Relationship between cigarette smoking and abdominal obesity

Background: Although smokers tend to have a lower body-mass index (BMI) than non-smokers, smoking may affect body fat (BF) distribution. Some studies have assessed the association between smoking, BMI and waist circumference (WC), but, to our knowledge, no population-based studies assessed the relation between smoking and BF composition. We assessed the association between amount of cigarette smoking, BMI, WC and BF composition. Method: Data was analysed from a cross-sectional population-based study including 6'187 Caucasians aged 32-76 and living in Switzerland. Height, weight and WC were measured. BF, expressed in percent of total body weight, was measured by electrical bioimpedance. Abdominal obesity was defined as a WC 0102 cm for men and 088 cm for women and normal WC as <94 cm for men and <80 cm for women. In men, excess BF was defined as %BF 028.1, 28.7, 30.6 and 32.6 for age groups 32-44, 45-54, 55-64 and 65-76, respectively; the corresponding values for women were 35.9, 36.5, 40.5 and 44.4. Cigarette smoking was assessed using a self-reported questionnaire. Results: 29.3% of men and 25.0% of women were smokers. Prevalence of obesity, abdominal obesity, and excess of BF was 16.9% and 26.6% and 14.2% in men and 15.0%, 33.0% and 27.5% in women, respectively. Smokers had lower age-adjusted mean WC and percent of BF compared to non-smokers. However, among smokers, mean age-adjusted WC and BF increased with the number of cigarettes smoked per day: among light (1-10 cig/day), moderate (11-20) and heavy smokers (>20), mean ± SE %BF was 22.4 ± 0.3, 23.1 ± 0.3 and 23.5 ± 0.4 for men, and 31.9 ± 0.3, 32.6 ± 0.3 and 32.9 ± 0.4 for women, respectively. Mean WC was 92.9 ± 0.6, 94.0 ± 0.5 and 96.0 ± 0.6 cm for men, and 80.2 ± 0.5, 81.3 ± 0.5 and 83.3 ± 0.7 for women, respectively. Compared with light smokers, the age-adjusted odds ratio (95% Confidence Interval) for excess of BF was 1.04 (0.58 to 1.85) for moderate smokers and 1.06 (0.57 to 1.99) for heavy smokers in men (p-trend = 0.9), and 1.35 (0.92 to 1.99) and 2.26 (1.38 to 3.72), respectively, in women (p-trend = 0.04). Odds ratio for abdominal obesity vs. normal WC was 1.32 (0.81 to 2.15) for moderate smokers and 1.95 (1.16 to 3.27) for heavy smokers in men (p-trend <0.01), and 1.15 (0.79 to 1.69) and 2.36 (1.41 to 3.93) in women (p-trend = 0.03). Conclusion: WC and BF were positively and dose-dependently associated with the number of cigarettes smoked per day in women, whereas only WC was dose dependently and significantly associated with the amount of cigarettes smoked per day in men. This suggests that heavy smokers, especially women, are more likely to have an excess of BF and to accumulate BF in the abdomen compared to lighter smokers.

Cholestérol, pression artérielle et fumée de cigarette dans la population en Suisse: le projet MONICA. [Cholesterol, blood-pressure and cigarette-smoking in switzerland - the MONICA-project].

Elevated plasma cholesterol, high blood pressure and cigarette smoking are three major risk factors for coronary heart disease. Within the framework of Switzerland's participation in the multicenter study MONICA (MONItoring of trends and determinants in CArdiovascular disease), proposed by the WHO, a first risk factor survey was conducted in a representative sample of the population (25-74 years) of two reporting units (cantons of Vaud and Fribourg, canton of Tessin). A high blood cholesterol level (>6,7 mmol/l) is the most common risk factor for coronary heart disease among the studied population. Among men, about 13% have elevated blood pressure, the proportion being about one in ten among women; these proportions increase with age and are slightly above these values in Tessin. Cigarette smoking is still a common behavior; between 25 and 45 years one third of the population (male and female) regularly smoke cigarettes.

