• Energy Research

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Little is known about the joint association between glycemic index (GI), glycemic load (GL), and alcohol intake with type 2 diabetes (T2D).The objective of this study was to examine whether alcohol intake alters the associations between carbohydrate quality (GI) or quality and quantity (GL) and T2D incidence in women.Participants from the Nurses' Health Study who were free of T2D, cardiovascular disease, or cancer (n = 81,827) at baseline in 1980 were followed for 26 y. Cumulative averages of GI, GL, total carbohydrates, and alcohol intake were calculated every 2-4 y from validated food-frequency questionnaires. Cox proportional hazard models were used to adjust for covariates.We documented 6950 cases of T2D during follow-up. After adjustment for lifestyle and dietary factors, the positive association between GL and T2D risk was attenuated in subjects with higher alcohol intakes. RRs that compared the top and bottom quintiles of GL were 1.29 (95% CI: 1.11, 1.49; P-trend < 0.001) in women with alcohol intakes of 0 to <5 g/d, 1.34 (95% CI: 0.93, 1.92; P-trend = 0.05) in women with alcohol intakes of 5 to <15 g/d, and 0.99 (95% CI: 0.60, 1.65; P-trend = 0.82) in women with alcohol intakes ≥15 g/d (P-interaction = 0.02). However, a higher intake of alcohol did not modify the positive association between GI and T2D (P-interaction = 0.76).Our findings suggest that a higher alcohol intake (≥15 g/d) attenuates the positive association between GL and T2D incidence.

We sought to characterize the effects of dietary macronutrient composition on various hormones implicated in the regulation of insulin sensitivity (IS) and energy expenditure (EE).Following 10-15% weight loss, 21 overweight subjects consumed 3 weight-loss maintenance diets [low fat (LF), low glycemic index (LGI) and very low carbohydrate (VLC)] in random order, each for 4 weeks. At baseline and at the end of each treatment period, fasting samples for fibroblast growth factor (FGF)-21, heme-oxygenase-1 (HO-1), chemerin, irisin, secreted frizzle-related protein (SFRP-4), total bile acids, ghrelin, gastrin inhibitory peptide (GIP), peptide-Y, and amylin; hepatic and peripheral IS; and EE were obtained. Analyses were controlled for age, gender, baseline body mass index, and diet sequence.FGF-21 decreased (P < 0.0001), with differential effect by macronutrient composition (mean change from baseline ± SEM: LF -49.4 ± 16.6, LGI -58.6 ± 16.3, VLC -76.7 ± 18.2 pg/mL, P = 0.0002). Change in FGF-21 was inversely associated with change in hepatic IS [Beta = -0.565 units/log(ng/mL), P = 0.02], but not with peripheral IS or EE. Heme-oxygenase-1 (HO-1) increased (P = 0.003), without differential effect by macronutrient composition (LF 0.40 ± 0.26, LGI 0.98 ± 0.63, VLC 0.49 ± 0.29 ng/mL, P = 0.07). Ghrelin increased (P = 0.0003), while chemerin decreased (P = 0.001) without macronutrient effect. Total bile acid, irisin, SFRP-4, GIP, peptide-Y and amylin levels did not change.FGF-21 levels decreased with dietary intervention in proportion to carbohydrate content, and correlated with hepatic insulin sensitivity, suggesting a pattern of improving FGF-21 resistance. HO-1 increased in response to dietary intervention, a tendency to greater increase in response to the LGI diet. Dietary intervention affected ghrelin and chemerin, independent of macronutrient composition. These findings may elucidate relationships between dietary composition, insulin sensitivity and metabolism.NCT00315354.

According to a commonly held view, the obesity pandemic is caused by overconsumption of modern, highly palatable, energy-dense processed foods, exacerbated by a sedentary lifestyle. However, obesity rates remain at historic highs, despite a persistent focus on eating less and moving more, as guided by the energy balance model (EBM). This public health failure may arise from a fundamental limitation of the EBM itself. Conceptualizing obesity as a disorder of energy balance restates a principle of physics without considering the biological mechanisms that promote weight gain. An alternative paradigm, the carbohydrate-insulin model (CIM), proposes a reversal of causal direction. According to the CIM, increasing fat deposition in the body-resulting from the hormonal responses to a high-glycemic-load diet-drives positive energy balance. The CIM provides a conceptual framework with testable hypotheses for how various modifiable factors influence energy balance and fat storage. Rigorous research is needed to compare the validity of these 2 models, which have substantially different implications for obesity management, and to generate new models that best encompass the evidence.