Study Title and Description
Storm in a coffee cup: caffeine modifies brain activation to social signals of threat.
Key Questions Addressed
|1||For [population], is caffeine intake above [exposure dose], compared to intakes [exposure dose] or less, associated with adverse effects on behavior*?|
Primary Publication Information
|Title||Storm in a coffee cup: caffeine modifies brain activation to social signals of threat.|
|Author||JE Smith,AD Lawrence,A Diukova,RG Wise,PJ Rogers,|
Secondary Publication Information
There are currently no secondary publications defined for this study.
Extraction Form: Behavior - Design Details - INCLUDED Studies
No arms have been defined in this extraction form.
|Question... Follow Up||Answer||Follow-up Answer|
|What outcome is being evaluated in this paper?||Behavior|
|What is the objective of the study (as reported by the authors)?||This study investigated the effects of caffeine on brain regions implicated in social threat processing and anxiety|
|Provide a general description of the methods as reported by the authors. Information should be extracted based on relevance to the SR (i.e., caffeine related methods)||Participants were restricted to individuals reporting no extreme sensitivity to caffeine (i.e. marked and distressing anxiety), but having a dietary caffeine intake of <280 mg per week, as the results of a prior study indicate this level of intake as around the threshold for withdrawal effects and tolerance (Rogers et al., 2010). Individuals reporting to have never consumed caffeine were excluded. Participants’ trait anxiety was assessed using the trait version of the Spielberger State-Trait Anxiety Inventory (STAI) (Spielberger, 1983). This was a double-blind crossover study, in which participants received 250 mg of caffeine or placebo in two fMRI sessions. They consumed a light (caffeine-free) snack 90 min prior to dosing. This dose of caffeine is equivalent to the caffeine present in 2–2.5 cups of ground coffee (Heatherley et al., 2006a), and has previously been found to modulate anxiety and blood pressure, particularly in non/infrequent caffeine consumers (Rogers et al., 2008, 2010). The treatment (caffeine/placebo) order was counterbalanced across participants, and the two fMRI sessions were spaced one week apart at the same time of day. The sessions began at 12.30 p.m. and participants received caffeine or placebo 30 min later. In both sessions, 1 h after treatment, participants performed a variant of the Emotional Face Processing Task (EFPT) (Hariri et al., 2002), then a simple visual task (SVT), while in the scanner. Participants’ current emotional states, alertness and blood pressure were assessed outside the scanner twice: before treatment (baseline) and 2 h after receiving caffeine or placebo (post-treatment). The behavioral data described here are self-rated anxiety and mental alertness assessed using items (single or groups of descriptors, e.g. I feel anxious/worried/nervous; I feel mentally alert/attentive/observant) taken from the Mood, Alertness and Physical Sensations Scales (MAPSS) (Rogers et al., 2010). Caffeine BP (Caffeine anhydrous powder; Direct Food Ingredients Limited, Macclesfield, Cheshire, UK) and placebo (cornflour) were administered in white size 1 cellulose capsules (Capsuline, Pompano Beach, Florida, FL, USA). These caffeine and placebo capsules were identical in appearance, and were swallowed with 50 ml of room temperature water. Change from baseline data were calculated for self-rated anxiety and mental alertness, and (systolic and diastolic) blood pressure, by subtracting the baseline data from the post-treatment data. These data were analyzed for effects of caffeine using paired t-tests (caffeine vs placebo). Effects of caffeine (caffeine vs placebo) and threat (angry/fearful faces vs happy faces) on face-matching accuracy (percentage correct) and reaction time (ms) were also assessed with paired t-tests. Statistical significance was set to P < 0.05, and all t-test and correlation analyses described above were conducted using SPSS 16.0.1 for Windows.|
|How many outcome-specific endpoints are evaluated?||1|
|What is the (or one of the) endpoint(s) evaluated? (Each endpoint listed separately)||Anxiety|
|List additional health endpoints (separately).|
|List additional health endpoints (separately)|
|What is the study design?||Controlled Trial|
|Randomized or Non-Randomized?||NCT|
|What were the diagnostics or methods used to measure the outcome?||Subjective|
|Optional: Name of Method or short description||Select questions from MAPSS questionnaire|
|Caffeine (general)||Caffeine (general)|
|What was the reference, comparison, or control group(s)? (e.g. high vs low consumption, number of cups, etc.)||Placebo vs 250 mg caffeine|
|What were the listed confounders or modifying factors as stated by the authors? (e.g. multi-variable components of models. Copy from methods)||None listed|
|Provide a general description of results (as reported by the authors).||Caffeine vs placebo increased anxiety [t(13)=4.58, P=0.0005] and diastolic blood pressure [t(13)=3.56, P=0.002], but did not affect systolic blood pressure (P> 0.1). Face matching was performed with high accuracy (>90%). Neither caffeine nor threat (angry/fearful faces vs happy faces) had an effect on face-matching accuracy or reaction time, and caffeine did not affect mental alertness (all P’s > 0.1).|
|Did the authors perform a dose-response analysis (or trend/related analysis)?||No|
|What were the authors's observations re: trend analysis?|
|What were the author's conclusions?||The observed changes in threat-related brain activation were accompanied by increased self-rated anxiety and blood pressure, as was expected from previous studies (Rogers et al., 2008, 2010). These results are consistent with converging lines of evidence from animal and human studies demonstrating involvement of the PAG, amygdala and mPFC wall in threat processing and anxiety (Keay and Bandler, 2001; Price, 2005; Wager et al., 2009).|
|What were the sources of funding?||Support for this study was provided by grants from the University of Bristol’s Faculty of Science, a Career Development Award from the Medical Research Council UK (to R.G.W) and The Wales Institute of Cognitive Neuroscience (to A.D.L.)|
|What conflicts of interest were reported?||The authors declare that over the past 3 years J.E.S. has received a PhD maintenance grant from Unilever Research and Development Vlaardingen, the Netherlands. P.J.R. has received consulting fees from Unilever; and grants for research from Cadbury, DSM, GSK and Unilever|
|Does the exposure (dose) need to be standardized to the SR?||No|
|Provide calculations/conversions for the exposure based on the decision tree in the guide (for all endpoints/exposure levels of interest).|
|List all the endpoint(s) followed by the dose (mg) which will be used in comparison to Nawrot. Characterize value as LOAEL/NOAEL, etc. if possible.||Anxiety LOAEL = 250 mg|
|Notes regarding selection/listing of endpoints and exposures/doses to be compared to Nawrot.||This study had a single exposure level (250 mg)|
|What is the importance of the study with respect to the adverseness of the outcome?||Important|
No baseline characteristics have been defined for this extraction form.
Results & Comparisons
No Results found.
|Arm or Total||Title||Description||Comments|
No quality dimensions were specified.
No quality rating data was found.