Clinical and pharmacogenetic study on smoking and smoking cessation

Currently, smoking cessation represents one of the main strategies to reduce the incidence of tobacco-related diseases in the population. Smoking can also influence pharmacotherapy through several pharmacokinetic or pharmacodynamic interactions. Some of the most concerned drugs are those metabolized by the cytochrome P450 (CYP) 1A2 enzyme (e.g. caffeine, theophylline, clozapine, olanzapine, duloxetine), whose activity is induced by the polycyclic aromatic hydrocarbons found in tobacco smoke. This can result in a clinically significant decrease in the pharmacological effect of the drugs and the need of higher doses in smokers. Conversely, upon smoking cessation, toxic plasma levels of the drugs can be reached. The main objective of this thesis was to study the interindividual variability in CYP1A2 induction in a large cohort of smokers, by measuring CYP1A2 activity before smoking cessation and one month later in continuously abstinent subjects. For this purpose, a clinical study was conducted, including 194 smokers from the general population who wished to participate in a smoking cessation program and therefore received medical counseling and substitution therapy (nicotine or varenicline). An analytical method for the simultaneous quantification of nicotine, its metabolites and varenicline in plasma was developed and validated using ultra performance liquid chromatography coupled with tandem mass spectrometry. This method was used to confirm abstinence at different time points during the follow-up. Moreover, it was used to determine plasma levels of the smoking cessation drugs, to be used in the study of their pharmacogenetics, which was the secondary objective of this thesis. High interindividual variability in CYP1A2 induction by smoking was observed, ranging from no change to approximately 7 times decreased CYP1A2 activity after smoking cessation. Several clinical and genetic factors were investigated in an attempt to explain this variability. Firstly, a significant influence of CYP1A2*1F and *1D alleles, of contraceptive use and of the number of cigarettes smoked per day on CYP1A2 induced activity was observed, and of CYP1A2*1F and the use of contraceptives on the basal activity. But no influence of these factors was found on CYP1A2 inducibility. Given that known genetic polymorphisms in CYP1A2 gene were shown to explain only poorly the observed variations in activity, additional genetic factors were studied. SNPs in the CYP oxidoreductase (POR) gene were found to influence CYP1A2 basal activity, but not the induction. Finally, a pathway-based approach allowed to identify SNPs in genes coding for nuclear receptors (CAR, RXRa, VDR, PXR) and induction-mediating receptors (AhR), which significantly influenced CYP1A2 inducibility and basal activity (SNPs in the gene coding for CAR and RXRa). As secondary objective of the study, the pharmacogenetics of nicotine and varenicline is being investigated. Therefore, the nicotine metabolite ratio is used in the attempt to better explain nicotine dependence and the failure/success of quitting smoking. A population pharmacokinetic model is being developed for varenicline, integrating clinical and genetic factors (genes coding for its metabolizing enzymes and transporters), with the purpose of trying to predict efficacy and side effects. These findings suggest that the influence of smoking on pharmacotherapy could be better managed by including clinical and possibly in the future genetic factors, in the assessment of the adaptations needed when a person starts or stops smoking.  - L'arrêt du tabac représente une des principales stratégies pour diminuer l'incidence des maladies causées par celui-ci. Le tabagisme peut influencer la thérapie médicamenteuse par des interactions pharmacocinétiques ou pharmacodynamiques. Parmi les médicaments concernés, il y a ceux métabolisés par le cytochrome P450 (CYP) 1A2 (caféine, théophylline, clozapine, olanzapine, duloxétine, etc), dont l'activité enzymatique est induite par les hydrocarbures aromatiques polycycliques présents dans la fumée de cigarette. Ceci peut se traduire par une diminution de l'effet pharmacologique du traitement et la nécessité d'augmenter les doses d'entretien chez les fumeurs. Au contraire, à l'arrêt de la cigarette, les taux plasmatiques des médicaments peuvent devenir toxiques. L'objectif principal de cette thèse était d'étudier la variabilité interindividuelle dans l'induction du CYP1A2 dans une large cohorte de fumeurs, par la mesure de l'activité du CYP1A2 avant l'arrêt de la cigarette, ainsi qu'un mois après chez les sujets abstinents. Pour ce faire, une étude clinique a été conduite, incluant 194 fumeurs de la population générale dans un programme d'arrêt du tabac offrant des consultations spécifiques et un traitement pharmacologique (nicotine ou varénicline). Une méthode analytique pour la quantification simultanée de la nicotine, ses métabolites et la varénicline dans le plasma par chromatographie liquide couplée à la spectrométrie de masse en tandem à été développée et validée. Cette méthode a été utilisée pour confirmer l'abstinence pendant l'étude et déterminer les taux plasmatiques des médicaments, dans le but d'étudier leur pharmacogénétique. Une grande variabilité interindividuelle dans l'induction du CYP1A2 par la fumée a été observée, parfois sans changement et pouvant aller jusqu'à une diminution d'environ 7 fois l'activité du CYP1A2 après l'arrêt de la cigarette. Plusieurs facteurs cliniques et génétiques ont été étudiés pour essayer d'expliquer cette variabilité. Tout d'abord, on a observé une influence significative: des allèles CYP1A2*1F et *1D, des contraceptifs et du nombre de cigarettes fumées par jour sur l'activité induite du CYP1A2, ainsi que l'influence de l'allèle *1F et des contraceptifs sur l'activité basale. Cependant, aucune influence de ces facteurs n'a été démontrée sur l'inductibilité du CYP1A2. Étant donné que les polymorphismes génétiques du CYP1A2 apportent peu de renseignements sur la variabilité de son activité, des facteurs génétiques supplémentaires ont été étudiés. Des polymorphismes dans le gène POR (CYP oxidoreductase) ont été associés à l'activité basale du CYP1A2, mais pas à l'induction. Finalement, une approche basée sur la voie de signalisation du CYP1A2 a permis d'identifier des polymorphismes dans des gènes codant pour des récepteurs nucléaires (CAR, RXRa, VDR, PXR) et d'autres liés à l'induction (AhR) qui influencent significativement l'inductibilité et l'activité basale (les SNPs du CAR et RXRa). L'objectif secondaire de cette étude était d'investiguer la pharmacogénétique de la nicotine et de la varénicline. Le ratio métabolique de la nicotine est utilisé pour mieux expliquer la dépendance à la nicotine et le succès/échec de l'arrêt de la cigarette. Un modèle pharmacocinétique de population est en cours de développement pour la varénicline, intégrant des facteurs cliniques et génétiques (gènes codant pour ses enzymes de métabolisme et transporteurs), pour tenter de prédire son efficacité et ses effets secondaires. Les résultats de cette thèse suggèrent que l'influence du tabagisme sur la pharmacothérapie serait mieux gérée par l'inclusion des facteurs cliniques et peut-être, dans le futur, génétiques, dans l'évaluation des adaptations nécessaires lorsqu'une personne fume ou arrête de fumer.  - l'arrêt du tabac représente une des principales stratégies pour diminuer l'incidence des maladies causées par celui-ci dans la population. Le tabagisme peut influencer les traitements médicamenteux, soit en modifiant leur élimination par l'organisme, soit en agissant sur leur mode d'action. Parmi les médicaments les plus concernés, on retrouve par exemple: la caféine, la théophylline, la clozapine, l'olanzapine, la duloxétine, dont l'élimination est accélérée par la fumée de cigarette (induction enzymatique). Ceci peut se traduire par une diminution de l'effet du traitement et la nécessité d'en augmenter les doses chez les fumeurs. Au contraire, à l'arrêt de la cigarette, on observe un ralentissement de la fonction enzymatique, qui a pour conséquence une augmentation du taux de médicament dans le sang, pouvant devenir toxique. L'objectif principal de cette thèse était d'étudier comment cette induction par le tabac varie dans une population de fumeurs, par la mesure de l'activité de l'enzyme avant l'arrêt de la cigarette, ainsi qu'un mois après chez les sujets abstinents. Pour ce faire, une étude clinique a été conduite, incluant 194 fumeurs de la population générale dans un programme d'arrêt du tabac offrant des consultations spécifiques et un traitement médicamenteux (nicotine ou varénicline). Une méthode analytique a été mise au point pour mesurer la quantité de nicotine, de ses produits de dégradation et de la varénicline dans le sang des participants à l'étude. De plus, cette méthode a été utilisée pour confirmer l'abstinence pendant l'étude. Une grande variabilité interindividuelle a été observée dans l'induction de l'enzyme par la fumée; il en résulte aucun changement d'activité chez certains sujets après l'arrêt de la cigarette, alors que pour d'autres elle peut être diminuée jusqu'à 7 fois. Plusieurs facteurs cliniques et génétiques ont été étudiés pour essayer d'expliquer cette variabilité. Premièrement, une influence sur l'activité de l'enzyme a été observée pour les contraceptifs hormonaux et le nombre de cigarettes fumées par jour, ainsi que pour certaines variations génétiques dans le gène codant pour l'enzyme d'intérêt, mais il η y a pas eu d'influence sur l'induction. Par la suite, des variations génétiques dans d'autres gènes influençant le fonctionnement de l'enzyme ont été associées soit avec son activité, soit avec son induction par le tabac. Finalement, l'étude propose également d'investiguer si le métabolisme de la nicotine a une influence sur la dépendance, les symptômes de sevrage et le succès/échec de l'arrêt de la cigarette. Des variations génétiques dans les gènes du métabolisme de la varénicline sont également étudiées en lien avec les quantités de varénicline mesurées dans le sang ainsi que les effets du médicament. Ceci permettra peut-être de prédire son efficacité et ses effets secondaires. Les résultats de cette thèse suggèrent que l'influence du tabagisme sur la thérapie médicamenteuse serait mieux gérée en tenant compte des facteurs cliniques et peut-être, dans le futur, de la génétique dans l'adaptation des traitements, que la personne soit fumeuse ou en phase d'arrêt.

