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Query: UMLS:C0278080 (physical dependence)
 1,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors present three case studies which suggest that smoking withdrawal symptoms in certain individuals may be due to removal of nicotine per se, implying that smokers may develop a true physical dependence on cigarettes. Nicotine replacement by use of an experimental chewing gum containing nicotine in various dosages successfully prevented or alleviated the abstinence symptoms of the subjects studied.
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PMID:The use of nicotine gum during cessation of smoking. 84 37

Smokeless tobacco practices are common in some parts of the world and the use seems to be increasing. Nicotine exposure is similar in smokeless tobacco users and smokers, often leading to strong physical dependence. As a rule, smokeless tobacco products contain high levels of nitrosamines with carcinogenic potency in experimental animals. Habitual use of oral tobacco can increase the risk of oral cancer, but the data are insufficient to assess in detail the risks associated with many types of smokeless tobacco. A recent study suggests that smokeless tobacco use is related to cardiovascular disease, which could be of great public health importance. The known and suspected health risks associated with the use of smokeless tobacco provide a basis for preventive action. In particular, efforts are needed to limit the introduction of such practices among young people, which may serve as a gateway to smoking.
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PMID:Smokeless tobacco. 874 96

This paper evaluates the hypothesis that Black smokers will respond differently than Whites to a smoking cessation intervention program where no adjustments are made in recognition of cultural differences. The responses of Black smokers who were recruited into the Lung Health Study (LHS) to the smoking cessation intervention are described. Black quit rates are compared with those of Whites. The LHS enrolled 5887 men and women smokers, aged 35-60 years, of whom 3923 were randomized to a group cessation intervention and 1964 to usual care. Blacks and Whites from six clinics who had complete covariate data (200 Blacks and 2868 Whites) were compared on baseline smoking characteristics and subsequent smoking cessation outcomes. Logistic models were constructed to adjust for baseline smoking variables and demographic characteristics to evaluate the effect of treatment group on smoking cessation among Blacks and Whites. At baseline, Blacks reported smoking fewer cigarettes than Whites, but had higher mean levels of salivary cotinine. The adjusted odds ratio of quitting at 1 year for the smoking intervention group vs. the usual care group was 1.48 for Blacks and 5.99 for Whites. This difference between Blacks and Whites was highly significant (p = 0.002). Across 5 years, the adjusted odds ratios of quitting were 1.87 for Blacks and 3.34 for Whites (p = 0.06). Although the treatment effect was stronger for Whites than for Blacks, over the 5 years of the study there was a significant treatment effect for Blacks. Indicators of physical dependence on nicotine at baseline were inconsistent in indicating whether Blacks were more dependent. We conclude that Blacks and Whites differed significantly in their response to the LHS group smoking intervention program.
Nicotine Tob Res 2001 Nov
PMID:Experience of Black participants in the Lung Health Study smoking cessation intervention program. 1169 5

Behavioural and pharmacological effects of Delta9-tetrahydrocannabinol (THC) and nicotine are well known. However, the possible interactions between these two drugs of abuse remain unclear in spite of the current association of cannabis and tobacco in humans. The present study was designed to analyse the consequences of nicotine administration on THC-induced acute behavioural and biochemical responses, tolerance and physical dependence. Nicotine strongly facilitated hypothermia, antinociception and hypolocomotion induced by the acute administration of THC. Furthermore, the co-administration of sub-threshold doses of THC and nicotine produced an anxiolytic-like response in the light - dark box and in the open-field test as well as a significant conditioned place preference. Animals co-treated with nicotine and THC displayed an attenuation in THC tolerance and an enhancement in the somatic expression of cannabinoid antagonist-precipitated THC withdrawal. THC and nicotine administration induced c-Fos expression in several brain structures. Co-administration of both compounds enhanced c-Fos expression in the shell of the nucleus accumbens, central and basolateral nucleus of the amygdala, dorso-lateral bed nucleus of the stria terminalis, cingular and piriform cortex, and paraventricular nucleus of the hypothalamus. These results clearly demonstrate the existence of a functional interaction between THC and nicotine. The facilitation of THC-induced acute pharmacological and biochemical responses, tolerance and physical dependence by nicotine could play an important role in the development of addictive processes.
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PMID:Behavioural and biochemical evidence for interactions between Delta 9-tetrahydrocannabinol and nicotine. 1181 92

