Smoking and mental health - NCSCT

More documents

Recommendations

Info

Smoking and mental health 3.3.1 Evidence from genetic studies A study of a population-based sample of female twins born in Virginia, USA, which used a co-twin control design and bivariate twin model, 49 found that the best-fitting model indicated that lifetime smoking and major depression were substantially genetically correlated. No environmental correlation between smoking and depression was detected. Similarly, Korhonen and colleagues, 50 in a sample of Finnish twins, reported a moderate genetic correlation and a more modest non-shared environmental correlation that was not statistically significant. Interestingly, the genetic relationship between depression and tobacco dependence is often found to appear stronger than the relationship between depression and smoking, eg Lyons and colleagues 51 reported a modest genetic correlation between depression and regular tobacco use, but a strong correlation between depression and tobacco dependence in men. Another study also reported modest genetic correlations between regular tobacco use and depression but slightly higher correlations between depression and tobacco dependence. 52 Modest environmental correlations were detected for both smoking-related phenotypes. 52 Such studies suggest that, although liability to smoking initiation is largely independent of liability to depression – perhaps more a function of peer influences or externalising tendencies – once smoking has been initiated, an individual’s degree of dependence is related to his or her genetic liability to depression. Consequently, individuals with a history (or family history) of depression could establish higher levels of dependence, and might find smoking cessation more difficult than others. Although results vary between studies, most findings support the existence of modest-to-moderate genetic correlations between major depression (or depressive symptoms) and smoking and/or tobacco dependence. Molecular genetic studies can be designed to identify the genes within which variation contributes to liability to both phenotypes. Such genes might be related to personality constructs (eg locus of control, neuroticism), or to neural systems such as dopaminergic or glutamatergic neurotransmission, which are both involved in depression and the establishment or maintenance of tobacco dependence. 53 3.3.2 Evidence from animal studies Evidence that nicotine has antidepressant-like effects is available from a range of animal models including the forced swim test, 54,56 and in studies of rats with an inbred 57,58 or induced behavioural phenotype characteristic of depression. 59 Nicotine also attenuates the reduction in sucrose preference evoked by chronic exposure to an unpredictable mild stressor, 60 which is thought to reflect the development of anhedonia (a reduced ability to respond to a pleasurable 42 © Royal College of Physicians 2013
Neurobiological and behavioural mechanisms linking smoking and mental disorders 3 reward), a major symptom of depression. This evidence suggests that nicotine has antidepressant-like activity in experimental animal models, and that it may act preferentially in animals which are particularly susceptible to a depressionlike behavioural phenotype. 59 Nicotine injections also enhance the ability of the brain to respond to pleasurable stimuli or events, and this reward enhancement has been observed following both experimenter-administered 61 and self-administered 62,63 nicotine. In intracranial self-stimulation, a procedure in which animals are trained to perform a task that results in stimulation of small electrodes located in pathways within the brain that mediate reward, nicotine injections decrease the electrical current required to maintain responding, 64,65 whereas abrupt withdrawal of nicotine, after a period of chronic infusion, increases the current required. 3,5 The withdrawal-evoked increase in brain reward sensitivity induced by nicotine self-administration persists for many days. 66 These findings indicate that the antidepressant properties of nicotine may arise from its ability to enhance mood by altering the way in which it is influenced by positive and negative stimuli, and that nicotine withdrawal may exacerbate the influence of negative stimuli. If the administration of the drug is controlled by the individual, its reward-enhancing properties may be increased and prolonged and may, therefore, contribute significantly to the addictive properties of the drug. There is evidence that mesolimbic dopaminergic neurons play a pivotal role in tobacco dependence (see Balfour 15 for a review), and that anhedonia and depression are associated with reduced mesolimbic DA release. 