A systematic review of longitudinal population-based studies on the predictors of smoking cessation in adolescent and young adult smokers

Le tabagisme est responsable de plus de 5 million de décès par an à travers le monde. En Suisse (2010), la prévalence de fumeurs chez les 14-19 ans était de 22% et la prévalence d'ex-fumeurs de 3%, taux qui reste relativement stable au fil des dernières années. La plupart des jeunes fumeurs désirant arrêter de fumer rencontrent des difficultés pour y parvenir. Les revues empiriques ont conclu que les programmes ayant pour but l'arrêt du tabagisme chez les jeunes ont une efficacité limitée. Afin de fournir une base solide de connaissances pour les programmes d'interventions contre le tabagisme, les déterminants de l'auto-cessation ont besoin d'être compris. Nous avons systématiquement recherché dans PUBMED et EMBASE des études longitudinales, basées sur la population, portant sur les déterminants de l'auto-cessation chez des adolescents et des jeunes adultes fumeurs. Nous avons passé en revue 4'502 titres et 871 abstracts, tous examinés indépendamment par deux et trois examinateurs, respectivement. Les critères d'inclusion étant : articles publiés entre janvier 1984 et août 2010, concernant les jeunes entre 10 et 29 ans et avoir une définition de cessation de fumer d'au moins 6 mois. Neuf articles ont été retenus pour une analyse détaillée. Les données suivantes ont été extraites de chaque article : le lieu de l'étude, la période étudiée, la durée du suivi, le nombre de collecte de données, la taille de l'échantillon, l'âge ou l'année scolaire des participants, le nombre de participants qui arrêtent de fumer, le status tabagique lors de la première collecte, la définition de cessation, les co-variantes et la méthode analytique. Le nombre d'études qui montrent une association significativement significative entre un déterminant et l'arrêt du tabagisme a été tabulé à partir de toutes les études qui ont évalués ce déterminant. Trois des neufs articles retenus ont défini l'arrêt du tabagisme comme une abstinence de plus de 6 mois et les six autres comme 12 mois d'abstinence. Malgré l'hétérogénéité des méthodes utilisées, cinq facteurs principaux ressortent comme prédicteur de l'arrêt du tabagisme : 1) ne pas avoir d'amis qui fument, 2) ne pas avoir l'intention de continuer de fumer dans le futur, 3) résister à la pression sociale, 4) être âgé de plus de 18 ans lors de la première cigarette, et 5) avoir un avis négatif au sujet du tabagisme. D'autres facteurs sont significatifs mais ne sont évalués que dans peu d'articles. La littérature au sujet des prédicteurs de cessation chez les adolescents et les jeunes adultes est peu développée. Cependant, nous remarquons que les facteurs que nous avons mis en évidence ne dépendent pas que de l'individu, mais aussi de l'environnement. La prévention du tabagisme peut se centrer sur les bienfaits de l'arrêt (p.ex., par rapport à l'asthme ou les performances sportives) et ainsi motiver les jeunes gens à songer d'arrêter de fumer. Une taxation plus lourde sur le prix des cigarettes peut être envisagée afin de retarder l'âge de la première cigarette. Les publicités anti-tabagiques (non sponsorisées par les entreprises de tabac) peuvent influencer la perception des jeunes par rapport au tabagisme, renforçant ou créant une attitude anti-tabagique. Les prochaines campagnes anti- tabac devraient donc tenir compte de ces différents aspects.

Dose-dependent positive association between cigarette smoking, abdominal obesity and body fat: cross-sectional data from a population-based survey.

