Professor Amanda Amos, Professor of Health Promotion, Centre for Population Health Sciences, University of Edinburgh

Preventing the uptake of smoking is a key element of tobacco control strategies across Europe. Smoking prevalence among young people is declining in many European countries. However in others, particularly in Central and Eastern Europe, rates among girls and young women are still increasing. Across Europe tobacco companies are developing new marketing strategies aimed at ensuring that young people continue to take up smoking, even in countries where there are restrictions on tobacco promotion.

This presentation will consider the opportunities for smoking prevention in Europe and some of the main challenges that need to be addressed. An overview will be given of current smoking patterns and trends in young people in Europe and what we know about what influences smoking uptake. Drawing on a review carried out for the British Department of Health, the presentation will outline the current evidence on the effectiveness of different types of smoking prevention interventions. New approaches that appear promising will be highlighted and gaps in the research evidence will be identified. The implications for tobacco control research, policy and practice will be discussed.

Dr Paul Aveyard

Current public health policies encourage smokers to worry about their continued smoking, encourage smokers to make abrupt attempts to stop smoking, and supporting these efforts when they do so. However, although most smokers are worried by their smoking and say they want to quit, relatively few are ready to stop smoking or try to do so. A much larger proportion of smokers try to control their smoking by reducing it. One view would be that encouraging smokers who feel that they cannot stop now to reduce their smoking would lead to improved population quit rates, because smokers who reduce are more likely to stop than those who take no action on their smoking. Another view, supported by US national guidelines, would be that this will divert smokers who would have quit abruptly to reduce smoking instead, and be happy with that state of affairs. In this lecture, I will look at the evidence that reduction could help two groups of smokers: smokers who are committed to stopping and smokers who have no immediate plans to quit. I will review the evidence on whether smoking reduction offers an effective route to cessation and the evidence and the evidence on the effectiveness of reduction methods. Among smokers with no immediate plans to quit, I will review the evidence that smoking reduction leads to cessation and the evidence on whether smoking reduction programmes divert smokers from the best (cessation) to a second best choice (reduction). I will also review the evidence on what is known about the efficacy of smoking reduction methods amongst this group of smokers.

John Britton

Around 30% of adults in living in the European Union – about 120 million people -- smoke tobacco, and represent a major current and future public health problem. Although the prevalence of smoking in the EU is falling slowly, trends in prevalence within individual countries differ substantially, as does the extent to which countries have introduced and implemented a wide range of tobacco control policies.

In this presentation I will review progress with a range of tobacco control policy initiatives in the EU, to identify priorities for future implementation, and to identify some priority areas for further research. Much of the evidence I will present will reflect work carried out by colleagues in the UK Centre for Tobacco Control Studies, on the measurement of prevalence in Europe, on pricing, point of sale promotion, smoke-free policy, health promotion and harm reduction. I will also explore some of the country characteristics that determine engagement with and success of tobacco control measures.

Caryn Lerman, Ph.D. University of Pennsylvania

The important goal of treating nicotine dependence can be realized by research that translates discoveries in basic neuroscience, pharmacology, genetics, and behavioral science to develop new treatment models that can be translated readily into the clinic and community. This presentation will review recent research aimed at elucidating the molecular, neural and behavioral basis of early nicotine abstinence symptoms that prompt smoking relapse, discuss efforts to translate these findings into improved and targeted pharmacotherapies for nicotine dependence treatment.

Jean-Pol Tassin, Directeur de Recherches Inserm, Université Paris VI

Tobacco is a potent reinforcing agent in humans, and nicotine is generally considered to be the major compound responsible for its addictive properties. However, animal experiments indicate some discrepancies between the effects of nicotine and those of other drugs of abuse. For example, the capacity of repeated nicotine to elevate dopamine levels in the nucleus accumbens is controversial and we have shown that repeated nicotine treatments in rats induce a behavioural sensitization which vanishes more quickly than that for other drugs of abuse. Furthermore, although psychostimulants and opiates induce a substantial locomotor hyperactivity both in rats and mice, nicotine is a weak locomotor stimulant in rats and generally fails to induce locomotor hyperactivity in mice at any dose. These differences could suggest that the addictive effects of tobacco are not only due to nicotine.

Actually, tobacco and tobacco smoke are known to contain monoamine oxidise inhibitors (MAOIs), such as harmane, norharmane or acetaldehyde. We have shown that MAOI pre-treatment allows the maintenance of behavioural sensitization to nicotine in rats, thus suggesting a role of MAOIs in the addictive properties of tobacco. More recently, tranylcypromine, a potent MAOI, was found to be able to trigger a locomotor response to nicotine in mice and nicotine self-administration in rats. Moreover, increases in extracellular 5-HT levels appeared to be crucial for these effects (Villegier et al., 2006).

Nicotine increases serotonergic neurons firing. However, this increased release of 5-HT -in absence of MAOI- is transient because of a retro-feedback inhibition on 5-HT1A autoreceptors. We have therefore proposed that MAOIs, because of their enhancing effects on extracellular 5-HT levels, compensate the consequences of the indirect inhibition of serotonergic cells by nicotine, thus suggesting a mechanism by which MAOI’s contained in tobacco smoke could act in synergy with nicotine to induce addiction (Tassin, 2008). Recent experiments using 5-HT1A agonists and antagonists have indicated that MAOIs contained in tobacco desensitize 5-HT1A autoreceptors to trigger the strong addictive properties of tobacco (Lanteri et al., 2009). In humans, nicotine replacement therapies are the most widely used form of pharmacological intervention, but seem to lack efficacy. Interestingly, most of tobacco smokers (> 80%) relapse after a few-week withdrawal, i.e. when inhibition of monoamine oxidises activity by tobacco and tobacco smoke is likely to have disappeared. MAOIs, or any compound able to desensitize 5-HT1A autoreceptors, may provide a more complete scheme of the addictive properties of tobacco in experimental models of reward.