03 May 2018 In Cancer
BACKGROUND: Racial disparities in the incidence of major cancers may be attributed to differences in the prevalence of established, modifiable risk factors such as obesity, smoking, physical activity and diet. METHODS: Data from a prospective cohort of 566,398 adults aged 50-71 years, 19,677 African-American and 450,623 Whites, was analyzed. Baseline data on cancer-related risk factors such as smoking, alcohol, physical activity and dietary patterns were used to create an individual adherence score. Differences in adherence by race, gender and geographic region were assessed using descriptive statistics, and Cox proportional hazards models were used to determine the association between adherence and cancer incidence. RESULTS: Only 1.5% of study participants were adherent to all five cancer-related risk factor guidelines, with marked race-, gender- and regional differences in adherence overall. Compared with participants who were fully adherent to all five cancer risk factor criteria, those adherent to one or less had a 76% increased risk of any cancer incidence (HR: 1.76, 95% CI: 1.70 - 1.82), 38% increased risk of breast cancer (HR: 1.38, 95% CI: 1.25 - 1.52), and doubled the risk of colorectal cancer (HR: 2.06, 95% CI: 1.84 - 2.29). However, risk of prostate cancer was lower among participants adherent to one or less compared with those who were fully adherent (HR: 0.79, 95% CI: 0.75 - 0.85). The proportion of cancer incident cases attributable to low adherence was higher among African-Americans compared with Whites for all cancers (21% vs. 19%), and highest for colorectal cancer (25%) regardless of race. CONCLUSION: Racial differences in the proportion of cancer incidence attributable to low adherence suggests unique opportunities for targeted cancer prevention strategies that may help eliminate racial disparities in cancer burden among older US adults
03 May 2018 In Cancer
BACKGROUND: Racial disparities in the incidence of major cancers may be attributed to differences in the prevalence of established, modifiable risk factors such as obesity, smoking, physical activity and diet. METHODS: Data from a prospective cohort of 566,398 adults aged 50-71 years, 19,677 African-American and 450,623 Whites, was analyzed. Baseline data on cancer-related risk factors such as smoking, alcohol, physical activity and dietary patterns were used to create an individual adherence score. Differences in adherence by race, gender and geographic region were assessed using descriptive statistics, and Cox proportional hazards models were used to determine the association between adherence and cancer incidence. RESULTS: Only 1.5% of study participants were adherent to all five cancer-related risk factor guidelines, with marked race-, gender- and regional differences in adherence overall. Compared with participants who were fully adherent to all five cancer risk factor criteria, those adherent to one or less had a 76% increased risk of any cancer incidence (HR: 1.76, 95% CI: 1.70 - 1.82), 38% increased risk of breast cancer (HR: 1.38, 95% CI: 1.25 - 1.52), and doubled the risk of colorectal cancer (HR: 2.06, 95% CI: 1.84 - 2.29). However, risk of prostate cancer was lower among participants adherent to one or less compared with those who were fully adherent (HR: 0.79, 95% CI: 0.75 - 0.85). The proportion of cancer incident cases attributable to low adherence was higher among African-Americans compared with Whites for all cancers (21% vs. 19%), and highest for colorectal cancer (25%) regardless of race. CONCLUSION: Racial differences in the proportion of cancer incidence attributable to low adherence suggests unique opportunities for targeted cancer prevention strategies that may help eliminate racial disparities in cancer burden among older US adults
08 December 2015 In Drinking & Driving

BACKGROUND: Alcohol is often mixed with various nonalcoholic beverages. While consumption of food with alcohol will decrease peak breath alcohol concentrations (BrAC), recent evidence has suggested that mixing alcohol with diet beverages can result in higher BrAC when compared with mixing the same amount of alcohol with sweetened beverages. The purpose of this study was to examine this phenomenon using two different moderate alcohol doses.

METHODS: Twenty participants (10 males) attended five sessions where they received 1 of 5 doses (0.91ml/kg vodka+3.64ml/kg of diet soda, 0.91ml/kg vodka+3.64 of regular soda, 1.82ml/kg vodka+7.28ml/kg diet soda, 1.82ml/kg vodka+7.28ml/kg regular soda, and a placebo beverage). BrAC was recorded repeatedly up to 180min after dose administration.

RESULTS: Participants had significantly higher BrAC when the mixer was diet as compared to regular for both alcohol dose conditions. No gender differences were observed.

CONCLUSIONS: Mixing alcohol with diet beverages can result in higher BrAC when compared to the same amount of alcohol administered with a similar sweetened beverage. Individuals who consume diet mixers with alcohol may reduce caloric intake but increase the harms associated with higher BrACs.

PURPOSE OF REVIEW: Alcohol consumption during adolescence greatly increases the likelihood that an alcohol use disorder will develop later in life. Elucidating how alcohol impacts the adolescent brain is paramount to understanding how alcohol use disorders arise. This review focuses on recent work addressing alcohol's unique effect on the adolescent brain.

RECENT FINDINGS: The unique and dynamic state of the developing adolescent brain is discussed with an emphasis on the developmentally distinct effect of alcohol on the dopaminergic reward system and corticolimbic structure and function. Reward neurocircuitry undergoes significant developmental shifts during adolescence, making it particularly sensitive to alcohol in ways that could promote excessive consumption. In addition, developing corticolimbic systems, including the prefrontal cortex and hippocampus, exhibit enhanced vulnerability to alcohol-induced damage. Disruption of white matter integrity, neurotoxicity and inhibition of adult neurogenesis may underlie alcohol-mediated cognitive dysfunction and lead to decreased behavioral control over consumption.

SUMMARY: In adolescents, alcohol interacts extensively with reward neurocircuitry and corticolimbic structure and function in ways that promote maladaptive behaviors that lead to addiction. Future work is needed to further understand the mechanisms involved in these interactions. Therapeutic strategies that restore proper reward neurochemistry or reverse alcohol-induced neurodegeneration could prove useful in preventing emergence of alcohol use disorders.

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