The effects of a priming dose of alcohol and drinking environment on snack food intake.

Alcohol consumption is a potential risk factor for being overweight. We aimed to investigate the effects of an alcohol priming dose and an alcohol-related environment on snacking behaviour. One hundred and fourteen social drinkers completed one of four experimental sessions either receiving a priming dose of alcohol (.6 g/kg) or soft drink in a bar-lab or a sterile lab. Participants provided ratings of appetite, snack urge, and alcohol urge before and after consuming their drinks. Participants completed an ad libitum snack taste test of savoury and sweet, healthy and unhealthy foods before completing the self-reports a final time. Appetite and snack urge increased more following alcohol consumption, and decreased to a lesser extent following the taste test relative to the soft drink. Total calories (including drink calories) consumed were significantly higher in the alcohol groups. There was a marginal effect of environment; those in the bar-lab consumed a higher proportion of unhealthy foods. These effects were more pronounced in those who were disinhibited. While alcohol may not increase food consumption per se, alcohol may acutely disrupt appetite signals, perhaps via processes of reward and inhibitory control, resulting in overall greater calorie intake. Individuals who are generally disinhibited may be more vulnerable to the effects of alcohol and drinking environments on eating behaviour.

Nematode modulation of inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a chronic disease arising due to a culmination of genetic, environmental, and lifestyle-associated factors and resulting in an excessive pro-inflammatory response to bacterial populations in the gastrointestinal tract. The prevalence of IBD in developing nations is relatively low, and it has been proposed that this is directly correlated with a high incidence of helminth infections in these areas. Gastrointestinal nematodes are the most prevalent parasitic worms, and they efficiently modulate the immune system of their hosts in order to establish chronic infections. Thus, they may be capable of suppressing unrelated inflammation in disorders such as IBD. This review describes how nematodes, or their products, suppress innate and adaptive pro-inflammatory immune responses and how the mechanisms involved in the induction of anti-nematode responses regulate colitis in experimental models and clinical trials with IBD patients. We also discuss how refinement of nematode-derived therapies should ultimately result in the development of potent new therapeutics of clinical inflammatory disorders.

The importance of glucocorticoids in alcohol dependence and neurotoxicity.

Alterations in hypothalamo-pituitary adrenal (HPA) function have been described in alcoholics and in rodents after chronic alcohol consumption but the role of glucocorticoids in alcohol consumption, and the mechanisms involved, has received little attention until recently. Both alcohol consumption and withdrawal from chronic alcohol intake raise circulating glucocorticoid levels, and prolonged high concentrations of glucocorticoids are known to have detrimental effects on neuronal function and cognition. This minireview covers the ways in which glucocorticoids may be involved in drinking behavior, from social drinking to dependence, and the negative consequences of alcohol consumption seen during withdrawal which may have a detrimental effect on treatment outcome. Research shows prolonged increases in brain glucocorticoid concentrations and decreased brain glucocorticoid receptor availability (consistent with increased levels of endogenous ligand) after withdrawal from chronic alcohol treatment. Evidence suggests that increased glucocorticoid levels in the brain after chronic alcohol treatment are associated with the cognitive deficits seen during abstinence which impact on treatment efficacy and quality of life. Studies on organotypic cultures also demonstrate the importance of glucocorticoids in the neuropathological consequences of alcohol dependence.

A new test to measure attentional bias and cognitive disinhibition in drinkers, based on the Hayling task.

AIMS: To generate and pilot unfinished sentences, based on the Hayling Task of disinhibition, which could be completed with alcohol or non-alcohol words. To determine whether drinking habits influenced responses on the new sentences, which may advance understanding of the cognitive processes underlying alcohol-related behaviours. METHODS: Three phases: I-Generation of appropriate sentences (via email correspondence); II-Sentence completion to establish proportion of alcohol-related and non-alcohol-related responses; III-A Hayling-style task using the sentences (laboratory-based). During the Hayling task, sentences were completed with the first word that came to mind (initiation task), and with a word that did not make semantic sense (inhibition task). In Phase III, the alcohol use disorder identification test (AUDIT) was also completed to determine whether drinking habits were related to responses. RESULTS: Fifteen sentences were generated and tested. Compared with low hazardous drinkers, higher hazardous drinkers gave more alcohol-related responses; persisted in giving alcohol responses in the inhibition task; and were slower to make non-alcohol-related responses. A positive correlation was found between AUDIT score and number of alcohol-related responses. CONCLUSIONS: A new alcohol-related sentence-completion tool, based upon the Hayling disinhibition task, was developed and piloted. Responses on the task were associated with measures of alcohol use disorders. The task can be used in research investigating the processes underlying the acute and chronic effects of alcohol, such as attentional bias and disinhibition. In future, the task could be used in conjunction with non-alcohol-related sentence completion tasks to investigate general and alcohol-specific processes of disinhibition.

The influence of alcohol on basic motoric and cognitive disinhibition.

It has been proposed that alcohol weakens control processes, which in turn supports the occurrence of disinhibited behaviours. Two studies were run, in parallel (both with 32 participants) using a between-subject design to investigate any disinhibiting effects of a moderate dose of alcohol (0.6 g/kg compared to placebo), previously found to trigger increased desire for alcohol. Disinhibiting effects were tested on basic motoric and cognitive control processes, using a go/no-go (GNG) and the Stroop task (ST) respectively. Although a higher proportion of participants wanted more alcohol under the alcohol preload (priming effect), this effect was not found to be significant. In the GNG task, correct response latency (RL) decreased from baseline [P = 0.008] while number of incorrect hits increased [P = 0.030] irrespective of treatment, indicating the formation of a habit-like response and motoric disinhibition. Although error rate did not differ between groups, an interaction occurred with regard to erroneous RL: participants under alcohol became quicker, while those under placebo became slower [P = 0.014]. In the ST, those preloaded with alcohol made significantly more errors [P = 0.021] and were quicker to complete the task [P = 0.044] compared with those preloaded with placebo, indicating a strong alcohol effect on cognitive disinhibition. The data suggest that a moderate dose of alcohol, which induces priming to want more alcohol, had disinhibiting effects both on a basic motoric and a cognitive inhibitory task. Thus the idea that priming may be mediated by the disinhibitory effects of alcohol is supported.