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I have read this answer to a different question which discusses a theory of the cause of type 2 Diabetes. It describes insulin resistance leading to a runaway positive feedback loop. The answer also suggests family or lifestyle factors being the cause of the insulin resistance.

I’m wondering if the current evidence we have suggests that any human could get Type 2 diabetes, or if it is possible that someone who is unambiguously human, (not a created via injecting non-human genetic material into a human egg for example,) who cannot get Type 2 Diabetes under any environment. For the purposes of a clean way to tell if something counts as Type 2 Diabetes, I'll specify that anything with the same underlying mechanism as something that is unambiguously Type 2 Diabetes counts as the same disease.

I suppose that I could formulate at least two forms of this question, by varying what counts as "any environment". The first form would include injecting fat into the person's liver. A second form would exclude all coerecion or direct modification of the person's body.

If we knew that someone who could not get Type 2 Diabetes existed, then I would argue that it would make sense to call Type 2 Diabetes a purely genetic disorder, even if the population with the disorder included every human except a single individual. Does that method of classification make sense?

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    Nothing in medicine is written in stone. There was no T2D in my family, yet when I was young, slim and pregnant, I had gestational diabetes, meaning I had a good chance of developing T2D later in life. My genetics (not my family's, particularly) predisposed me to this problem, but didn't guarantee it. Apr 25, 2020 at 1:41

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I think you're confused by what is meant as a genetic disease. A disease like Huntingdon's Chorea is a genetic disease because we know the genetics, and we know that it occurs due to mutation in an autosomal dominant gene so the chance of inheritance is 50% with almost 100% penetrance.

Diseases like T2DM have a genetic basis so that we know some groups are way more susceptible than others.

The large variation in prevalence rates of type 2 diabetes among ethnic groups living in similar environments, the increased risk to siblings of affected individuals, and the high concordance rate for the disease in monozygotic twins compared with dizygotic twins indicate that this disease has a significant genetic component (rev. in 6). Studies in twins, and particularly in twins reared apart, have also produced high heritability estimates for BMI, ranging between 0.6 and 0.9 (7). However, the extent to which this familial aggregation reflects a small number of genes with major effects, a large number of genes each with small effect (polygenic inheritance), and environmental factors shared among family members remains unknown. For example, certain aspects of the intrauterine environment, such as the blood supply from the placenta, are shared more strongly between monozygotic compared with dizygotic twins, and intrauterine effects are known to have a significant impact on the future development of diabetes (8).

but we don't consider it 100% genetic because for many if not most people it can be prevented by an appropriate life style, and it's the change in lifestyles that have caused the current epidemics of this disease.

https://diabetes.diabetesjournals.org/content/53/5/1181

https://pubmed.ncbi.nlm.nih.gov/17098087/

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  • DId I say it was 100% penetrant? Apr 25, 2020 at 4:15
  • I suppose that there’s the disease itself and the predisposition to the disease, and those are two different things. What I have gotten out of this answer is that it does not make sense to say that the disease is 100% genetic, since lifestyle changes can mitigate/prevent the disease. But, (given the evidence brought up in this answer) it may be the case that the predisposition to the disease is determined by genes to the extent that an individual who cannot get T2D might be possible. But we do not currently know for sure, since the genetics involved are relatively complex.
    – Ryan1729
    Apr 25, 2020 at 4:16

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