The previous post explained Dr. James V. Neel’s thrifty gene hypothesis and the notion of “starvation mode” that grew from it.
Pushback and rethinking
Neel’s original thrifty gene hypothesis received various criticisms, some of which could be attributed to plain old common sense, with no scientific training required. For instance, because of all the fruits and fish so easily available to them, Pacific Islanders and similar populations have not historically experienced famine or starvation. So they had no need for thrifty genes — and yet tend to be quite fleshy. Also, there are contemporary hunter-gatherer populations who do not accumulate large bodily fat stores between famines. It was also pointed out that in a time of famine, death occurs mainly from infection, rather than loss of adipose tissue.
It became evident that the thrifty genotype hypothesis was over-simplified, yet could not be completely abandoned. Consequently, other researchers and Dr. Neel himself proposed modified or alternative hypotheses. He published a revisionist look at his previous work, and an expanded form of the original idea that called for…
… a more complex theory of several related diseases such as diabetes, obesity, and hypertension (see also metabolic syndrome) being caused by physiological systems adapted for an older environment being pushed beyond their limits by environmental changes.
He still believed that the “thrifty genotype” concept was viable, and had some other things to say about it in relation to non-insulin-dependent diabetes mellitus (NIDDM), such as:
[W]hy is the predisposition to NIDDM so frequent? Explanations based on the “thrifty genotype” hypothesis continue to be invoked. Over the past 35 years, it has become increasingly clear that essential hypertension and obesity share many of the epidemiological features of NIDDM. Both are diseases of civilization, with a very gradual onset.
In 2008, it was proposed that Dr. Neel’s theory “may provide an evolutionary basis for genetic predisposition to Metabolic Syndrome…” Dr. Neel had originally said that obesity-prone animals could survive through famines better than animals that did not, in good times, tend toward obesity. And sure enough, experiments showed that mice who are genetically prone to obesity actually could withstand prolonged food deprivation better than slimmer kinds of mice. This became interesting when science started to identify genes that predispose humans to Metabolic Syndrome.
Clues?
A recent thesis by Grayson James Hughes that was published by the University of Arizona notes that by the early 2000s “there were five subtypes of diabetes identified in younger patients, each containing distinct insulin resistances and different genetic causes.” One of the elaborations on Dr. Neel’s original thought was dubbed the “thrifty phenotype” hypothesis, having to do with malnutrition in newborns that could lead to flawed insulin production. Here is a description of that phenomenon, originally published in Epidemiology of Diabetes:
[T]he thrifty phenotype hypothesis or fetal origins hypothesis suggests that poor nutrition during fetal development will lead to restricted intrauterine growth, as well as phenotype changes. These changes include low birth weight and body size, reduced metabolism, and alterations of glucose-insulin metabolism that will likely cause nutritional problems in later life.
And Dr. Neel himself still believed that there was somehow more to all this than met the eye.
(To be continued…)
Your responses and feedback are welcome!
Source: “The ‘Thrifty Genotype’ in 1998,” UMich.edu, 1999
Source: “Factors that contribute to metabolic syndrome,” ScienceDirect.com, 2008
Source: “The Thrifty Gene Hypotheses: A Total Review,” Arizona.edu, 2022
Source: “The Epidemic and Prevalence of Diabetes in the United States,” ScienceDirect.com, 2019
Image by Brendan/CC BY 2.0
FAQs and Media Requests: 