ABSTRACT: BACKGROUND: Although smokers tend to have a lower body-mass index than non-smokers, smoking may favour abdominal body fat accumulation. To our knowledge, no population-based studies have assessed the relationship between smoking and body fat composition. We assessed the association between cigarette smoking and waist circumference, body fat, and body-mass index. METHODS: Height, weight, and waist circumference were measured among 6,123 Caucasians (ages 35-75) from a cross-sectional population-based study in Switzerland. Abdominal obesity was defined as waist circumference>=102 cm for men and >=88 cm for women. Body fat (percent total body weight) was measured by electrical bioimpedance. Age- and sex-specific body fat cut-offs were used to define excess body fat. Cigarettes smoked per day were assessed by self-administered questionnaire. Age-adjusted means and odds ratios were calculated using linear and logistic regression. RESULTS: Current smokers (29% of men and 24% of women) had lower mean waist circumference, body fat percentage, and body-mass index compared with non-smokers. Age-adjusted mean waist circumference and body fat increased with cigarettes smoked per day among smokers. The association between cigarettes smoked per day and body-mass index was non-significant. Compared with light smokers, the adjusted odds ratio (OR) for abdominal obesity in men was 1.28 (0.78-2.10) for moderate smokers and 1.94 (1.15-3.27) for heavy smokers (P=0.03 for trend), and 1.07 (0.72-1.58) and 2.15 (1.26-3.64) in female moderate and heavy smokers, respectively (P<0.01 for trend). Compared with light smokers, the OR for excess body fat in men was 1.05 (95% CI: 0.58-1.92) for moderate smokers and 1.15 (0.60-2.20) for heavy smokers (P=0.75 for trend) and 1.34 (0.89-2.00) and 2.11 (1.25-3.57), respectively in women (P=0.07 for trend). CONCLUSION: Among smokers, cigarettes smoked per day were positively associated with central fat accumulation, particularly in women.

Predicting smoking cessation and its relapse in HIV-infected patients: the Swiss HIV Cohort Study.

OBJECTIVES: The aim of the study was to assess whether prospective follow-up data within the Swiss HIV Cohort Study can be used to predict patients who stop smoking; or among smokers who stop, those who start smoking again. METHODS: We built prediction models first using clinical reasoning ('clinical models') and then by selecting from numerous candidate predictors using advanced statistical methods ('statistical models'). Our clinical models were based on literature that suggests that motivation drives smoking cessation, while dependence drives relapse in those attempting to stop. Our statistical models were based on automatic variable selection using additive logistic regression with component-wise gradient boosting. RESULTS: Of 4833 smokers, 26% stopped smoking, at least temporarily; because among those who stopped, 48% started smoking again. The predictive performance of our clinical and statistical models was modest. A basic clinical model for cessation, with patients classified into three motivational groups, was nearly as discriminatory as a constrained statistical model with just the most important predictors (the ratio of nonsmoking visits to total visits, alcohol or drug dependence, psychiatric comorbidities, recent hospitalization and age). A basic clinical model for relapse, based on the maximum number of cigarettes per day prior to stopping, was not as discriminatory as a constrained statistical model with just the ratio of nonsmoking visits to total visits. CONCLUSIONS: Predicting smoking cessation and relapse is difficult, so that simple models are nearly as discriminatory as complex ones. Patients with a history of attempting to stop and those known to have stopped recently are the best candidates for an intervention.

Adolescent's suicide attempts: populations at risk, vulnerability, and substance use.

Adolescence corresponds to a transition period that requires adaptation and change capacities and skills. Most young people succeed with this challenge, whereas a minority fail. In order to identify with the teenage culture, become autonomous, and differentiate from their parents, some adolescents choose to use drugs, beginning with the use of cigarettes, alcohol, cannabis, followed by other illicit drugs such as opiates and stimulants. A high proportion of these adolescents attempt suicide, which is the primary cause of death during adolescence in many European countries. Who are the "vulnerable" adolescents? What are the mechanisms that can explain the varieties of drug-use initiation or suicide attempts? Can "protective factors" be identified? What kind of strategies might be developed at a social and political level in order to prevent or to minimize drug abuse and suicide attempts, among other harmful behaviors? These issues will be discussed on the basis of the recent literature and in the light of a recent study carried out in the French-speaking part of Switzerland on large cohorts of adolescent drug users. Unresolved critical issues are noted and future needed research is suggested.

Increased 24-hour energy expenditure in cigarette smokers.

We studied the effect of smoking on energy expenditure in eight healthy cigarette smokers who spent 24 hours in a metabolic chamber on two occasions, once without smoking and once while smoking 24 cigarettes per day. Diet and physical exercise (30 minutes of treadmill walking) were standardized on both occasions. Physical activity in the chamber was measured by use of a radar system. Smoking caused an increase in total 24-hour energy expenditure (from a mean value [+/- SEM] of 2230 +/- 115 to 2445 +/- 120 kcal per 24 hours; P less than 0.001), although no changes were observed in physical activity or mean basal metabolic rate (1545 +/- 80 vs. 1570 +/- 70 kcal per 24 hours). During the smoking period, the mean diurnal urinary excretion of norepinephrine (+/- SEM) increased from 1.25 +/- 0.14 to 1.82 +/- 0.28 micrograms per hour (P less than 0.025), and mean nocturnal excretion increased from 0.73 +/- 0.07 to 0.91 +/- 0.08 micrograms per hour (P less than 0.001). These short-term observations demonstrate that cigarette smoking increases 24-hour energy expenditure by approximately 10 percent, and that this effect may be mediated in part by the sympathetic nervous system. The findings also indicate that energy expenditure can be expected to decrease when people stop smoking, thereby favoring the gain in body weight that often accompanies the cessation of smoking.

