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An 18-mo randomized trial of a low-glycemic-index diet and weight change in Brazilian women.
Sichieri, R, Moura, AS, Genelhu, V, Hu, F, Willett, WC
The American journal of clinical nutrition. 2007;(3):707-13
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Abstract
BACKGROUND Despite interest in the glycemic index diets as an approach to weight control, few long-term evaluations are available. OBJECTIVE The objective was to investigate the long-term effect of a low-glycemic-index (LGI) diet compared with that of a high-glycemic-index (HGI) diet; all other dietary components were equal. DESIGN After a 6-wk run-in, we randomly assigned 203 healthy women [body mass index (in kg/m2): 23-30] aged 25-45 y to an LGI or an HGI diet with a small energy restriction. The primary outcome measure was weight change at 18 mo. Secondary outcomes included hunger and fasting insulin and lipids. RESULTS Despite requiring a run-in and the use of multiple incentives, only 60% of the subjects completed the study. The difference in glycemic index between the diets was approximately 35-40 units (40 compared with 79) during all 18 mo of follow-up, and the carbohydrate intake from energy remained at approximately 60% in both groups. The LGI group had a slightly greater weight loss in the first 2 mo of follow-up (-0.72 compared with -0.31 kg), but after 12 mo of follow-up both groups began to regain weight. After 18 mo, the weight change was not significantly different (P = 0.93) between groups (LGI: -0.41 kg; HGI: -0.26 kg). A greater reduction was observed in the LGI diet group for triacylglycerol (difference = -16.4 mg/dL; P = 0.11) and VLDL cholesterol (difference = -3.7 mg/dL; P = 0.03). CONCLUSIONS Long-term weight changes were not significantly different between the HGI and LGI diet groups; therefore, this study does not support a benefit of an LGI diet for weight control. Favorable changes in lipids confirmed previous results.
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Serum lipids, lipid-lowering drugs, and the risk of breast cancer.
Eliassen, AH, Colditz, GA, Rosner, B, Willett, WC, Hankinson, SE
Archives of internal medicine. 2005;(19):2264-71
Abstract
BACKGROUND Experimental evidence suggests that statins protect against breast carcinogenesis by interrupting cell cycle progression and promoting apoptosis. Evidence in humans is limited and inconsistent. The relation between serum cholesterol levels and breast cancer risk is itself unclear; because cholesterol is the precursor to sex steroid hormones, higher levels could plausibly increase risk. METHODS The associations of statins, general lipid-lowering drugs, and reported cholesterol levels with breast cancer risk were assessed in the Nurses' Health Study, with 6 to 12 years of follow-up. A total of 79,994 women aged 42 to 69 years and free of cancer were followed prospectively for up to 12 years. Current statin use, including duration, was assessed retrospectively in 2000 in 75,828 women. Self-reported serum cholesterol level was assessed prospectively between 1990 and 2000 in 71,921 women. RESULTS Overall, we documented 3177 incident cases of invasive breast cancer. Compared with nonusers, current lipid-lowering drug users experienced similar breast cancer risk (multivariate relative risk [RR], 0.99; 95% confidence interval [CI], 0.86-1.13). Current use of statins also was not significantly associated with breast cancer risk (RR, 0.91; 95% CI, 0.76-1.08). Associations by duration of current use were similarly null. Self-reported serum cholesterol levels were not associated with breast cancer risk in postmenopausal women with levels of 240 mg/dL or higher (> or = 6.22 mmol/L) compared with less than 180 mg/dL (< 4.66 mmol/L) (RR, 1.04; 95% CI, 0.91-1.17). CONCLUSION Overall, these data suggest that serum cholesterol levels and the use of lipid-lowering drugs in general and of statins in particular are not substantially associated with breast cancer risk.