitations, the evidence supports the notion that environmentally-induced mitochondrial dysfunction is associated with autism spectrum disorders. A different study has also found a role for mitochondrial dysfunction in Parkinson’s Disease (synopsis here).
Prenatal Organochlorine Compound Exposure, Rapid Weight Gain, and Overweight in Infancy. Study finding prenatal DDE exposure to be associated with rapid weight gain in the first 6 months and elevated BMI later in infancy, among infants of normal-weight mothers.
Widely Used Pesticides with Previously Unknown Endocrine Activity Revealed as in Vitro Anti-Androgens. Study finding that which finds many agricultural pesticides disrupt male hormones. These include some which had previously not been tested for this yet are commonly found in food. Synopsis by EHN here.
Prenatal environmental exposures, epigenetics, and disease. This review summarizes recent evidence that prenatal exposure to diverse environmental chemicals dysregulates the fetal epigenome, with potential consequences for subsequent developmental disorders and disease manifesting in childhood, over the lifecourse, or even transgenerationally.
Toxic Chemicals in Pregnant Women? An uncomplicated Q&A with Dr Sarah Janssen, MD, about the difficult issues presented by research finding that pregnant women have a range of possibly harmful chemicals in their bodies.
Green Cleaning Spruces Up Environment. WebMD asks: what does “going green” actually mean, when it comes to cleaning products? The answer, they say, has to do with the fact that much of the cleaning we do “isn’t cleaning, it’s polluting”.
Home Pesticide Chemical May Hurt Kids’ Cognition. Data analyzed for almost 350 children found that increase in exposure to piperonyl butoxide — a chemical mixed with pyrethroid pesticides to improve its efficacy — was associated with delayed mental development at age 3 years. Original study here.
Clorox comes clean: Company discloses all ingredients in all products. The maker of bleach, Pine-Sol and other popular cleaning products has announced it will disclose the specific preservatives, dyes and fragrances it uses in its cleaning, disinfecting and laundry products sold in the U.S. and Canada.
First Chemicals Banned In European Union. Chemical & Engineering News provide a lucid explanation of what the new chemical phase-outs under REACH actually mean. The phase-outs have in places been mis-described as bans.