IPH response to Department of Health (UK) Standardised Packaging of Tobacco Products

Enhanced tobacco control policies and programmes are an important component of any strategic approach to improving population health and tackling health inequalities. The consultation on standardised packaging of tobacco products in the UK is particularly timely in view of the recent publication of the Ten Year Tobacco Strategy for Northern Ireland (DHSSPS, 2012). In this strategy the Department expressed its support for the introduction of further measures to reduce the influence of tobacco advertising and promotion upon children e.g. the introduction of plain packaging for cigarettes and hand rolling tobacco.  IPH key points •    The extent of tobacco-related harm across the island of Ireland and across the UK is unacceptable. Increasingly comprehensive and effective tobacco-control interventions are required. •    IPH recommends the adoption of option 2: require standardised packaging of tobacco products. •    IPH acknowledges that as plain packaging has not yet been introduced in any country, it is not possible at this time to accurately forecast the extent and nature of this intervention on population level health outcomes in the UK context. •    The proposed approach appears comprehensive in addressing the direct and indirect ways in which elements of tobacco packaging can promote brand appeal and can portray impressions in respect of tobacco-related harm. Consideration should be given to include specific provisions relating to roll-your-own (RYO) tobacco packaging. Any approach needs to be regularly reviewed to take into account attempts to bypass restrictions and evaluate responses in respect of consumer choices. •    IPH considers that the introduction of plain packaging has the potential to support the achievement of the goals set out in the Ten Year Tobacco Control Strategy for Northern Ireland ( DHSSPS, 2012). •    Among children in Northern Ireland who reported trying their first cigarette, around one quarter were aged 11 or under and three quarters were 14 or under when they did so (DHSSPS, 2012).  The very young age of these children is concerning on many levels including their susceptibility to sophisticated branding and marketing techniques linked to tobacco packaging.

Address by Michea¡l Martin to the Conference - Legislating for Tobacco Free Society

