A multidisciplinary team of researchers finds no evidence to support the widely held view that the “thrifty genotype” theory explains racial differences in the prevalence of obesity and type 2 diabetes. The thrifty genotype theory posits that humans developed a genotype to efficiently absorb and store nutrients to cope with feast-famine cycles, but this has become maladaptive in affluent and sedentary societies.
However, there is nothing "to suggest that minority populations are especially genetically susceptible" to obesity, and consequently T2DM, when energy is abundant, the researchers say.
"Genetics plays a role (in the development of T2DM) — it does in everything," Dr. Montoya stated. “But 90-plus-percent can be explained by environmental causes."
What appears to play a much bigger role "is poverty, housing segregation, education, nutrition … and access to health care," he asserted.
"The research community for many years has been looking for genetic causes to explain ethnic differences," he said. "They have been so focused on genetics that they have lost the big picture."
"Genes specific to a group that account for a disease do not mean that those genes cause the disease," Dr. Montoya explained. "The differences can be explained through nongenetic factors … In fact, the vast majority can be explained by nongenetic causes."
In their paper, Dr. Montoya and colleagues call for an interdisciplinary approach to genetic epidemiologic research. "Genetic epidemiological researchers need to move beyond the mere recognition of ethnorace as socially constructed and towards the practice of studying ethnoracial health disparities as the biological embodiment of sociopolitical processes," Dr. Montoya and colleagues argue.
The challenge, they conclude, is to link "population health parameters, including environmental exposures and social conditions, with both pathophysiology and genetic risk estimates."
The team, led by anthropologist Dr. Michael Montoya, of the University of California at Irvine, report their findings in a paper titled "Racialized Genetics and the Study of Complex Diseases," published in the Spring issue of Perspectives in Biology and Medicine. Perspect Biol Med 2007;50:203-227.
New BG test – The BIGTT test: A novel test for the simultaneous measurement of pancreatic beta-cell function, insulin sensitivity, and glucose tolerance has been developed and validated. Non-diabetic individuals without impaired glucose tolerance were examined in order to derive equations that are more accurate than those that are currently available for estimating the insulin sensitivity index (S1) and the acute insulin response (AIR). The test is based on an oral glucose tolerance test (OGTT). Information on sex and body mass index is combined with analysis of plasma glucose and serum insulin levels (OGTT) in the fasting state, (measured up to 8 times during 4 hours [full models]) to provide estimates of S1 and AIR that are highly correlated with indexes obtained from a frequently sampled intravenous glucose tolerance test. Because of the simplicity of these models they can be implemented in large-scale metabolic, genetic, and epidemiological studies. Diabetes Care,30 (257-262): Hansen T, Drivsholm T, Urhammer S, Palacios R, Volund A, Borch-Johnsen K, Pedersen O The BIGTT test: a novel test for simultaneous measurement of pancreatic beta-cell function, insulin sensitivity, and glucose tolerance