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For those who want to know more of the science behind nicotine (and other) addictions, here's some snippets taken from the last ten years of medical research:
On Nicotine addiction:
“Nicotine exposure can have long lasting effects on nervous system function, some of which must contribute to nicotine dependence. Up-regulation, an increase in numbers of nicotinic acetylcholine receptors, occurs on exposure to nicotine at high concentrations”
“Nicotine is a powerful stimulant of the sympathoadrenal system, causing the release of peripheral catecholamines and activation of catecholamine biosynthesis. In previous reports, we have studied the mechanisms by which short-term nicotine treatment regulates tyrosine hydroxylase (TH-the precursor to dopamine) in adrenal medulla. In this report, we study the effects of chronic nicotine treatment on adrenal TH gene expression....Chronic nicotine administration also elicited a sustained increase in adrenal TH gene transcription rate, which persisted for up to 7 days after the final nicotine injection... These results demonstrate that repeated nicotine injections administered chronically over 1 to 2 weeks lead to sustained stimulation of the TH gene and consequent induction of TH gene expression in rat adrenal medulla. These studies support the hypothesis that chronic nicotine administration produces long-lasting cellular changes in central nervous system that lead to sustained transcriptional responses.”
“Few studies have evaluated the impact of smoking cessation on objective measures of sleep. The present study assessed the long-term effects of tobacco smoking abstinence on sleep and depression. A total of 15 chronic smokers with Hamilton Rating Scale for Depression (HAM-D) scores of less than 9 were evaluated. Subjects were screened for baseline data when they were smoking chronically. They underwent a 5-week psychological treatment for tobacco smoking, after which their depressive symptoms and sleep architecture were evaluated at 1, 2, 4, 6, 9, and 12 months of abstinence. We report the results of the seven patients who completed 1 year of evaluations and of those patients who achieved only partial abstinence. Polysomnographic recordings were taken, level of depression was measured with the HAM-D, and urinary cotinine levels also were evaluated. HAM-D scores were analyzed with and without sleep items. Nicotine abstinence reduced latency to rapid eye movement sleep and increased HAM-D scores, suggesting that chronic smokers have depressive symptoms that may be controlled by nicotine administration.”
“Nicotine is a developmental neurotoxicant but the proposed "sensitization-homeostasis" model postulates that even in adulthood nicotine permanently reprograms synaptic function. We administered nicotine to rats throughout gestation or in adulthood, simulating plasma levels in smokers, with evaluations on Day 105, 110, 120, 130 and 180……Our results indicate that the effects of nicotine withdrawal in adults show persistent changes after nicotine exposure, commensurate with the sensitization-homeostasis model. These effects may contribute to lifelong vulnerability to readdiction.”
“The present studies were done to investigate the effect of long-term nicotine treatment against nigrostriatal damage in non-human primates. Monkeys were administered nicotine in drinking water for 6 months to provide chronic but intermittent delivery as with smoking. Plasma nicotine levels ranged from 10 to 15 ng/mL, which were within the range in cigarette smokers………….results indicating that nicotine acts at the striatal level to restore/maintain dopaminergic function. These data further support the possibility that nicotine contributes to the lower incidence of Parkinson's disease in smokers.”
“Our results show that…changes in serotonin content and serotonin 1A receptor expression, are present when nicotine is withdrawn, even after a long time, suggesting a role of serotonin in mood disorders eventually occurring following smoking cessation.”
On the genetics of addiction in general:
“Several twin studies have been published in the substance dependence field, all showing significantly higher rates of dependence among twins than among non-twin siblings and higher rates among monozygotic than di-zygotic twins. Published heritability estimates include 34% for males dependent on heroin, 55% for males dependent on alcohol, 52% for females dependent on marijuana, and 61% for cigarette-dependent twins of both sexes. More studies of heritability are needed across drug types and sexes, but the evidence suggests significant genetic contribution to the risk of addiction comparable to that seen in other chronic illnesses.”
“In women, genetic risk factors have a moderate impact on the probability of ever using cannabis and a strong impact on the liability to heavy use, abuse, and, probably, dependence. By contrast, the family and social environment substantially influences risk of ever using cannabis, but plays little role in the probability of developing heavy cannabis use or abuse.”
“Twins were recruited through alcohol and drug treatment programs. With structural equation modeling, genetic and environmental estimates were obtained for use and DSM-III abuse/dependence of sedatives, opioids, cocaine, stimulants, and cannabis as well as any illicit drug. Analyses were conducted separately for males and females. Models included thresholds based on population prevalence of use or abuse/dependence and ever having been in treatment. Genetic influences were found for most measures. They were generally stronger for males than females and for clinical diagnoses of abuse/dependence compared to use. Common environmental influences played a greater role in use than abuse/dependence.”
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