Non-communicable chronic disease is now the biggest killer on the planet. Surpassing war, tobacco, and HIV, the diseases of metabolic syndrome account not only for most of the disease burden in the developed world, but also for the majority of the 35 million deaths per annum in the developing world as well[16]. The cause of this increase is routinely ascribed to the continued advancement of the obesity epidemic, which, in turn, is ascribed to global caloric surfeit.
However, there are four separate lines of reasoning that question this thesis. Firstly, while obesity prevalence and diabetes prevalence correlate, they are not concordant[17]. There are countries with populations who are obese without being diabetic (such as Iceland, Mongolia, and Micronesia), and there are countries with populations who are diabetic without being obese, such as India, Pakistan, and China (they manifest a diabetes prevalence of 11%; the United States, one of the world’s most obese country, has a 9.3% diabetes prevalence).
This is further elaborated by looking at years of life lost from diabetes versus obesity[18]. Many normal weight people (up to one-third) succumb to type 2 diabetes as well.
Secondly, although it is true that 80% of the obese population harbour at least one of the diseases of the metabolic syndrome (hypertension, dyslipidaemia, fatty liver disease, and type 2 diabetes), 20% of morbidly obese individuals do not (termed “metabolically healthy obese” or MHO), and have normal life spans[19],[20],[21]. Conversely, up to 40% of normal weight adults harbour the same diseases of the metabolic syndrome, including hypertension, dyslipidaemia, fatty liver disease, and CVD[22],[23]. Thirdly, the secular trend of diabetes in the United States from 1988 to 2012 has demonstrated a 25% increase in prevalence in both the obese and the normal weight population[24]. Thus, obesity, and by inference, caloric balance, does not explain the worldwide pandemic of non-communicable disease. Although obesity is clearly a marker for the pathology, it is clearly not the cause — because normal weight people get metabolic syndrome, too.
Finally, lipodystrophy is a disease syndrome characterised by too little, rather than too much body fat[25]. Yet these patients have the highest risks for CVD and type 2 diabetes of all; clearly unrelated to calories or obesity.
Current thinking about obesity and related diseases holds that quantifying calories is the principal concern and target for intervention. The basis for this directive is that consumed calories, regardless of their sources, are equivalent; i.e. ‘a calorie is a calorie’. Rather, a focus on the sources of those calories consumed (i.e. processed versus real food) and on the metabolic changes that result from consuming foods of different types needs to be addressed[26]. In particular, calorie-focused thinking is inherently biased against high-fat foods, many of which appear to be protective against obesity and the diseases of metabolic syndrome, and supportive of refined starch and sugar replacements, which are clearly detrimental, and exclusive of their calories and effects on weight gain[27],[28].
Shifting the focus away from quantitative and toward qualitative food distinctions (i.e. that the diseases of metabolic syndrome are due to food-induced changes in physiology; for example, neurohormonal and mitochondrial metabolic pathways) is required to see chronic disease abatement. This cannot be accomplished through arithmetic caloric restriction (i.e. calorie counting). Calorie balance sheets — targeting ‘calories in’ and/or ‘calories out’ — reinforce the message of overeating and inactivity as the underlying causes, rather than the resultant effects, of this aberrant physiology[29].
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