Thank you Chairman I would like to extend a warm welcome to our keynote speakers, David Byrne of the European Commission, Derek Yach from the World Health Organisation, and Paul Quinn representing Congressman Marty Meehan who sends his apologies. When we include the speakers who will address later sessions, this is, undoubtedly, one of the strongest teams that have been assembled on tobacco control in Europe. The very strength of the team underlines what I see as a shift – a very necessary shift – in the way we perceive the tobacco issue. For the last twenty years, we have lived out a paradox. It isn´t a social side issue. I make no apology for the bluntness of what I´m saying, and will come back, a little later, to the radicalism I believe we need to bring – nationally – to this issue. For starters, though, I want to lay it on the line that what we´re talking about is an epidemic as deadly as any suffered by human kind throughout the centuries. Slower than some of those epidemics in its lethal action, perhaps. But an epidemic, nonetheless. According to the World Health Organisation tobacco accounted for just over 3 million annual deaths in 1990, rising to 4.023 million annual deaths in 1998. The numbers of deaths due to tobacco will rise to 8.4 million in 2020 and reach roughly 10 million annually by 2030. This is quite simply ghastly. Tobacco kills. It kills in many different ways. It kills increasing numbers of women. It does its damage directly and indirectly. For children, much of the damage comes from smoking by adults where children live, study, play and work. The very least we should be able to offer every child is breathable air. Air that doesn´t do them damage. We´re now seeing a global public health response to the tobacco epidemic. The Tobacco Free Initiative launched by the World Health Organisation was matched by significant tobacco control initiatives throughout the world. During this conference we will hear about the experiences our speakers had in driving these initiatives. This Tobacco Free Initiative poses unique challenges to our legal frameworks at both national and international levels; in particular it raises challenges about the legal context in which tobacco products are traded and asks questions about the impact of commercial speech especially on children, and the extent of the limitations that should be imposed on it. Politicians, supported by economists and lawyers as well as the medical profession, must continue to explore and develop this context to find innovative ways to wrap public health considerations around the trade in tobacco products – very tightly. We also have the right to demand a totally new paradigm from the tobacco industry. Bluntly, the tobacco industry plays the PR game at its cynical worst. The industry sells its products without regard to the harm these products cause. At the same time, to gain social acceptance, it gives donations, endowments and patronage to high profile events and people. Not good enough. This model of behaviour is no longer acceptable in a modern society. We need one where the industry integrates social responsibility and accountability into its day-to-day activities. We have waited for this change in behaviour from the tobacco industry for many decades. Unfortunately the documents disclosed during litigation in the USA and from other sources make very depressing reading; it is clear from them that any trust society placed in the tobacco industry in the past to address the health problems associated with its products was misplaced. This industry appears to lack the necessary leadership to guide it towards just and responsible action. Instead, it chooses evasion, deception and at times illegal activity to protect its profits at any price and to avoid its responsibilities to society and its customers. It has engaged in elaborate ´spin´ to generate political tolerance, scientific uncertainty and public acceptance of its products. Legislators must act now. I see no reason why the global community should continue to wait. Effective legal controls must be laid on this errant industry. We should also keep these controls under review at regular intervals and if they are failing to achieve the desired outcomes we should be prepared to amend them. In Ireland, as Minister for Health and Children, I launched a comprehensive tobacco control policy entitled “Towards a Tobacco Free Society“. OTT?Excessive?Unrealistic? On the contrary – I believe it to be imperative and inevitable. I honestly hold that, given the range of fatal diseases caused by tobacco use we have little alternative but to pursue the clear objective of creating a tobacco free society. Aiming at a tobacco free society means ensuring public and political opinion are properly informed. It requires help to be given to smokers to break the addiction. It demands that people are protected against environmental tobacco smoke and children are protected from any inducement to experiment with this product. Over the past year we have implemented a number of measures which will support these objectives; we have established an independent Office of Tobacco Control, we have introduced free nicotine replacement therapy for low-income earners, we have extended our existing prohibitions on tobacco advertising to the print media with some minor derogations for international publications. We have raised the legal age at which a person can be sold tobacco products to eighteen years. We have invested substantially more funds in health promotion activities and we have mounted sustained information campaigns. We have engaged in sponsorship arrangements, which are new and innovative for public bodies. I have provided health boards with additional resources to let them mount a sustained inspection and enforcement service. Health boards will engage new Directors of Tobacco Control responsible for coordinating each health board´s response and for liasing with the Tobacco Control Agency I set up earlier this year. Most recently, I have published a comprehensive Bill – The Public Health (Tobacco) Bill, 2001. This Bill will, among other things, end all forms of product display and in-store advertising and will require all retailers to register with the new Tobacco Control Agency. Ten packs of cigarettes will be banned and transparent and independent testing procedures of tobacco products will be introduced. Enforcement officers will be given all the necessary powers to ensure there is full compliance with the law. On smoking in public places we will extend the existing areas covered and it is proposed that I, as Minister for Health and Children, will have the powers to introduce further prohibitions in public places such as pubs and the work place. I will also provide for the establishment of a Tobacco Free Council to advise and assist on an ongoing basis. I believe the measures already introduced and those additional ones proposed in the Bill have widespread community support. In fact, you´re going to hear a detailed presentation from the MRBI which will amply illustrate the extent of this support. The great thing is that the support comes from smokers and non-smokers alike. Bottom line, Ladies and Gentlemen, is that we are at a watershed. As a society (if you´ll allow me to play with a popular phrase) we´ve realised it´s time to ´wake up and smell the cigarettes.´ Smell them. See them for what they are. And get real about destroying their hold on our people. The MRBI survey makes it clear that the single strongest weapon we have when it comes to preventing the habit among young people is price. Simple as that. Price. Up to now, the fear of inflation has been a real impediment to increasing taxes on tobacco. It sounds a serious, logical argument. Until you take it out and look at it a little more closely. Weigh it, as it were, in two hands. I believe – and I believe this with a great passion – that we must take cigarettes out of the equation we use when awarding wage increases. I am calling on IBEC and ICTU, on employers and trade unions alike, to move away from any kind of tolerance of a trade that is killing our citizens. At one point in industrial history, cigarettes were a staple of the workingman´s life. So it was legitimate to include them in the ´basket´ of goods that goes to make up the Consumer Price Index. It isn´t legitimate to include them any more. Today, I´m saying that society collectively must take the step to remove cigarettes from the basket of normality, from the list of elements which constitute necessary consumer spending. I´m saying: “We can no longer delude ourselves. We must exclude cigarettes from the considerations we address in central wage bargaining. We must price cigarettes out of the reach of the children those cigarettes will kill.” Right now, in the monthly Central Statistics Office reports on consumer spending, the figures include cigarettes. But – right down at the bottom of the page – there´s another figure. Calculated without including cigarettes. I believe that if we continue to use the first figure as our constant measure, it will be an indictment of us as legislators, as advocates for working people, as public health professionals. If, on the other hand, we move to the use of the second figure, we will be sending out a message of startling clarity to the nation. We will be saying “We don´t count an addictive, killer drug as part of normal consumer spending.” Taking cigarettes out of the basket used to determine the Consumer Price Index will take away the inflation argument. It will not be easy, in its implications for the social partners. But it is morally inescapable. We must do it. Because it will help us stop the killer that is tobacco. If we can do it, we will give so much extra strength to health educators and the new Tobacco Control Association. This new organisation of young people who already have branches in over fifteen counties, is represented here today. The young adults who make up its membership are well placed to advise children of the dangers of tobacco addiction in a way that older generations cannot. It would strengthen their hand if cigarettes move – in price terms – out of the easy reach of our children Finally, I would like to commend so many public health advocates who have shown professional and indeed personal courage in their commitment to this critical public health issue down through the years. We need you to continue to challenge and confront this grave public health problem and to repudiate the questionable science of the tobacco industry. The Research Institute for a Tobacco Free Society represents a new and dynamic form of partnership between government and civil society. It will provide an effective platform to engage and mobilise the many different professional and academic skills necessary to guide and challenge us. I wish the conference every success.

General Scheme of the Public Health (Standardised Packaging of Tobacco) Bill

The purposes of this Act are to : (a) reduce the appeal of tobacco and tobacco products, (b) increase the effectiveness of health warnings on tobacco products, and (c)reduce the ability of the packaging of tobacco and tobacco products to mislead consumers about the harmful effects of smoking in the public interest,by providing for the standardisation of the labelling and physical features of retailpackaging of tobacco products and the requirements for the appearance of cigarettes. Click here to download PDF 125KB Read the Reports of the Joint Committee on Health and Children – General Scheme of the Public Health (Standardised Packaging of Tobacco) Bill 2013 here  

Simple steps to a healthy heart

The number of deaths from coronary heart disease in Northern Ireland has dropped significantly, according to recent figures. However, the Public Health Agency is urging everyone to take steps to protect their heart and reduce their chances of developing the disease during National Heart Month (February).Despite the number of deaths dropping significantly in recent years, coronary heart disease is still the number one killer across the country. Over 2,200 people died in Northern Ireland from coronary heart disease in 2010 compared to just over 2,300 people in 2009 - an overall reduction of 100 province-wide. The latest figure reveals the positive downward trend is continuing - in 2008, there were 2,410 deaths, 2,493 in 2007 and 2,554 in 2006, while in 1979 there were nearly 5,000 deaths. Throughout National Heart Month in February, the PHA is calling for people to follow a number of steps in a bid to reduce their chances of developing the disease.Smoking is a major risk factor and, the more cigarettes you smoke, the higher the risk, according to Dr Christine McMaster, Consultant in Public Health Medicine, with responsibility for cardiovascular disease in the PHA."The reduction in smoking over the past number of years through public education, stop smoking programmes and smoke free legislation has had a major impact on reducing deaths from heart disease. However, 24% of the population in Northern Ireland still smoke, putting them at risk of developing the disease."People who suffer from high blood pressure also run an increased risk of developing coronary heart disease. High blood pressure is a silent, but treatable condition. In order to minimise the risk, I would urge everyone over the age of 45 to have their blood pressure measured every five years by their GP," said Dr McMaster.Simple lifestyle changes will also reduce the risk of heart disease, including eating at least five servings of fruit and vegetables a day, avoiding saturated fats, limiting alcohol intake and taking at least 30 minutes of exercise a day, five days a week.Dr McMaster described the reduction in deaths from coronary heart disease over the past few years as "a big success story". "It shows that people can take very positive steps to reduce their risk of heart disease by getting their blood pressure checked and adopting a healthier lifestyle; in particular by not smoking," he added. "The message is clear during National Heart Month - you only have one heart and you can take steps to keep it healthy."

Mental health and growing up factsheet. Cannabis and mental health: information for young people.

About this leaflet This is one in a series of leaflets for parents, teachers and young people entitled Mental Health and Growing Up. These leaflets aim to provide practical, up-to-date information about mental health problems (emotional, behavioural and psychiatric disorders) that can affect children and young people. This leaflet gives you some basic facts about cannabis and also how it might affect your mental health. Introduction Lots of young people want to know about drugs. Often, people around you are taking them, and you may wonder how it will make you feel. You may even feel under pressure to use drugs in order to fit in, or be â?~coolâ?T. You may have heard that cannabis is no worse than cigarettes, or that it is harmless. What is cannabis? The cannabis plant is a member of the nettle family that has grown wild throughout the world for centuries. People have used it for lots of reasons, other than the popular relaxing effect. It comes in two main forms: ï,§ resin, which is a brown black lump also known as bhang, ganja or hashish ï,§ herbal cannabis, which is made up of the dried leaves and flowering tops, and is known as grass, marijuana, spliff, weed, etc. Skunk cannabis is made from a cannabis plant that has more active chemicals in it (THC), and the effect on your brain is stronger. Because â?~streetâ?T cannabis varies so much in strength, you will not be able to tell exactly how it will make you feel at any particular time. What does it do to you? When you smoke cannabis, the active compounds reach your brain quickly through your bloodstream. It then binds/sticks to a special receptor in your brain. This causes your nerve cells to release different chemicals, and causes the effects that you feel. These effects can be enjoyable or unpleasant. Often the bad effects take longer to appear than the pleasant ones. ï,§ Good/pleasant effects: You may feel relaxed and talkative, and colours or music may seem more intense. ï,§ Unpleasant effects: Feeling sick/panicky, feeling paranoid or hearing voices, feeling depressed and unmotivated. Unfortunately, some people can find cannabis addictive and so have trouble stopping use even when they are not enjoying it. The effects on your mental health Using cannabis triggers mental health problems in people who seemed to be well before, or it can worsen any mental health problems you already have. Research has shown that people who are already at risk of developing mental health problems are more likely to start showing symptoms of mental illness if they use cannabis regularly. For example if someone in your family has depression or schizophrenia, you are at higher risk of getting these illness when you use cannabis. The younger you are when you start using it, the more you may be at risk. This is because your brain is still developing and can be more easily damaged by the active chemicals in cannabis. If you stop using cannabis once you have started to show symptoms of mental illness, such as depression, paranoia or hearing voices, these symptoms may go away. However, not everyone will get better just by stopping smoking. If you go on using cannabis, the symptoms can get worse. It can also make any treatment that your doctor might prescribe for you, work less well. Your illness may come back more quickly, and more often if you continue to use cannabis once you get well again. Some people with mental health problems find that using cannabis makes them feel a bit better for a while. Unfortunately this does not last, and it does nothing to treat the illness. In fact, it may delay you from getting help you need and the illness may get worse in the longer term. [For the full factsheet, click on the link above]This resource was contributed by The National Documentation Centre on Drug Use.

Mental health and growing up factsheet. Drugs and alcohol - what parents need to know.