67 Similar mechanisms are thought to contribute to the psychopathology of nicotine withdrawal. 68 Thus, it seems likely that increases in DA release evoked in the nucleus accumbens, the principal terminal field of the mesolimbic dopaminergic system, not only mediate the reinforcing properties of nicotine in general but also contribute specifically to the amelioration of anhedonia in depression. This hypothesis provides an explanation for the role of depression in tobacco dependence that has clear face validity. However, it hides a conundrum. Many depressed patients smoke heavily, in a way that is likely to generate blood nicotine levels which desensitise many of the neuronal nicotinic receptors in the brain and in turn mediate the effects of nicotine on DA release. 15,69 Thus, the hypothesis above does not provide a complete explanation for the mechanism through which tobacco smoke may serve as an antidepressant. In some of the forced swim test studies 56,58 nicotine was given either acutely or repeatedly as a subcutaneous injection, a route of administration that is likely to result in stimulation of neuronal nicotinic receptors. In other studies nicotine was given in drinking water 57 or by continuous subcutaneous infusion, 70 thus maintaining blood nicotine concentrations at a level that desensitises nicotinic receptors but, perhaps, models more closely the pattern of exposure experienced by heavy smokers. Interestingly, there is evidence that nicotinic receptor antagonists also demonstrate antidepressant-like activity in this test, 54 which © Royal College of Physicians 2013 43
Page 1 and 2:
PDF not for circulation Smoking and
Page 3 and 4:
Contents Members of the Tobacco Adv
Page 5 and 6: Contents 4.4.3 Attention deficit hy
Page 7 and 8: Contents 6.4.3 Staff knowledge 122
Page 9 and 10: Contents 10.5 Tobacco policy and me
Page 11 and 12: Contributors Anthony Aclet - Specia
Page 13 and 14: Contributors Jill Williams - Associ
Page 15 and 16: 1 Mental disorders 1.1 What is a me
Page 17 and 18: Mental disorders 1 1.3 Common menta
Page 19 and 20: Mental disorders 1 1.4.4 Somatisati
Page 21 and 22: Mental disorders 1 In addition to s
Page 23 and 24: Mental disorders 1 not diagnosed un
Page 25 and 26: Mental disorders 1 Similar to many
Page 27 and 28: Mental disorders 1 12 Chang CK, Hay
Page 29 and 30: Mental disorders 1 52 Young S, Toon
Page 31 and 32: Smoking among people with mental di
Page 53 and 54: Neurobiological and behavioural mec
Page 55: Neurobiological and behavioural mec
Page 77 and 78: Epidemiology of the association bet
Page 99 and 100: Smoking cessation interventions for
Page 107 and 108:
Smoking cessation interventions for
Page 109 and 110:
Page 111 and 112:
Page 113 and 114:
Page 115 and 116:
Page 117 and 118:
Page 119 and 120:
Page 121 and 122:
Page 123 and 124:
Page 125 and 126:
6 Population strategies to prevent
Page 127 and 128:
Population strategies to prevent sm
Page 129 and 130:
Page 131 and 132:
Page 133 and 134:
Page 135 and 136:
Page 137 and 138:
Page 139 and 140:
Page 141 and 142:
Page 143 and 144:
Page 145 and 146:
Smoking and mental disorders: speci
Page 147 and 148:
Page 149 and 150:
Page 151 and 152:
Page 153 and 154:
Page 155 and 156:
Page 157 and 158:
Page 159 and 160:
Page 161 and 162:
Page 163 and 164:
Page 165 and 166:
Page 167 and 168:
Page 169 and 170:
Page 171 and 172:
Page 173 and 174:
Page 175 and 176:
Page 177 and 178:
Page 179 and 180:
The economic cost of smoking in peo
Page 181 and 182:
Page 183 and 184:
Page 185 and 186:
Page 187 and 188:
Page 189 and 190:
Page 191 and 192:
Page 193 and 194:
Page 195 and 196:
Page 197 and 198:
Ethical and legal aspects 9 pose co
Page 199 and 200:
Ethical and legal aspects 9 less an
Page 201 and 202:
Ethical and legal aspects 9 patient
Page 203 and 204:
10 Summary and conclusions 10.1 Smo
Page 205 and 206:
Summary and conclusions 10 10.4 Smo
Page 207 and 208:
Summary and conclusions 10 although
Page 209 and 210:
11 Key conclusions and recommendati
Page 211 and 212:
Key conclusions and recommendations
Page 213 and 214:
Page 215:
show all

Smoking and mental health - NCSCT

Create successful ePaper yourself

Delete template?

Save as template?