Obesity and chronic disease: have we missed the point?

Evidence in science requires time, but when that evidence arrives, it may suggest that we need to think about things differently. In the case of research into the relationship of obesity to chronic disease, the accumulating weight of evidence has meant a rethink of what obesity means, and what we are trying to achieve in “treating” obesity.

After three decades of rapid increases in mean national bodyweight, we now seem to accept that we have a problem. Around one in two Australians are overweight (body mass index [BMI] > 25 kg/m2), and more than one in three are obese (BMI > 30 kg/m2).2 However, now that the message has hit home, the evidence relating obesity to chronic disease has started to shift. Some question whether obesity really is the issue. Should we be focusing instead on those factors (such as lifestyle, environment and social factors) that may (or may not) cause obesity?

Why the change of heart? There is little doubt that obesity is linked with the dysmetabolism associated with much chronic disease, and particularly type 2 diabetes. But there are also more distal drivers, which may or may not require obesity in the causal pathway for chronic disease to occur, and these may not be considered if the focus is purely on obesity.

This has become clear with the concept of “metaflammation”3 — a form of low-grade, persistent systemic and chronic inflammation, which is associated with much, and perhaps most, chronic disease. While the classical form of inflammation has a healing role in acute disease, metaflammation, because of its persistence, may have a causal role in aggravating and perpetuating chronic disease. Linked not just to obesity, it is also associated with a range of “inducers”, some of which directly cause obesity (overnutrition, inactivity, stress), but also many that are not direct causes.4 These include environmental factors like pollution and passive smoking, a newly identified group of endocrine-disrupting chemicals, and social and occupational factors such as inequality, perceived injustice and even shift work.

Together, these make up a group of inducers of chronic disease that could be called “anthropogens” — human-made environments, their by-products, and associated lifestyles. Some of these may be detrimental to human health; all have arisen since the industrial revolution and seem to be foreign to our ancient physiology. These anthropogens may be considered to be the “germs” behind many chronic diseases.

A focus just on the proximal causes of obesity and associated individual behaviours could have the adverse impact of blaming individuals for the environment that surrounds them. It deflects criticism from more distal social and environmental causes, where the recognition of an anthropogen-based causality would get to the heart of chronic disease causation. Given this, what would be the point of targeting the “fit fat” — the 35% of obese individuals who have no obvious health risk (apart from mechanical and possibly psychological issues) — and ignoring the approximately 25% of lean people who fit the “lean unhealthy” phenotype and have all the risks expected of the obese?5 The current focus is on visceral fat, which gets close to the issue, but we need to think about what is causing visceral adiposity in the first place.

All this points to obesity as an intermediary as much as an offender in chronic disease — it is a sentinel of problems in the broader environment. This is not to suggest that weight loss is not a justifiable goal; of course it is. But to do the job properly, it should be accompanied by broader initiatives aimed at targeting the anthropogens that are using obesity as their cover.