I had thought, like scholars such as Vaclav Smil:
https://inference-review.com/article/good-eats that the present obesity crisis was due to an over-supply of carbohydrate-rich food. But then I stumbled across a reply to this by Edward Archer, and had a brief re-think:
“It should be obvious that a large food supply does not inevitably lead to obesity. After all, a large body of water does not inevitably cause drowning and an abundance of atmospheric air does not automatically lead to hyperventilation. Just as one individual drowns in a bathtub while another swims easily in an ocean, obesity is surging in nations with relatively small food supplies, such as Botswana and Nigeria. At the same time, many individuals in nations with a surfeit of food, such as Switzerland and Norway, remain lean and healthy. The size of the macro-environment—that is, the body of water, air supply, and food supply—is not relevant, nor even related to these outcomes. There is no valid relationship between a nation’s food supply and its levels of obesity and metabolic diseases. Compared to Switzerland, New Zealanders spend a greater percentage of household income on food and have a smaller per capita food supply. Nonetheless, New Zealanders have an obesity prevalence approximately 250% greater than the Swiss. From 1910 until the 1960s, the per capita food supply in the US decreased from 3,500 calories to 3,100. This reduction was accompanied by an increase in body mass. Both logic and empirical data refute the notion that a surfeit of food, whether as a result of lower costs or a larger supply, is a causal factor in obesity and metabolic dysfunction.
So, what then is the cause? For Archer, it all lies in individual physiological differences:
“As my work has shown, it is not what one eats and drinks that causes obesity and cardio-metabolic diseases, but what one’s body does with the foods consumed. Known as nutrient-partitioning, this physiologic process determines how many calories one eats and drinks, and whether the body burns or stores those calories as fat or muscle. An individual’s metabolic phenotype determines both habitual caloric consumption and the metabolic fate of consumed fats, proteins, and carbohydrates—the nutrient-partitioning building fat or muscle mass. The amount and effects of consumed foods and beverages, as well as the concomitant risk of obesity and cardio-metabolic disease, are entirely dependent on the metabolic phenotype and nutrient-partitioning of the individual in question. It is well-established that different people can eat and drink the same foods and beverages, yet have widely disparate metabolic responses. Diet-centric arguments ignore individual differences in metabolic phenotype and the resulting fate of consumed foods and beverages.”
But, these differences surely existed in the past, so why the obesity crisis now, in particular?
“In both children and adults, the frequency of the most obese phenotypes is increasing exponentially compared to other phenotypes. Examinations of US data over the last decade indicate that these patterns of exponential skewing are continuing unabated. There were no significant changes in the US food supply and dietary patterns over the last decade, nor any social, cultural, educational, economic, or psychological factors that support inferences of causality. Diet-centric conjectures and speculations originating in the social sciences of economics, psychology, and sociology have no explanatory nor predictive power with respect to the increasingly strong positive skew in body mass distributions in industrialized nations and intergenerational increases in severe obesity. They also cannot account for the intra-individual shifts toward the upper end of the distribution as a function of age.”
The cause, at the end of the day, is postulated to be iatrogenic artificial selection:
“The increased use of Caesarian sections allowed both larger fetuses and the metabolically compromised mothers who produced them to survive and reproduce. In earlier human evolutionary history, macrosomic fetuses and their mothers died in childbirth due to complications arising from cephalo-pelvic asymmetry—a head too large to exit the birth canal. This evolutionary constraint on the size of the fetus is known as the obstetric dilemma. Increasingly frequent non-vaginal childbirths circumvented natural selection and replaced it with iatrogenic artificial selection for larger and fatter humans. The result was an exponential increase in the frequency of obese and metabolically compromised phenotypes in the global population. This iatrogenic artificial selection explains both the increasing skew of body mass distributions in industrialized nations, as well as the exponential increase in severe obese phenotypes in the US.”
Could the explosion in obsess people thus be due to an increase in C-sections? First, how frequent are C-sections? Well, in the US the figure is one in three births, and Australia getting there at about 30 percent, which could support Archer’s thesis, but there will still be statistical rumblings as obesity rates are higher that C-section rates. There is also inflation due to fears of litigation with normal births.
But, there are countries with exploding, or if you like, expanding, obesity, but lower C-section rates. Thus, in places such as Nigeria and Botswana, there is high obesity, but low C-sections, and perhaps the C-section rate should be higher to prevent maternal deaths. But, that is a separate issue. The point to be made is that this is counter-evidence to Archer’s hypothesis, since we would be expecting the opposite of iatrogenic artificial selection, but this, we are not seeing.
I then go back to the holistic explanation, that it is quantity of the wrong sorts of food, high carbohydrate processed food, with a lifestyle involving little sustained physical activity, making people fat. The evolutionary explanations fall because they cannot account for the way the obesity crisis has happened so fast, within decades, while the shuffle of genes is much slower. Still, once the collapse of Western civilisation comes, soon, and the horseman of starvation rides again, we will see an empirical testing of the hypothesis, for all the good it will do.