Research demonstrates a negative relationship between alcohol use and affect, but the value of deprecation is unknown and thus cannot be included in estimates of the cost of alcohol to society. This paper aims to examine this relationship and develop econometric techniques to value the loss in affect attributable to alcohol consumption.

Data Availability: There are restrictions prohibiting the provision of data in this manuscript. The data were obtained from a third party, UK Biobank, upon application. Interested parties can apply for data from UK Biobank directly, at www.ukbiobank.ac.uk . UK Biobank will consider data applications from bona fide researchers for health-related research that is in the public interest. By accessing data from UK Biobank, readers will be obtaining it in the same manner as we did.

Introduction

The potential benefits of light alcohol consumption has long been described in terms of greater happiness, reduced anxiety and positive changes in other affective states [1]. The pursuit of happiness is an unalienable right in some jurisdictions [2] and the UK Government explicitly referenced the presumed positive effect of alcohol on well-being in the 2012 Alcohol Strategy [3]. However, there is a reliable and consistent relationship between greater alcohol use and negative affect [3]. Initiatives that reduce alcohol consumption should, therefore, be expected to elicit improvements to a population’s affective state.

Although the directionality of the relationship between alcohol use and affect has historically been difficult to determine, attention to possible underlying mechanisms suggests that greater alcohol use results in a net detriment to the consumer’s affective state, or personal utility. Unidirectional models typically fit data more accurately than bidirectional models where personal utility also influences alcohol use [4, 5]. Models also suggest a J-shaped association curve between consumption and various measures of personal utility. For example, depression is lowest, and happiness is greatest, in light drinkers [6–10]; however, moderate and heavy consumption of alcohol, even in the absence of a disorder, tends to reverse any protective effect and increase the risk of mental health problems to a level above that observed in those who abstain [6–8]. In short, abstaining appears to be a risk factor for decreased personal utility, but moderate or heavy alcohol consumption is a higher risk factor. Some explain this trend as the “sick quitter” effect, which occurs when a subset of abstainers refrains from drinking due to other health factors that increase their risk of adverse effects. These factors serve as latent confounders and falsely inflate the risk attributable to abstaining [11]. Further, in the population suffering from comorbid depression and alcohol use disorder or dependence, alcohol problems are typically the initial disorder [4, 5].

One mechanism underlying this relationship may include a role for alcohol in circadian dysfunction. Even in moderate amounts, alcohol has been shown to disrupt the circadian rhythm and interrupt transcription of regulatory genes in related networks, including CLOCK, CRY1, CRY2, ARNTL, & PER2 [12–15]. Circadian-related single nucleotide polymorphisms have been associated with comorbid depression and alcohol abuse [16]. Alcohol consumption has also been observed to lower serotonin levels and morph the shape of the concentration curve to mimic that found in those diagnosed with depression [14]. This body of evidence points to alcohol as a causal factor in circadian dysregulation, which in turn may progress depression via potentiation of risk factors for depression including serotonin levels, altered emotional regulation, or deficits in sociality. Another possible mechanism centres on brain-derived neurotrophic hormone (BNDF), a stimulator of neurogenesis and necessary for the growth and repair of neural cells. Altered BDNF expression has been a prime candidate in the epigenetic exploration of depression. In adolescent rats, binge drinking is associated with a reduction in BDNF expression, which is in turn associated with decreased survival time of neural progenitor cells and the display of a depressive phenotype [17]. In sum, the weight of observational, genetic and neuroscientific evidence together indicates that increasing levels of alcohol consumption causes a deterioration in personal utility.

Studies are increasingly seeking to capture the intangible benefits of initiatives and interventions that seek to improve health [18–20], anxiety and depression [21], and are doing so in monetary terms [22–25]. For alcohol, however, the value of reducing consumption has typically focussed on quantifiable outcomes such as the price of hospital admission and costs to economic productivity [26–28]; intangible costs and benefits are less prominent in estimates. This focus is notable, as the presumed affective benefits of alcohol have been used to counterbalance policies aimed at reducing alcohol consumption and therefore harm [3]. Policymakers and consumers may, therefore, ask whether the cost of any reduction in alcohol consumption on affect is worthwhile. Policymakers, for example, may consider interventions to improve personal utility in populations through targeting interventions at alcohol consumption and may wish to know whether efforts are cost-effective. Consumers, meanwhile, may lack the necessary information to compare the consequences of alcohol, such as negative affect, with consequences of other consumption decisions. Money is, by nature, fungible and exchangeable for a range of goods and services. Providing a value for the affective consequences of alcohol use allows consumers the option to consider the combined financial, health and personal utility costs of their alcohol use and consider ways to invest their resources to maximise personal utility. Placing a value on the personal utility consequences of alcohol use facilitates this decision-making for both policy makers and consumers.

Shadow pricing methods [29] can be used to determine the price of non-market goods [30], including the affective benefits derived from clean air and green landscapes [31], the value of fear in response to crime [32] and aircraft noise [33]. The method is derived from observations that wages often vary systematically by the unpleasantness of employment, that is, that a higher wage is necessary to offset occupations that are unpleasant to compensate and therefore attract employees [34, 35]. With respect to alcohol consumption, personal utility (U) can be expressed as a function of affective state. Alcohol consumption is associated with a reduction in U but that U increases as household income increases [36–38]. We therefore define the shadow price of alcohol as the compensating differential, the increase in household income, required to offset the effect of an alcohol-induced detriment in affect.

In sum, the aims of this work are, first, to determine the nature and relationship between alcohol consumption and personal utility, and, second, to apply econometric models to estimate the relative value of any change. This investigation uses data from UK Biobank, a prospective cohort study based in the United Kingdom (UK) [39]. Biobank records a wealth of data from respondents, aged 37 to 73 years of age, including alcohol use, and includes two measures relating to affect. A neuroticism scale [40] describing levels of anxiety and depression, and a brief depression scale [41]. Depression is associated with panic, social anxiety, and post-traumatic stress disorder [42] whereas neuroticism [40] is an aspect of personality that is not only associated with anxiety and depression, but further predicts mortality in older men [43]. Further, a smaller group of respondents were followed up using the measures of interest so providing an opportunity to consider both between and within changes. For completeness, we use both scales each in cross-sectional and longitudinal analysis, excepting that the reduced numbers in the longitudinal analyses may leave it underpowered. We undertake analyses in parallel. We consider results from both longitudinal and cross-sectional analyses for both depression and neuroticism in deriving estimates. We restrict analyses to only those consuming alcohol as the reasons for abstinence cannot be accounted for in models.