Changes in density of on-premises alcohol outlets and impact on violent crime, Atlanta, Georgia, 1997-2007.

INTRODUCTION: Regulating alcohol outlet density is an evidence-based strategy for reducing excessive drinking. However, the effect of this strategy on violent crime has not been well characterized. A reduction in alcohol outlet density in the Buckhead neighborhood of Atlanta from 2003 through 2007 provided an opportunity to evaluate this effect. METHODS: We conducted a community-based longitudinal study to evaluate the impact of changes in alcohol outlet density on violent crime in Buckhead compared with 2 other cluster areas in Atlanta (Midtown and Downtown) with high densities of alcohol outlets, from 1997 through 2002 (preintervention) to 2003 through 2007 (postintervention). The relationship between exposures to on-premises retail alcohol outlets and violent crime were assessed by using annual spatially defined indices at the census block level. Multilevel regression models were used to evaluate the relationship between changes in exposure to on-premises alcohol outlets and violent crime while controlling for potential census block-level confounders. RESULTS: A 3% relative reduction in alcohol outlet density in Buckhead from 1997-2002 to 2003-2007 was associated with a 2-fold greater reduction in exposure to violent crime than occurred in Midtown or Downtown, where exposure to on-premises retail alcohol outlets increased. The magnitude of the association between exposure to alcohol outlets and violent crime was 2 to 5 times greater in Buckhead than in either Midtown or Downtown during the postintervention period. CONCLUSIONS: A modest reduction in alcohol outlet density can substantially reduce exposure to violent crime in neighborhoods with high density of alcohol outlets. Routine monitoring of community exposure to alcohol outlets could also inform the regulation of alcohol outlet density, consistent with Guide to Community Preventive Services recommendations.

Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans.

BACKGROUND: Prospective studies in humans examining the effects of fructose consumption on biological markers associated with the development of metabolic syndrome are lacking. Therefore we investigated the relative effects of 10 wks of fructose or glucose consumption on plasma uric acid and RBP-4 concentrations, as well as liver enzyme (AST, ALT, and GGT) activities in men and women. METHODS: As part of a parallel arm study, older (age 40-72), overweight and obese male and female subjects (BMI 25-35 kg/m2) consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 wks. Fasting and 24-h blood collections were performed at baseline and following 10 wks of intervention and plasma concentrations of uric acid, RBP-4 and liver enzyme activities were measured. RESULTS: Consumption of fructose, but not glucose, led to significant increases of 24-h uric acid profiles (P < 0.0001) and RBP-4 concentrations (P = 0.012), as well as plasma GGT activity (P = 0.04). Fasting plasma uric acid concentrations increased in both groups; however, the response was significantly greater in subjects consuming fructose (P = 0.002 for effect of sugar). Within the fructose group male subjects exhibited larger increases of RBP-4 levels than women (P = 0.024). CONCLUSIONS: These findings suggest that consumption of fructose at 25% of energy requirements for 10 wks, compared with isocaloric consumption of glucose, may contribute to the development of components of the metabolic syndrome by increasing circulating uric acid, GGT activity, suggesting alteration of hepatic function, and the production of RBP-4.

Circulating concentrations of monocyte chemoattractant protein-1, plasminogen activator inhibitor-1, and soluble leukocyte adhesion molecule-1 in overweight/obese men and women consuming fructose- or glucose-sweetened beverages for 10 weeks.

CONTEXT: Results from animal studies suggest that consumption of large amounts of fructose can promote inflammation and impair fibrinolysis. Data describing the effects of fructose consumption on circulating levels of proinflammatory and prothrombotic markers in humans are unavailable. OBJECTIVE: Our objective was to determine the effects of 10 wk of dietary fructose or glucose consumption on plasma concentrations of monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor-1 (PAI-1), E-selectin, intercellular adhesion molecule-1, C-reactive protein, and IL-6. DESIGN AND SETTING: This was a parallel-arm study with two inpatient phases (2 wk baseline, final 2 wk intervention), conducted in a clinical research facility, and an outpatient phase (8 wk) during which subjects resided at home. PARTICIPANTS: Participants were older (40-72 yr), overweight/obese (body mass index = 25-35 kg/m(2)) men (n = 16) and women (n = 15). INTERVENTIONS: Participants consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 wk. Blood samples were collected at baseline and during the 10th week of intervention. MAIN OUTCOME MEASURES: Fasting concentrations of MCP-1 (P = 0.009), PAI-1 (P = 0.002), and E-selectin (P = 0.048) as well as postprandial concentrations of PAI-1 (P < 0.0001) increased in subjects consuming fructose but not in those consuming glucose. Fasting levels of C-reactive protein, IL-6, and intercellular adhesion molecule-1 were not changed in either group. CONCLUSIONS: Consumption of fructose for 10 wk leads to increases of MCP-1, PAI-1, and E-selectin. These findings suggest the possibility that fructose may contribute to the development of the metabolic syndrome via effects on proinflammatory and prothrombotic mediators.

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.

Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose- or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults.