01 February 2017 In Social and Cultural Aspects

Background and aims The 2011 UN Summit on Non-Communicable Disease failed to call for global action on alcohol marketing despite calls in the World Health Organization (WHO) Global Action Plan on Non-Communicable Diseases 2013-20 to restrict or ban alcohol advertising. In this paper we ask what it might take to match the global approach to tobacco enshrined in the Framework Convention on Tobacco Control (FCTC), and suggest that public health advocates can learn from the development of the FCTC and the Code of Marketing on infant formula milks and the recent recommendations on restricting food marketing to children.

Methods Narrative review of qualitative accounts of the processes that created and monitor existing codes and treaties to restrict the marketing of consumer products, specifically breast milk substitutes, unhealthy foods and tobacco.

Findings The development of treaties and codes for market restrictions include: (i) evidence of a public health crisis; (ii) the cost of inaction; (iii) civil society advocacy; (iv) the building of capacity; (v) the management of conflicting interests in policy development; and (vi) the need to consider monitoring and accountability to ensure compliance.

Conclusion International public health treaties and codes provide an umbrella under which national governments can strengthen their own legislation, assisted by technical support from international agencies and non-governmental organizations. Three examples of international agreements, those for breast milk substitutes, unhealthy foods and tobacco, can provide lessons for the public health community to make progress on alcohol controls. Lessons include stronger alliances of advocates and health professionals and better tools and capacity to monitor and report current marketing practices and trends.

01 February 2017 In Drinking & Eating Patterns

BACKGROUND: The Alcohol Harm Paradox refers to observations that lower socioeconomic status (SES) groups consume less alcohol but experience more alcohol-related problems. However, SES is a complex concept and its observed relationship to social problems often depends on how it is measured and the demographic groups studied. Thus this study assessed socioeconomic patterning of alcohol consumption and related harm using multiple measures of SES and examined moderation of this patterning by gender and age.

METHOD: Data were used from the Alcohol Toolkit Study between March and September 2015 on 31,878 adults (16+) living in England. Participants completed the AUDIT which includes alcohol consumption, harm and dependence modules. SES was measured via qualifications, employment, home and car ownership, income and social-grade, plus a composite of these measures. The composite score was coded such that higher scores reflected greater social-disadvantage.

RESULTS: We observed the Alcohol Harm Paradox for the composite SES measure, with a linear negative relationship between SES and AUDIT-Consumption scores (beta = -0.036, p<0.001) and a positive relationship between lower SES and AUDIT-Harm (beta = 0.022, p<0.001) and AUDIT-Dependence (beta = 0.024, p<0.001) scores. Individual measures of SES displayed different, and non-linear, relationships with AUDIT modules. For example, social-grade and income had a u-shaped relationship with AUDIT-Consumption scores while education had an inverse u-shaped relationship. Almost all measures displayed an exponential relationship with AUDIT-Dependence and AUDIT-Harm scores. We identified moderating effects from age and gender, with AUDIT-Dependence scores increasing more steeply with lower SES in men and both AUDIT-Harm and AUDIT-Dependence scores increasing more steeply with lower SES in younger age groups.

CONCLUSION: Different SES measures appear to influence whether the Alcohol Harm Paradox is observed as a linear trend across SES groups or a phenomenon associated particularly with the most disadvantaged. The paradox also appears more concentrated in men and younger age groups.

15 December 2016 In Social and Cultural Aspects

This paper reviews the evidence for the effectiveness and cost-effectiveness of policies to reduce alcohol-related harm. Policies focus on price, marketing, availability, information and education, the drinking environment, drink-driving, and brief interventions and treatment. Although there is variability in research design and measured outcomes, evidence supports the effectiveness and cost-effectiveness of policies that address affordability and marketing. An adequate reduction in temporal availability, particularly late night on-sale availability, is effective and cost-effective. Individually-directed interventions delivered to at-risk drinkers and enforced legislative measures are also effective. Providing information and education increases awareness, but is not sufficient to produce long-lasting changes in behaviour. At best, interventions enacted in and around the drinking environment lead to small reductions in acute alcohol-related harm. Overall, there is a rich evidence base to support the decisions of policy makers in implementing the most effective and cost-effective policies to reduce alcohol-related harm.

15 December 2016 In Liver Disease

The susceptibility to developing alcohol dependence and significant alcohol-related liver injury is determined by a number of constitutional, environmental and genetic factors, although the nature and level of interplay between them remains unclear. The familiality and heritability of alcohol dependence is well-documented but, to date, no strong candidate genes conferring increased risk have emerged, although variants in alcohol dehydrogenase and acetaldehyde dehydrogenase have been shown to confer protection, predominantly in individuals of East Asian ancestry. Population contamination with confounders such as drug co-dependence and psychiatric and physical co-morbidity may explain the essentially negative genome-wide association studies in this disorder. The familiality and hereditability of alcohol-related cirrhosis is not as well-documented but three strong candidate genes PNPLA3, TM6SF2 and MBOAT7, have been identified. The mechanisms by which variants in these genes confer risk and the nature of the functional interplay between them remains to be determined but, when elucidated, will undoubtedly increase our understanding of the pathophysiology of this disease. The way in which this genetic information could potentially inform patient management has yet to be determined and tested.

Page 8 of 27

Disclaimer

The authors have taken reasonable care in ensuring the accuracy of the information herein at the time of publication and are not responsible for any errors or omissions. Read more on our disclaimer and Privacy Policy.