(AEON ESSAYS)  Pam Weintraub, DECEMBER 22, 2016 — ‘Virtually zero.’ That’s a reasonable estimate of the probability that public health authorities in the foreseeable future will successfully curb the worldwide epidemics of obesity and diabetes, at least according to Margaret Chan, the director general of the World Health Organization (WHO) – a person who should know. Virtually zero is the likelihood, Chan said at the National Academy of Medicine’s annual meeting in October, that she and her many colleagues worldwide will successfully prevent ‘a bad situation’ from ‘getting much worse’. That Chan also described these epidemics as a ‘slow-motion disaster’ suggests the critical nature of the problem: ‘population-wide’ explosions in the prevalence of obesity along with increases in the occurrence of diabetes that frankly strain the imagination: a disease that leads to blindness, kidney failure, amputation, heart disease and premature death, and that was virtually non-existent in hospital inpatient records from the mid-19th century, now afflicts one in 11 Americans; in some populations, as many as one in two adults are diabetic.

In the midst of such a public health crisis, the obvious question to ask is why. Many reasons can be imagined for any public health failure, but we have no precedents for a failure of this magnitude. As such, the simplest explanation is that we’re not targeting the right agent of disease; that our understanding of the aetiology of both obesity and diabetes is somehow flawed, perhaps tragically so.

Researchers in harder sciences have a name for such situations: ‘pathological science’, defined by the Nobel Laureate chemist Irving Langmuir in 1953 as ‘the science of things that aren’t so’. Where experimental investigation is prohibitively expensive or impossible to do, mistaken assumptions, misconceived paradigms and pathological science can survive indefinitely. Whether this is the case with the current epidemics is an all-too-regrettable possibility: perhaps we’ve simply misconceived the reality of the link between diet, lifestyle and the related disorders of obesity and diabetes? As the Oxford scholar Robert Burton suggested in The Anatomy of Melancholy (1621), in cases in which the cures are ‘imperfect, lame, and to no purpose’ it’s quite possible that the causes are misunderstood.

The history of obesity and nutrition research suggests that this is indeed what has happened. In the decades leading up to the Second World War, German and Austrian clinical investigators had concluded that common obesity was clearly caused by a hormonal disturbance; starting in the1960s, other research would link that disturbance to the sugar in our diets. But the German and Austrian thinking evaporated with the war, and the possibility that sugar was to blame never took hold, dismissed by a nutrition community who, by the 1970s, became fixated on dietary fat as the trigger of our chronic diseases. Now, with an explosion of the epidemic and compelling new research, it’s time to reconsider both our causal thinking on obesity and diabetes, and the possibility that sugar is playing the critical role.

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