Editing Insulin resistance (section)

=== Adaptive explanations ===
Some scholars go as far as to claim that neither insulin resistance, nor obesity really are metabolic disorders ''per se'', but simply adaptive responses to sustained caloric surplus, intended to protect bodily organs from [[lipotoxicity]] (unsafe levels of lipids in the bloodstream and tissues): "Obesity should therefore not be regarded as a [[pathology]] or disease, but rather as the normal, physiologic response to sustained caloric surplus... As a consequence of the high level of lipid accumulation in insulin target tissues including skeletal muscle and liver, it has been suggested that exclusion of glucose from lipid-laden cells is a compensatory defense against further accumulation of lipogenic substrate."<ref>{{cite journal | vauthors = Unger RH, Scherer PE | title = Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity | journal = Trends in Endocrinology and Metabolism | volume = 21 | issue = 6 | pages = 345–52 | date = June 2010 | pmid = 20223680 | pmc = 2880185 | doi = 10.1016/j.tem.2010.01.009 }}</ref>

Other prevailing thoughts that insulin resistance can be an evolutionary adaptation include the [[thrifty gene hypothesis]]. This hypothesis raises the point that if there is a genetic component to insulin resistance and Type 2 diabetes, these phenotypes should be selected against.<ref name=":3">{{cite journal | vauthors = Neel JV | title = Diabetes mellitus: a "thrifty" genotype rendered detrimental by "progress"? | journal = American Journal of Human Genetics | volume = 14 | issue = 4 | pages = 353–62 | date = December 1962 | pmid = 13937884 | pmc = 1932342 }}</ref> Yet, there has been an increase in mean insulin resistance in both the normoglycemic population as well as the diabetic population.<ref>{{cite journal | vauthors = Ioannou GN, Bryson CL, Boyko EJ | title = Prevalence and trends of insulin resistance, impaired fasting glucose, and diabetes | journal = Journal of Diabetes and Its Complications | volume = 21 | issue = 6 | pages = 363–70 | date = 2007-11-01 | pmid = 17967708 | doi = 10.1016/j.jdiacomp.2006.07.005 }}</ref>

J.V. Neel posits that in ancient human ancestors, during periods of heightened famine, genes facilitating increased glucose storage would have conferred an advantage. However, in today's modern environment, this is no longer the case.<ref name=":3" />

Evidence contradicts Neel's hypothesis in studies of the Pima Indians, which suggest that individuals with higher insulin sensitivity tended to have higher weights, whereas those with insulin resistance tended to weigh less on average within this demographic.<ref>{{cite journal | vauthors = Swinburn BA, Nyomba BL, Saad MF, Zurlo F, Raz I, Knowler WC, Lillioja S, Bogardus C, Ravussin E | display-authors = 6 | title = Insulin resistance associated with lower rates of weight gain in Pima Indians | journal = The Journal of Clinical Investigation | volume = 88 | issue = 1 | pages = 168–73 | date = July 1991 | pmid = 2056116 | pmc = 296017 | doi = 10.1172/JCI115274 }}</ref>

Modern hypotheses propose that insulin [[metabolism]] serves as a socio-ecological adaptation, with insulin serving as the mechanism for allocating energy to different body components and insulin sensitivity being an adaptation to regulate this energy allocation. The Behavioral Switch Hypothesis suggests that insulin resistance leads to two methods of altering reproductive and behavioral strategies. These strategies are termed "r to K" and "soldier to diplomat." The "r to K" strategy involves directing insulin through the placenta to the fetus, resulting in weight gain in the fetus but not the mother, indicating an increase in parental investment (K strategy). In the "soldier to diplomat" strategy, the insensitivity of skeletal muscle to insulin could redirect glucose to the brain, which does not require insulin receptors. This has been shown to enhance cognitive development across various studies.<ref>{{cite journal | vauthors = Watve MG, Yajnik CS | title = Evolutionary origins of insulin resistance: a behavioral switch hypothesis | journal = BMC Evolutionary Biology | volume = 7 | pages = 61 | date = April 2007 | issue = 1 | pmid = 17437648 | pmc = 1868084 | doi = 10.1186/1471-2148-7-61 | bibcode = 2007BMCEE...7...61W | doi-access = free }}</ref>