J Lanini et al, 2015. Acute personalized habitual caffeine doses improve attention and have selective effects when considering the fractionation of executive functions. Human Psychopharmacology, published online ahead of print.

ABSTRACT:

Caffeine is widely used, often consumed with food, and improves simple and complex/executive attention under fasting conditions. We investigated whether these cognitive effects are observed when personalized habitual doses of caffeine are ingested by caffeine consumers, whether they are influenced by nutriments and if various executive domains are susceptible to improvement. This was a double-blind, placebo-controlled study including 60 young, healthy, rested males randomly assigned to one of four treatments: placebo fasting, caffeine fasting, placebo meal and caffeine meal. Caffeine doses were individualized for each participant based on their self-reported caffeine consumption at the time of testing (morning). The test battery included measures of simple and sustained attention, executive domains (inhibiting, updating, shifting, dual tasking, planning and accessing long-term memory), control measures of subjective alterations, glucose and insulin levels, skin conductance, heart rate and pupil dilation. Regardless of meal intake, acute habitual doses of caffeine decreased fatigue, and improved simple and sustained attention and executive updating. This executive effect was not secondary to the habitual weekly dose consumed, changes in simple and sustained attention, mood, meal ingestion and increases in cognitive effort. We conclude that the morning caffeine “fix” has positive attentional effects and selectively improved executive updating whether or not caffeine is consumed with food.

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D P Evatt et al, 2015. A brief manualized treatment for problematic caffeine use: a randomized trial. Journal of Consulting and Clinical Psychology, published online ahead of print.

ABSTRACT:

Objective: The goal of the present investigation was to develop and test a brief therapist-guided manualized treatment for problematic caffeine use, including cognitive-behavioral strategies and 5 weeks of progressively decreased consumption.

Method: Individuals seeking treatment for problematic caffeine use (mean daily caffeine consumption of 666 mg at baseline) were randomized using a waitlist-control design to receive immediate treatment (N = 33) or delayed treatment (∼6 weeks later; N = 34). A 1-hr treatment session designed to help individuals quit or reduce caffeine consumption was provided by a trained counselor along with a take-home booklet. After the treatment session, participants completed daily diaries of caffeine consumption for 5 weeks. They returned for follow-up assessments at 6, 12, and 26 weeks and had a telephone interview at 52-weeks posttreatment.

Results: Treatment resulted in a significant reduction in self-reported caffeine use and salivary caffeine levels. No significant posttreatment increases in caffeine use were observed for up to 1 year follow-up. Comparisons to the waitlist-control condition revealed that reductions in caffeine consumption were due to treatment and not the passing of time, with a treatment effect size of R2 = .35 for the model.

Conclusion: A brief 1-session manualized intervention with follow-up was efficacious at reducing caffeine consumption. Future researchers should replicate and extend these findings, as well as consider factors affecting dissemination of treatment for problematic caffeine use to those in need.

 

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E Loftfield et al, 2015. Association of Coffee Consumption With Overall and Cause-Specific Mortality in a Large US Prospective Cohort Study. American Journal of Epidemiology, published online ahead of print.

ABSTRACT:

Concerns about high caffeine intake and coffee as a vehicle for added fat and sugar have raised questions about the net impact of coffee on health. Although inverse associations have been observed for overall mortality, data for cause-specific mortality are sparse. Additionally, few studies have considered exclusively decaffeinated coffee intake or use of coffee additives. Coffee intake was assessed at baseline by self-report in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Hazard ratios were estimated using Cox proportional hazards models. Among 90,317 US adults without cancer at study baseline (1998-2001) or history of cardiovascular disease at study enrollment (1993-2001), 8,718 deaths occurred during 805,644 person-years of follow-up from 1998 through 2009. Following adjustment for smoking and other potential confounders, coffee drinkers, as compared with nondrinkers, had lower hazard ratios for overall mortality (<1 cup/day: hazard ratio (HR) = 0.99 (95% confidence interval (CI): 0.92, 1.07); 1 cup/day: HR = 0.94 (95% CI: 0.87, 1.02); 2-3 cups/day: HR = 0.82 (95% CI: 0.77, 0.88); 4-5 cups/day: HR = 0.79 (95% CI: 0.72, 0.86); ≥6 cups/day: HR = 0.84 (95% CI: 0.75, 0.95)). Similar findings were observed for decaffeinated coffee and coffee additives. Inverse associations were observed for deaths from heart disease, chronic respiratory diseases, diabetes, pneumonia and influenza, and intentional self-harm, but not cancer. Coffee may reduce mortality risk by favorably affecting inflammation, lung function, insulin sensitivity, and depression.

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