EDCs – an invisible cause of obesity | World Obesity Federation

EDCs – an invisible cause of obesity

NewsEDCs – an invisible cause of obesity

While poor dietary patterns and lack of physical activity are commonly blamed for the modern obesity epidemic, Tim Lobstein and Kelly Brownell argue that a third type of obesogen may be equally important, and is much harder to avoid.

For up to a century the ‘calories in - calories out’ view of weight gain has dominated the discussion on the primary causes of the obesity epidemic which now affects much of the world. Yet in the last two decades a third cause of adiposity has become increasingly recognised, with over 500 scientific papers published since 2000 including over 300 in the last five years. 

This third factor? Endocrine-disrupting chemicals (EDCs) – the man-made industrially-produced compounds that are becoming increasingly widespread in the environment and demonstrably able to affect human hormone systems. These compounds can be found in a wide range of products and environments. They are added to plastic beverage bottles, they are used for food wrapping, they are painted inside tin cans, and put into cosmetics, they are sprayed onto crops, they are incorporated in carpets and furnishing materials and released in traffic fumes and tyre dust. They are known to affect human reproduction and can raise the risk of certain cancers, and most recently they have been shown to affect adipose tissue formation, appetite control and weight gain.

In a review published this month in Obesity Reviews we suggest that EDCs are likely to increase the risk of obesity as much as a poor diet, or watching TV, and that policies for obesity prevention need to take EDCs into account.  The link between overweight and EDC exposure is hard to dispute: children in the USA with higher urinary levels of one of the most common EDCs, bisphenol A (BPA) had twice the prevalence of obesity compared with children with lower levels (Bhandari et al). A meta-analysis found that, for every 1.0 ng/mL increase in urinary BPA above a baseline of 1.0 ng/mL, the odds for obesity increased by 17% in children and 15% in adults (Wu et al). This is highly relevant to western populations where 10% of the population have urinary BPA levels exceeding 5.0 ng/mL.

How does this compare with known risk factors for obesity? A review of childhood obesity prevalence attributable to maternal overweight, maternal obesity, and excessive gestational weight gain, suggested these factors account for 10% to 22% of the risk of obesity (Voerman et al). Watching TV increases the odds for developing obesity by 13% for every hour of TV-watching each day (Zhang et al). Consumption of less healthful diets (refined grains, red meat, sugar-sweetened beverages) increases obesity risk between 5% and 14%, according to Schlesinger et al’s 2019 meta-analysis

Equally modest effects on obesity prevalence are reported in studies of sugar-sweetened beverage consumption. The Spanish SUN project found a daily 200ml serving of regular soda was associated with a 15% increase in risk of obesity, and a 330ml serving of beer associated with a 19% risk. Interestingly, a serving of diet soda was linked with a 9% obesity risk – a finding echoed in a meta-analysis of soda consumption by Qin et al which found sugar-sweetened beverages increased obesity risk by 12% per 250ml portion, but diet soda increased risk of obesity by 21% per portion.

The paradoxical finding of no-sugar beverages linked to obesity may simply be due to people living with obesity switching to diet drinks. But another explanation could be that beverage consumption in all forms raises the risk of increasing EDC consumption – mainly from the plasticisers in plastic bottles and plastic-lined cans. Ultra-processed foods and beverages have recently been linked to EDC exposure: children consuming higher levels of ultra-processed food had more EDC metabolites in their urine, in a dose-response association (Martinez Steele at al).

Having made the case that EDCs need to be taken seriously in obesity prevention, we ask: What policies are being recommended and where are they being taken up? We surveyed over 60 scientific reviews of EDCs and their relation to obesity and found three types of recommendation: (i) individual action to reduce exposure through limiting consumption of EDC-containing products, (ii) medical interventions to counter the effects of EDCs on endocrine systems and to educate patients, and (iii) tougher regulation on the use of EDCs, with increased safety testing and prohibitions on the use of products that are suspected of causing harm.

We then looked at 60 inter-governmental, national and expert policy documents concerned with obesity prevention, including publications from the World Health Organization, the European Commission, and a range of national government departments and agencies. Of these 60 documents only six referred to toxins in the environment as potentially relevant to obesity, and only one document actually specified EDCs and the need for regulatory action. This mismatch between the evolving science of EDCs and their limited recognition in governmental policy is alarming.

We know that policy change in this area is difficult: it requires willingness in government and pressure from civil society, and will be resisted by current commercial interests. However, policies which achieve multiple goals simultaneously could be especially attractive, and policies already in place to reduce EDCs in line with the Sustainable Development Goals for protecting the environment and reducing harm to health may also help to achieve the Word Health Assembly’s targets for preventing further increases in overweight and obesity. This is a good example of a win-win or ‘double duty’ policy combination of the sort identified in the Lancet Obesity Commission. It is good in theory, but for EDCs significant regulatory action is proving difficult to achieve, and is strongly resisted by commercial interests and by governments with economic ties to their continued production.

Lastly, we fear that a narrative of individual agency or personal responsibility to defend against obesogenic chemicals unfortunately echoes the narratives of stigma and blame for weight gain in other contexts, and can divert attention from corporate determinants of health. There are few opportunities for personal responsibility when it comes to avoiding persistent and pervasive pollutants in the environment. Compared with sugar-sweetened beverages or snack foods, EDCs are invisible and potentially obesogenic in relatively small quantities. They are found in a wide variety of products and environments, with highest exposure likely to be from plastics used in food and beverage production, but also in many household products, in transport pollutants and in water supplies.

It needed legislation to remove lead pollution from water supplies and car exhaust, to take asbestos out of the building trade, and it will need legislation to regulate EDCs. Individuals cannot be blamed for their consumption of EDCs and cannot reasonably be asked to reduce their own exposure.

Tim Lobstein and Kelly Brownell

Read the original article

Find 'Endocrine-disrupting chemicals and obesity risk: A review of recommendations for obesity prevention policies' by Tim Lobstein and Kelly Brownell in our journal Obesity Reviews.