BACKGROUND: Insulin resistance, which can lead to a number of diseases including 
type 2 diabetes and coronary heart disease, is believed to have evolved as an 
adaptation to periodic starvation. The "thrifty gene" and "thrifty phenotype" 
hypotheses constitute the dominant paradigm for over four decades. With an 
increasing understanding of the diverse effects of impairment of the insulin 
signaling pathway, the existing hypotheses are proving inadequate.
PRESENTATION OF THE HYPOTHESIS: We propose a hypothesis that insulin resistance 
is a socio-ecological adaptation that mediates two phenotypic transitions, (i) a 
transition in reproductive strategy from "r" (large number of offspring with 
little investment in each) to "K" (smaller number of offspring with more 
investment in each) and (ii) a transition from "stronger to smarter" or "soldier 
to diplomat" i.e. from relatively more muscle dependent to brain dependent 
lifestyle. A common switch could have evolved for the two transitions since the 
appropriate environmental conditions for the two transitions are highly 
overlapping and interacting.
TESTING THE HYPOTHESIS: Gestational insulin resistance diverts more energy 
through the placenta, resulting in increased investment per offspring. On the 
other hand, insulin resistance is associated with reduced ovulation. The insulin 
signaling pathway is also related to longevity. Insulin resistance diverts more 
nutrients to the brain as compared to muscle. Also, hyperinsulinemia has direct 
positive effects on cognitive functions of the brain. The hypothesis gets 
support from known patterns in human clinical data and recent research on the 
molecular interactions in the insulin signaling pathway. Further we state many 
predictions of the hypothesis that can be tested experimentally or 
epidemiologically.
IMPLICATIONS OF THE HYPOTHESIS: The hypothesis can bring about a significant 
change in the line of treatment as well as public health policies for the 
control of metabolic syndrome.