Aims: To update epidemiological data on alcohol and breast cancer, with special emphasis on light alcohol consumption, and to review mechanisms of alcohol mediated mammary carcinogenesis. Methods: For epidemiological data, in November 2011 we performed a literature search in various bibliographic databases, and we conducted a meta-analysis of data on light alcohol drinking. Relevant mechanistic studies were also reviewed to November 2011. Results: A significant increase of the order of 4% in the risk of breast cancer is already present at intakes of up to one alcoholic drink/day. Heavy alcohol consumption, defined as three or more drinks/day, is associated with an increased risk by 40–50%. This translates into up to 5% of breast cancers attributable to alcohol in northern Europe and North America for a total of approximately 50 000 alcohol-attributable cases of breast cancer worldwide. Up to 1–2% of breast cancers in Europe and North America are attributable to light drinking alone, given its larger prevalence in most female populations when compared with heavy drinking. Alcohol increases estrogen levels, and estrogens may exert its carcinogenic effect on breast tissue either via the ER or directly. Other mechanisms may include acetaldehyde, oxidative stress, epigenetic changes due to a disturbed methyl transfer and decreased retinoic acid concentrations associated with an altered cell cycle. Conclusions: Women should not exceed one drink/day, and women at elevated risk for breast cancer should avoid alcohol or consume alcohol occasionally only.

Alcohol misuse is a common presentation to the Emergency Department (ED). The International Classification of Diseases ICD-10 for alcohol misuse, both under F10 and Y90/Y91, is not straightforward. The practicalities of coding ED attendances reveal an increasing detachment from ICD-10 (currently under review). Early identification [sometimes using blood alcohol concentrations (BACs)] and brief advice (IBA) can reduce unscheduled alcohol-related ED re-attendance. The UK Government Department of Health has implemented use of the terms ‘Hazardous Drinking’, ‘Harmful Drinking’ and ‘Dependent Drinking’ in its Public Service Agreements aimed at reducing harm by alcohol. Simplifying coding might increase IBA usage. We suggest that coding improvements in ICD-11 should update Y91 (currently ‘clinical assessment’)—with ICD-10 Y90 remaining for BAC to classify a patient's ‘alcohol status’. Y90 and Y91 together would indicate the urgency for early IBA and/or speciality referral, aiming to reduce the prevalence of ‘Dependent Drinking’.

Among the tasks facing those who code alcohol-related disorders in an international classification of disease are an examination of the multiple places in which the involvement of alcohol and other psychoactive substances (and their associated disorders) are captured and finding out how this can be optimized for clinical and epidemiological purposes. It is important to adjust the current coding system so that the involvement of alcohol in injuries is routinely recorded. The suggestions by Touquet and Harris (2012) for enhancing the International Classification of Diseases (ICD) system are valuable input for this process, pointing to the importance of codes that can be used in the emergency-department environment both for capturing alcohol's involvement and to point to the necessary therapeutic response.

Aims: Early ethanol consumption could be a risk factor for young brain integrity and its maturation, and also for the development of addictive behaviors in adulthood. Neuronal nitric oxide synthase (nNOS) expressing neurons are specifically located in the subgranular layer (SGL) of dentate gyrus and may be relevant for hippocampal neurogenesis. The focus of this work is aimed to determine local changes in the nNOS-like immunoreactive (nNOS-LIR) cell populations of the SGL after chronic ethanol exposure in young adult and mature adult rats. Methods: We used the nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase (NADPH-d) reaction as a qualitative marker of nNOS enzyme activity. We also analyzed the nNOS-LIR cell density by the nNOS immunocytochemistry in order to compare these two methods of labeling. Dorsal striatum (CPu) was also analyzed in order to compare two neural areas with high nNOS-LIR cell density. Results: The young adult group showed less hippocampal NADPH-d⁺ cell density than the mature adult group. Interestingly, the NADPH-d⁺ cell density was increased in the SGL of the young adult ethanol-treated group, whereas it decreased in the mature adult ethanol-treated group, when compared with their respective controls. No change was observed in any of the groups for the hippocampal nNOS-LIR cell density and no differences could be established in CPu for nNOS-LIR and NADPH-d⁺ cell densities in any of the groups studied. Conclusion: The NADPH-d expression is affected by chronic ethanol exposure in opposite ways between both age groups studied. Further studies are needed to evaluate the relative importance of these findings, especially when considering human subjects.