Edited by Helaine E. Resnick, PhD, MPH
Diet May Modulate Diabetes Risk Associated With TCF7L2
A new study in this issue of Diabetes Care (p. 3803) examines how a genetic polymorphism that has been shown to increase diabetes risk may be modulated by adherence to a Mediterranean diet. The transcription factor 7-like 2 (TCF7L2) polymorphisms are known to be associated with people with the TT genotype who are at a significantly higher risk to develop diabetes compared with their CT and CC counterparts. The new report by Corella et al. focused on genotyping TCF7L2 in more than 7,000 participants who were enrolled in the PREvención con DIetaMEDiterránea (PREDIMED) study. This randomized controlled trial included individuals at high risk of cardiovascular disease (CVD), defined as type 2 diabetes or three or more CVD risk factors such as hypertension, smoking, dyslipidemia, or family history of early CVD. Participants were randomized to one of two dietary interventions—a Mediterranean diet with extra virgin olive oil, a Mediterranean diet with mixed nuts, or a control group that was advised to reduce dietary fat intake. Prerandomization adherence to a Mediterranean diet was also assessed. Median follow-up time was 4.8 years, and the primary end point was a composite of stroke, myocardial infarction, or cardiovascular death. The focus of the new investigation was whether TCF7L2-rs7903146 polymorphism modulated the impact of Mediterranean diet adherence on CVD risk. Results indicated that when prerandomization adherence to a Mediterranean diet was low, TT individuals exhibited the expected increases in fasting glucose, but when their adherence was high, these increases were absent. This pattern was also observed for total cholesterol, LDL cholesterol, and triglycerides. Similarly, TT individuals in the trial had higher incidence of stroke in the control group, but this risk showed a (nonsignificant) downward trend when adherence to a Mediterranean diet was high. These results suggest that behavioral and genetic factors may interact in meaningful ways to reduce the risk of diabetes and its complications. The implications of these findings are potentially far-reaching in that they speak to the impact that behavior modification may have on the unfavorable impact of inherited factors. — Helaine E. Resnick, PhD, MPH
Bridging the Gap to Optimal Diabetes Care
This issue of Diabetes Care includes detailed analyses concerning barriers to the provision of optimal diabetes care as well as recommendations aimed at overcoming these barriers. A new report by the Diabetes Working Group (DWG) (p. 3843), a consortium of organizations and individuals, used three sets of clinical guidelines to identify 29 specific standards of care for people with diabetes. The group then designed six clinical vignettes involving three people with type 1 diabetes and three with type 2 diabetes representing patients typically seen by diabetes care professionals. Diabetes care professionals were asked to determine the amount of time and resources required to achieve the predefined standards of care for each of the six patient profiles. Using economic modeling, provider costs were analyzed in relation to reimbursement, and a “reimbursement gap” was quantified. Results of these analyses indicated not only that provider costs exceeded reimbursement for all six patient profiles, but that meeting the standards of care resulted in diabetes providers losing between $470,000 and $750,000 per year depending on their case mix. In a best-case scenario, the results of the new report show that a diabetes care professional treating adult patients would need a 19% increase in reimbursement to break even. The investigators point out the obvious: these financial losses place pressure on providers in ways that are unfavorable for the provision of optimal care. In the new report, the DWG offers a number of provider-focused strategies to address these challenges. The strategies, which are grouped into three categories—care management, payment reform, and workforce supply—include recommendations involving topics as diverse as information technology and the revision of billing codes. Although the DWG acknowledges that some of its suggestions may not be feasible in certain settings, it nevertheless points out that without meaningful changes, the receipt of guideline-based care will remain unrealistic. — Helaine E. Resnick, PhD, MPH
Link Between Age at Menarche and Diabetes Risk Is Not Fully Explained by Obesity
Results from a large case-cohort study presented in this issue of Diabetes Care (p. 3526) suggest that obesity explains only part of the association between early menarche and subsequent risk of type 2 diabetes. The investigators examined data from the European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct case-cohort study, a collaboration among 26 clinical centers in eight countries. The new results are based on information from 15,168 women, 5,995 of whom had diabetes. As part of their analytic strategy, the investigators divided the women into quintiles according to their age at menarche, with age 13 years identified as the middle quintile in this cohort. The data from this study confirmed previous observations indicating that earlier age at menarche was associated with elevated risk of developing type 2 diabetes later in life. Compared to the middle quintile of age at menarche, women who reached menarche in the earliest quintile (age 8–11 years) were 70% more likely to develop diabetes (adjusted for a number of lifestyle and other factors). When adult BMI was also considered in these analyses, women with early menarche were still 42% more likely to develop diabetes, an association that remained statistically significant. It was important to note that women who reached menarche at older ages were not protected against diabetes later in life. The investigators indicate that although mechanisms underpinning the association between age at menarche and diabetes risk remain unclear, the impact of differential exposure to sex hormones on metabolic disease throughout an individual’s life span may play a role. From a public health point of view, these findings suggest that in addition to prevention of obesity in adulthood, a focus on prevention of early menarche may be a strategy to reduce the risk of diabetes in women. — Helaine E. Resnick, PhD, MPH
Genetic Variation May Help to Explain Response to Caloric Restriction
New data in this issue of Diabetes Care (p. 3442) suggest that genetic variation near the IRS1 gene helps to explain the long-term response to specific features of caloric restriction. The new report is based on data from 738 overweight or obese participants who participated in the Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial. This 2-year trial involved randomizing participants to four diets consisting of various combinations of macronutrients and a reduction of caloric intake by 750 kcal/day from baseline. The study’s 2 X 2 factorial design resulted in two groups that followed a high-fat diet (40%) and two that followed a low-fat diet (20%). Participants were assessed at baseline and at 6 and 12 months for the metabolic syndrome using the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria. They were also genotyped for two variants near IRS1—rs1522813 and rs2943641. The investigators focused on carriers of the A-allele to determine if there was an interaction between this genetic factor and diet on reversion of the metabolic syndrome in this high-risk population. Although both diets resulted in similar reductions in metabolic syndrome status during follow-up, the data indicated that among participants carrying the rs1522813 A-allele, reversion of the metabolic syndrome at 2 years was nearly three times higher in the high-fat group compared with the low-fat group. A similar relationship was not observed for rs2943641. These results suggest that in managing the metabolic syndrome, response to diet may be modulated by genetic factors, an idea that has implications for tailoring dietary interventions in the future. — Helaine E. Resnick, PhD, MPH
