to test between the adaptive 'thrifty gene' idea and the non-adaptive 'drifty gene' idea because it would be possible to find signatures of positive selection in the human genome, at genes that are linked to both obesity and type 2 diabetes, if the 'thrifty gene' hypothesis is correct. two comprehensive studies have been performed seeking such signatures of selection. ayub et al. (2014) searched for signatures of positive selection at 65 genes linked to type 2 diabetes, and wang and speakman (2016) searched for signatures of selection at 115 genes linked to obesity. in both cases there was no evidence for such selection signatures at a higher rate than in random genes selected for matched gc content and recombination rate. these two papers provide strong evidence against the thrifty gene idea, and indeed against any adaptive explanation which relies on selection during our recent evolutionary history, but rather provide strong support the 'drifty gene' interpretation. search for thrifty genes many attempts have been made to search for one or more genes contributing to thrift. modern tools of genome wide association studies have revealed many genes with small effects associated with obesity or type 2 diabetes but all of them together explain only between 1.4 and 10% of population variance. this leaves a large gap between the pregenomic and emerging genomic estimates of heritability of obesity and type 2 diabetes, sometimes called the "missing heritability problem." the reasons for this discrepancy are not completely understood. a likely possibility is that the missing heritability is explained by rare variants of large effect that are found only in limited populations. these would be impossible to detect by standard whole genome sequencing approaches even with hundreds of thousands of participants. the extreme endpoint of this distribution are the so-called 'monogenic' obesities where most of the impact on body weight can be tied to a mutation in a single gene that runs in a single family. the classic example of such a genetic effect is the presence of mutations in the leptin gene. an important unanswered question is whether such rare variants exist because of chance mutations, population founder events and maintenance by processes such as drift, or whether there is any selective advantage involved in their maintenance and spread. an example of such a rare variant effect was recently discovered among samoan islanders. among the islanders the variant is extremely common, but in other populations it is extremely rare or absent. the variant predisposes to obesity but strangely is protective against type 2 diabetes. based on cell studies it was suggested the variant may protect individuals against periods of 'famine' and there is also evidence that it has been under positive selection. the most likely scenario then is that this rare variant was established in the islanders by a founder effect among a small initial colonising population, and was able to spread because of a selective advantage it conferred within that small group. hence, in small populations under particular environmental conditions it may be feasible that the 'thrifty gene' idea is correct. it remains to be seen if rare variants that fill the gap in the missing heritability estimates are also 'thrifty genes' or if they are rare chance events sustained by drift, as implicated for the common variants currently linked to obesity and type 2 diabetes.