The thrifty gene hypothesis, introduced in 1962 by James V. Neel, M.D., Ph.D., originated as an effort to explain diabetes, and then expanded to potentially account for obesity as well. (He later noted that this paper was written “before the clear distinction between type I and type I1 diabetes had been drawn, but in retrospect it was directed at type II.”) Dr. Neel defined thrifty as “exceptionally efficient in the intake and/or utilization of food.” The provocative paper suggested ways to test the hypothesis, and the through line boiled down to:
In this essay an hypothesis has been advanced which envisions diabetes mellitus as an untoward aspect of a “thriftiness” genotype which is less of an asset now than in the feast-or-famine days of hunting and gathering cultures.
In the late 1960s, people thought this sounded likely, and that type II diabetes had a genetic origin, though nobody could pinpoint the exact genes involved. The prevalence of such a gene or genes could have occurred in order to survive intermittent starvation. The idea that humans might be genetically hardwired to accumulate body fat and then hold onto it made a certain amount of sense, because throughout most of history, food insecurity was the norm for just about everyone.
In the old days, salt and spices were incredibly valuable because they preserved food. The existence of, and trade in, spices made it somewhat easier to alleviate the ravages of famines caused by weather, enemy action, and the like. Several gigantic advances in human ingenuity had to happen before we could know the confidence that comes from having a stash of canned goods in the basement.
But, according to Neel’s theory, genetic progress did not keep pace, and humans are still under the influence of a genotype that wants to prepare us for a famine that we will never actually experience. (While this may be true of the majority of people in developed countries, such confidence is certainly not universal.)
The thrifty gene hypothesis proposed that one of the chief survival instincts is the imperative to absorb whatever food is available, in order to store fat so the body has energy to burn when times are hard and food is scarce. Also, that another survival instinct is based on built-in safeguards that prevent the body from letting go of that stored fat. One of the details is a belief that trying too hard to lose weight, by limiting caloric intake, can actually have the opposite effect, by sending the body into “starvation mode” which makes it try even more desperately to conserve its stored fat.
Starvation a la mode
A fitness guru known as Jay, whose work has appeared in at least a dozen major publications, explains the thinking behind the starvation mode school of thought:
[T]he fundamental concept behind what causes starvation mode is this: Being in too much of a caloric deficit is supposedly capable of stopping weight loss. When you eat too little and/or burn too much, your body’s survival response is to hold on to all of your fat and slow your metabolism enough to prevent you from losing anything (or potentially even cause you to gain additional fat).
Jay says there is no such thing as “starvation mode,” and that a caloric deficit always produces weight loss. There is, however, such a thing as adaptive thermogenesis, meaning that the metabolism does slow down during weight loss — but adaptive thermogenesis is never influential enough to either stop weight loss, or to cause weight gain.
(To be continued…)
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Source: “Diabetes Mellitus: A ‘Thrifty’ Genotype Rendered Detrimental by “Progress”?,” NIH.gov, 1962
Source: “Starvation Mode: Is It A Myth?,” AWorkoutRoutine.com, 11/19/22
Image by Esteban Chiner/CC BY-SA 2.0