A potent toxin that alters hormones and metabolism, sugar sets the stage for epidemic levels of obesity and diabetes
‘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.
When researchers and public health authorities today discuss their failure to curb the rising tide of obesity and diabetes, they offer the explanation that these disorders are ‘multifactorial and complex’, implying that failure is somehow understandable. But this obscures the reality that prescriptions to prevent and treat the two depend almost entirely on two simple causal concepts, neither one of which is necessarily correct.
The first assumption equates obesity and Type 2 diabetes (the common form of the disease, formerly known as ‘adult-onset’ until it began appearing in children as well). Because obesity and Type 2 diabetes are so closely associated in both individuals and populations, the assumption is that it’s the obesity – or at least the accumulation of excess fat – that causes the diabetes. By this logic, whatever causes obesity is ultimately the cause of the diabetes as well.
The second assumption then strives to explain ‘the fundamental cause’ of the obesity itself: an energy imbalance between calories consumed on one hand, and calories expended on the other hand.
This thinking, espoused by the WHO and virtually every other medical authority, is a paradigm in the true Kuhnian sense of the word. Researchers and public health authorities describe obesity as a disorder of ‘energy balance’. This conception underlies virtually all aspects of obesity research from prevention through treatment, and, by association, diabetes. As such, it has also shaped how we think about the role of what is now, finally, considered a prime suspect – refined or ‘added’ sugars, and specifically, sucrose (table sugar) and high-fructose corn syrup.
The WHO and other health organisations have recently taken to arguing that sugar and particularly sugary beverages should be taxed heavily or regulated. But they do so not because they say sugar causes disease – using the same definition of causality that we use when we say cigarettes cause lung cancer – but, rather, because, from their perspective, sugar represents ‘empty calories’ that we eat in excess. By this thinking, we still get fatter because we eat too much or exercise too little. The solution is to eat in moderation, and consume sugar in moderation or balance it with more physical activity.
The energy balance paradigm implies that the only way in which foods influence our body fat is through their energy content, or calories – that is, through the energy that we absorb without excreting, and so make available to be oxidised or stored. This is the only variable that matters. It’s the implication of the phrase ‘a calorie is a calorie’, which, by the 1960s, had become a mantra of nutrition and obesity researchers, evoked invariably to support the dogma that only calories count when it comes to understanding and treating human obesity.