Information about drugs and alcohol - what parents need to know: information for parents, carers and anyone who works with young people. About this leaflet This is one in a series of leaflets for parents, teachers and young people entitled Mental Health and Growing Up. These leaflets aim to provide practical, up-to-date information about mental health problems (emotional, behavioural and psychiatric disorders) that can affect children and young people. This leaflet offers practical advice for parents, teachers and carers who are worried that a young person is misusing drugs or alcohol. Why do I need to know about a young person using drugs or alcohol? Many young people smoke, drink alcohol and may try drugs. It is important you are aware of this and do not ignore it as a time when they are just having fun or experimenting. It doesnââ,‰"¢t take much for the young people to soon lose control and to need help to recover from this problem. How common is it? By the age of 16, up to half of young people have tried an illegal drug. Young people are trying drugs earlier and more are drinking alcohol. What are the different types of drugs which cause problems? The most commonly used, readily available and strongly addictive drugs are tobacco and alcohol. There are numerous others that can be addictive. Alcohol and cannabis are sometimes seen as ââ,¬Ëogatewayââ,‰"¢ drugs that lead to the world of other drugs like cocaine and heroin. Drugs are also classed as ââ,¬Ëolegalââ,‰"¢ andââ,¬Ëoillegalââ,‰"¢. The obviously illegal drugs include cannabis (hash), speed (amphetamines), ecstasy (E), cocaine and heroin. Using ââ,¬Ëolegalââ,‰"¢ drugs (like cigarettes, alcohol, petrol, glue) does not mean they are safe or allowed to be misused. It just means they may be bought or sold for specific purposes and are limited to use by specific age groups. There are clear laws regarding alcohol and young people. For more detailed information on various drugs, their side-effects and the law, see ââ,¬ËoFurther Informationââ,‰"¢ at the end of the factsheet. Why do young people use drugs or alcohol? Young people may try or use drugs or alcohol for various reasons. They may do it for fun, because they are curious, or to be like their friends. Some are experimenting with the feeling of intoxication. Sometimes they use it to cope with difficult situations or feelings of worry and low mood. A young person is more likely to try or use drugs or alcohol if they hang out or stay with friends or family who use them. What can be the problems related to using drugs or alcohol? Drugs and alcohol can have different effects on different people. In young people especially the effects can be unpredictable and potentially dangerous. Even medications for sleep or painkillers can be addictive and harmful if not used the way they are prescribed by a doctor. Drugs and alcohol can damage health. Sharing needles or equipment can cause serious infections, such as HIV and hepatitis. Accidents, arguments and fights are more likely after drinking and drug use. Young people are more likely to engage in unprotected sex when using drugs. Using drugs can lead to serious mental illnesses, such as psychosis and depression. When does it become addiction or problem? It is very difficult to know when exactly using drugs or alcohol is more than just ââ,¬Ëocasualââ,‰"¢. Addiction becomes more obvious when the young person spends most of their time thinking about, looking for or using drugs. Drugs or alcohol then become the focus of the young personââ,‰"¢s life. They ignore their usual work, such as not doing their schoolwork, or stop doing their usual hobbies/sports such as dancing or football. How do I know if there is a problem or addiction? Occasional use can be very difficult to detect. If the young person is using on a regular basis, their behaviour often changes. Look for signs such as: ïâ?s§ unexplained moodiness ïâ?s§ behaviour that is ââ,¬Ëoout of character' ïâ?s§ loss of interest in school or friends ïâ?s§ unexplained loss of clothes or money ïâ?s§ unusual smells and items like silver foil, needle covers. Remember, the above changes can also mean other problems, such as depression, rather than using drugs. What do I do if I am worried? If you suspect young person is using drugs, remember some general rules. ïâ?s§ Pay attention to what the child is doing, including schoolwork, friends and leisure time. ïâ?s§ Learn about the effects of alcohol and drugs (see websites listed below). ïâ?s§ Listen to what the child says about alcohol and drugs, and talk about it with them. ïâ?s§ Encourage the young person to be informed and responsible about drugs and alcohol. ïâ?s§ Talk to other parents, friends or teachers about drugs - the facts and your fears and seek help. If someone in the family or close friend is using drugs or alcohol, it is important that they seek help too. It may be hard to expect the young person to give up, especially if a parent or carer is using it too. My child is abusing drugs. What do I do? ïâ?s§ If your child is using drugs or alcohol, seek help. ïâ?s§ Do stay calm and make sure of facts. ïâ?s§ Don't give up on them, get into long debates or arguments when they are drunk, stoned or high. ïâ?s§ Donââ,‰"¢t be angry or blame themââ,‰?othey need your help and trust to make journey of recovery. Where can I get help? You can talk in confidence to a professional like your GP or practice nurse, a local drug project or your local child and adolescent mental health. They can refer your child to relevant services and they will be able to offer you advice and support. You may also be able to seek help through a school nurse, teacher or social worker. You can find this information from your local area telephone book or council website, or ask for the address from your health centre. [For the full factsheet, click on the link above]This resource was contributed by The National Documentation Centre on Drug Use.

Building Evidence for Dementia Prevention

As was the case in 2010 when the National Institutes of Health issued a consensus statement on the prevention of Alzheimer’s and other dementias, there remains a lack of firm evidence for dementia prevention. Because of the difficulties in studying this phenomenon, no modifiable risk factors for dementia have been definitively established, and no pharmaceutical or nutritional supplements been proven to prevent Alzheimer’s disease or cognitive decline. However, longitudinal observational studies have identified several factors associated with dementia. A recent review article summarizes the current epidemiological evidence about Alzheimer’s and other dementias, and presents three ongoing large scale randomized control trials (RCTs) that focus on preventing dementia. The review argues that there is substantial evidence for many factors that, in combination, might reduce the risk of, or delay the onset of, dementia. Although no specific cure for dementia exists, and no specific pathway between risk factor and disease onset has been identified, several cardiovascular, stress, toxicity, and psychosocial variables have been repeatedly associated with dementia. Protective factors, such as high education, physical exercise, and not smoking cigarettes, have been identified as well. Intervention studies that account for these multiple factors may well identify strategies for preventing or delaying dementia. However, the protective effects and risk factors suggested by observational data have yet to be assessed in RCT research. The role of such factors in reducing or increasing the risk for dementia needs to be more specifically defined. Three ongoing RCT studies in Europe show promise in this area, as they target multiple risk and protective factors by promoting healthy lifestyle changes and medical treatment of vascular diseases. These are: FINGER, a Finnish trial involving 1,200 older adults at risk for dementia. This intervention features nutritional guidance, physical activity, cognitive and social engagement, and medical management of risk factors. Participants were involved in previous, intensive observational studies of vascular health and health behavior, so FINGER will provide a level of relevant information about its research subjects that is normally impossible for clinical RCTs to attain;MAPT, a multicenter study of 1,680 frail older adults in France. This study will compare the efficacy of omega-3 dietary supplementation with a multidomain training intervention that involves physical and cognitive training. The study will include follow-up assessments after five years;PreDIVA, a Dutch study of 3,534 community dwelling participants between 70 and 78 years old, recruited from primary care clinics. This study will compare standard medical care with a multicomponent vascular health intervention. The study will last for six years and measure both dementia and disability outcomes. These studies are an important step in dementia research, using earlier observational studies as the basis for rigorously assessed interventions. Although a cure for dementia has not been identified, this new research may identify preventive strategies against dementia. �� Source: Mangialasche F, Kivipelto M, et al. (2012). Dementia prevention: current epidemiological evidence and future perspective. Alzheimer’s Research and Therapy 4:6.