EXCESS INTRAUTERINE NUTRITION IN THE ; EPIDEMIC OF TYPE 2 DIABETES AMONG llNDIGENOUS PEOPLES

those reported in the general population, about 3%. While others had also observed high rates of GOM in aboriginal populations, this was the first time that it had been noted in communities in which T20M was uncommon. We therefore speculated that GOM might be one of the earliest manifestations of carbohydrate intolerance in some aboriginal populations as they experience acculturation and a dramatic change In Iffestyle. We also wondered whether the high rates of GOM that we had observed could be an important contributing factor in the initiation and progressk>n of the nOM epidemic in these populations. This has k! d to a decadelong search for answers to these questions. High birth weigh (HBW) is a frequent complication of GOM and of pregnancy in women with preexisting diabetes. We therefore reasoned that if the appearance of GOM were one of the earliest stages in the T20M epidemic among Saskatchewan aboriginal people, we ought to find that increasIng rates of HBW had preceded overt T20M in this population. Subsequently, we were exdted to find that HBW rates had increased from 12.6% to 19.2% between 1975 and 1984 in northern Saskatchewan (predomi· nantly aboriginal), but from only 10.2% to 12.8% In the south (predominantly non-aboriginal) [4]. This was consistent with a canadian Inuit/Indian survey that had reported an increase in HBW rates from 12 to 22 % over the period of 1962 to 19B3. We were aware of the seminal work done in the southwestern United States shOWing that the offspring of Pima women with nOM and GOM had increased rates of HBW and a propensity to develop early age NOrth America aboriginal people, and other indigenous peoples worldwide, are experi* endng an epidemic of type 2 diabetes mellitus (T20M) and its complications. Both genetic and environmental factors have been implicated in this epidemic, but the possible diabetogenic role of the intrauterine milieu has also attracted increasing attention. Most attention has focused on the relationship between low birth weight (LBW) and T2DM [1,2]. For example, the Widely quoted thrifty phenotype hypothesis suggests that impaired islet cell development caused by maternal/fetal malnutrition increases the risk for nOM in adulthood. While conditions leading to fetal malnutrition and LaW may be important for the subsequent development of nOM under certain drcumstances and in some populations, they are unlikely to explain the rapidly increasing rates of nOM in populations experiencing acculturation. We believe that recent findings from our work, and evidence from research among the Pima Indians, now suggest that excess, rather than inadequate, fetal nutrition may have become the overriding intrauterine factor in the pathogenesis of nOM among canadian, and possibly other, indigenous peoples. A key element in this hypothesis is the role of diabetes (gestational diabetes and nOM), as well as gestational-impaired glucose intolerance (GIGT), during pregnancy. We first became intrigued by the possible role of gestational diabetes (GOM) in the epidemic of nOM among Saskatchewan aboriginal people in the early 19905, when we conducted a diabetes prevalence study on three northern Saskatchewan reserves [3]. A1thoogh we found that rates of nOM paralleled increasing rates of obesity, the overall prevalence of nOM was still quite low. In contrast, an unexpected finding was that rates of GOM, up to 15%, were several times higher than ; EXCESS INTRAUTERINE NUTRITION IN THE ; EPIDEMIC OF TYPE 2 DIABETES AMONG llNDIGENOUS PEOPLES