Are the products used to build our buildings also making us fat? Are our diet sodas giving us cancer?

As though it isn’t hard enough to watch our diets, as insurers we have to worry about what it all means for liability emerging risk too. We can help with the emerging risk, but we have to leave the dieting to you.

Obesity is on the rise across the developed world. Until recently, most of us had assumed that was because we kept eating “unhealthy” foods and eating too much overall. In the United States, after a brief pause, childhood obesity has begun rising again, despite some efforts to improve diet. Research has been emerging that suggests another likely culprit: chemical exposures.

Scientists coined the term “obesogen” to describe chemicals that seem to result in increased risk of obesity. Might these chemicals result in liability for causing the obesity epidemic?

Obesogens appear to exert their effects and contribute to the obesity epidemic by several different mechanisms, including altering our body’s hormonal regulation, which scientists call “endocrine disruption.” The endocrine disruptors include familiar risks such as bisphenol A, some flame retardants, phthalates and metal compounds, but in the last year some new candidates have emerged. These emerging obesogens include salts of dibutyltin and dibenzoates, both of which are commonly used in building products.

Bisphenol A is well studied in the scientific literature because of its endocrine-disrupting effects, but its links to obesity were discovered more recently. The way it works is that adipose tissue—fat cells and associated structures—performs many endocrine functions, such as controlling appetite. The ubiquitous exposure of people worldwide to bisphenol A, primarily from plastics, appears to impact the endocrine function of adipose tissue on top of its other effects on hormonal balance. Furthermore, the link has proved durable across human studies, animal studies and in vitro mechanistic studies. (Editor’s Note: Mechanistic studies examine cellular and molecular interactions that can help explain how, for example, disease states can be induced by toxic exposures.)

The growing level of scientific evidence for this link is strong enough to show that bisphenol A can, in principle, induce obesity. It is far from clear whether it will become possible to link any specific case of obesity to bisphenol A exposure, which is necessary to establish liability.

Phthalates, which are used in plastics including toys and medical tubing and in cosmetics, have fallen under suspicion in recent years for contributing to the obesity epidemic. The most prominent phthalate is di(2-ethylhexyl) phthalate, or DEHP. The research linking DEHP to endocrine disruption is well settled, but the specific links to obesity are being worked out. Research published in 2018 brought several epidemiological studies to light suggesting that DEHP and other phthalates could play a significant role in the increasing obesity burden.

One of the newer compounds to emerge as a risk for obesity in the last year is dibutyltin chloride. Its chemical cousin, tributyltin, has been used in marine antifouling paints and was one of the first materials identified as an obesogen. While tributyltin’s commercial uses have been curtailed, dibutyltin compounds remain common. For instance, dibutyltin is a heat stabilizer in plastics and is used to make hot water PVC pipes in our homes. The scientific evidence for these compounds’ obesogenic effects is very new, but one recent study directly examines this possibility both in vitro and in mice. It showed that dibutyltin salts could cause obesity by interfering with the genes that control adipose tissue.

Another newly emerging obesogen is diethylene glycol dibenzoate, or DEGDB. This relatively unknown compound has been in use as a plasticizer for many years, but its popularity is growing as a substitute for phthalates in some building materials such as vinyl flooring. A study published last year compared its endocrine disrupting and obesogenic effects to those of bisphenol A. DEGDB was demonstrated to increase fat production in animals. With this initial research, DEGDB might prove to be yet another “regrettable substitution.”

As we confront the risk of obesity, artificial sweeteners have long been one solution to reduce calorie intake, but these sweeteners are often seen by the public—and by insurers—as riskier than the natural products (like sugar) they replace. Aspartame, in particular, is sometimes alleged to cause cancer, and the web is full of dark conspiracies about how aspartame is even “linked to” Monsanto and former U.S. Defense Secretary Donald Rumsfeld.

Underwriters are inevitably influenced by this climate of artificial sweetener fear. But the science comes to a very different conclusion. With a relatively large amount of literature, scientists have struggled to consistently find anything harmful from aspartame.

For example, a quick Internet search will tell you that fears abound about aspartame’s ability to cause leukemia, brain tumors, type 2 diabetes, obesity, inflammation, attention-deficit hyperactivity disorder and even dementia, stroke and depression. While scientific literature for all these harms exists, Praedicat has found that all this literature, on balance, soundly rejects the hypothesis of human harm despite the occasional study showing an association.

Alas, science rarely stands still. A whole new line of research is emerging on the potential for aspartame to affect our metabolism via disrupting the community of flora and fauna that live in our gut, a.k.a., the gut microbiome. Microbiome disruption is the newest hypothesis that has gained some traction in the scientific community to explain the rise of obesity.

Of all the great ironies, can it be that our diet sodas are making us fat? Randomized controlled trials comparing sugary beverages to diet sodas have concluded otherwise, but the hunt for aspartame harms seems likely to continue.