An economics literature has examined several determinants of addiction to cigarettes, including family habits, prices and discount rates. One area which is currently underexplored within this setting is the role of genetics in addiction formation. Both prices (Gruber & Zinman, 2001) and genes (Ding et al, 2009; Fletcher & Lehrer, 2011) have been found to drive smoking behaviour, but the interaction has not been explored. Our project will investigate how individuals differ in their response to health policies based on prices, and how genetics play a role in this.

In stage one of the project, we hypothesise that two mechanisms interact to partially determine the habit formation of smoking and other drug taking for young ALSPAC members. Firstly, young individuals consider the price of cigarettes when deciding whether to smoke. We will exploit price changes along two dimensions. As cohort members age, changes in taxes on cigarettes vary the price. Additionally, the ALSPAC children were born across a 21 month period and consequently for a given age, the price of a cigarette will vary. This will allow us to identify the effect of price changes upon the first age of smoking.

Secondly, an individual's response to their first cigarette will depend among other things, upon their genotype. Variations in both the speed of nicotine metabolism and dopamine and serotonin transmitters create heterogeneous adverse or positive reactions of a first cigarette, and subsequent dependence. We will investigate whether the response to a price change is less effective in individuals with certain genotypes.

In the second phase of the project we will explore the implications for the ALSPAC children of forming an addiction. Nicotine, alcohol or cannabis can themselves have detrimental effects on individuals. Retrospective information on smoking habits, prices and genotype will be combined with outcomes for 16 year old children. We will explore the effect on behavioural outcomes, obesity, expectations for the future, achievement against test scores and criminal activity. The methodology will exploit genetic variations in an instrumental variable setting. Assuming that genotype drives child outcomes only through its effect on smoking dependence allows estimation of the causal effect of addiction.

There are important policy implications inherent in this study. If the responsiveness of drug dependence to price changes varies across genotype, a group of individuals will require stronger intervention methods than prices alone. This is particularly true if we find adverse effects of forming an addiction on later outcomes for children.

Variables

We plan to make use of the genetic information for mothers and children of ALSPAC. The gene CYP2A6 drives the metabolism of nicotine and cotinine as well as other drugs and toxins.[1] There are different variants of activity of CYP2A6, and ALSPAC contains data on two in particular - CYP2A6*2 and CYP2A6*9 - which indicate slow functionality. CYP2A6*2 and CYP2A6*9 was measured for children and mothers. Lerman & Berrettial (2003) note the importance to control for maternal genes in order to separate the effects from the child's inherited genotype and familial smoking behaviour which is driven by parental genes. We would therefore request the genotype data for both generations. We hypothesise that children with differing activity of the gene will have different responses to smoking the first cigarette, and subsequent development of a smoking habit. Smoking is indeed found less likely in individuals with these variants and, for those who do smoke, quantities reported are lower[2]. Also, through its metabolism of other toxins, variants of CYP2A6 may drive the response to other drugs including alcohol and cannabis.

In addition, two genes contained in the ALSPAC genotyping archive which link to dopamine and serotonin transmitters are

SLC6A4 (5HTT) and MAOA. Variants in these genes lead to differential signals of pleasure upon consuming drugs, which again may drive the early stage addiction and dependence to the drugs.

At ages 14 and 16 questionnaires recorded the age ALSPAC children first smoked, drank an alcoholic drink and took drugs, the intensity with which they consumed them and records how the drugs affected them. For example, there is information on whether they felt ill after smoking. We will explore whether the reaction to the first experience of a drug differs by genotype.

The confounding variables are grouped into several categories. We will control for family smoking habits through the history of maternal and partner's reported smoking status. This will be important to the extent that children mimic the smoking behaviour of their parents. Additionally, as smoking behaviour is non-random across socio-economic groups we will control for education and occupation of parents. It is a concern that smoking behaviour is indicative of discount rates, whereby individuals with high discount rates place little weight on future periods relative to the present. To control for this, we will utilise the variables on diet, fitness and gambling.

[1]Hughes et al (1984), Ingelman-Sundberg, Nakajima M, Yamamoto T, Nunoya K, et al.(1996), Messina ES et al (1997), Benowitz NL, Jacob P III (1994).

[2] Schoedel et al (2004).