Nicotine is one of the most widely abused psychoactive drugs and far more people trying it progress to regular use than those trying heroin, cocaine, or alcohol. Since the early 20th century, it has been understood that tobacco use is driven largely by nicotine's pharmacological actions. Nicotine produces reinforcing effects, tolerance and physical dependence, and pharmacological effects that smokers enjoy, such as modulation of mood, appetite, and task performance. Pharmacokinetic properties of tobacco-based nicotine products optimize abuse potential. Cigarette smoke inhalation delivers high nicotine concentrations to the brain and other organs within 10 s of inhalation. Nicotine's acute effects dissipate in a few minutes, encouraging the smoker to smoke frequently throughout the day to maintain its pleasurable effects and prevent withdrawal symptoms. Nicotine and other constituents of smoke also provide sensory stimuli which, through repeated pairings, become conditioned reinforcers and further strengthen tobacco self-administration, creating an extremely persistant behavior. Nicotine replacement medications provide relief of cigarette withdrawal symptoms and are effective aids in smoking cessation; however, sustaining long-term abstinence can still be very difficult.
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PMID:Pharmacologic Determinants of Tobacco Dependence. 1186 69

The involvement of mu-opioid receptors in different behavioral responses elicited by nicotine was explored by using mu-opioid receptor knock-out mice. The acute antinociceptive responses induced by nicotine in the tail-immersion and hot-plate tests were reduced in the mutant mice, whereas no difference between genotypes was observed in the locomotor responses. The rewarding effects induced by nicotine were then investigated using the conditioning place-preference paradigm. Nicotine produced rewarding responses in wild-type mice but failed to produce place preference in knock-out mice, indicating the inability of this drug to induce rewarding effects in the absence of mu-opioid receptors. Finally, the somatic expression of the nicotine withdrawal syndrome, precipitated in dependent mice by the injection of mecamylamine, was evaluated. Nicotine withdrawal was significantly attenuated in knock-out mutants when compared with wild-type mice. In summary, the present results show that mu-opioid receptors are involved in the rewarding responses induced by nicotine and participate in its antinociceptive responses and the expression of nicotine physical dependence.
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PMID:Attenuation of nicotine-induced antinociception, rewarding effects, and dependence in mu-opioid receptor knock-out mice. 1248 88

Cigarette smoking is a leading cause of mortality and morbidity and a particularly common and intractable addictive disorder. Research shows that nicotine is a sine qua non of tobacco addiction and that it produces the hallmark effects of addictive drugs: sensitization, tolerance, physical dependence, and euphoria/elation. Research on the development of smoking reveals that although smoking prevalence has declined from a peak in the mid-1990s, close to 30% of twelfth graders still smoke. Smoking in adolescents is related to development of physical dependence, ethnicity, impulsivity, affective disorder, and peer influences. However, which of these exerts the greatest causal effects is unknown, and their influence no doubt varies across individuals and across development. Once dependence on tobacco smoking is established, evidence suggests that tobacco motivation is strongly influenced by a reduction in withdrawal symptoms, an expectation of stress reduction, and conditioned reinforcement. Nicotine motivation may also be influenced by modulation in stimulus incentive value.
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PMID:Motivational influences on cigarette smoking. 1474 23

Understanding the basic and clinical pharmacology of nicotine provides a basis for improved prevention and treatment of tobacco addiction. Nicotine acts on nicotinic cholinergic receptors in the brain to release dopamine and other neurotransmitters that sustain addiction. Neuroadaptation and tolerance involve changes in both nicotinic receptors and neural plasticity. Nicotine addiction can occur in the context of physical dependence characterized by self-medication to modulate negative affect and/or to relieve withdrawal symptoms, as well as, in light or occasional smokers, primarily for positive reinforcement in specific situations. Nicotine is metabolized primarily by CYP2A6. Its clearance exhibits considerable individual variability that is determined by genetic, racial, and hormonal (sex) factors. Genetically slow metabolism of nicotine appears to be associated with a lower level of dependence. Nicotine dependence is highly heritable and appears to be influenced by genes coding for some nicotine receptor subtypes, some neurotransmitter genes, and genes involved in neural connectivity. Novel pharmacotherapies for nicotine dependence include partial agonists for nicotinic receptors and nicotine vaccines. Pharmacogenetic studies suggest various candidate genes and a nicotine metabolism phenotype that influence outcome. Human pharmacology studies of nicotine and smoking behavior also provide a basis for assessing the benefits and risks of long-term nicotine use for harm reduction and for a potential cigarette regulatory strategy that includes reducing nicotine content of cigarettes to nonaddictive levels.
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PMID:Clinical pharmacology of nicotine: implications for understanding, preventing, and treating tobacco addiction. 1830 52

The endogenous opioid system has been reported to participate in nicotine behavioural responses. The aim of the study was to determine the contribution of the endogenous peptides derived from prodynorphin in acute and chronic nicotine responses, mainly those related to its addictive properties. Locomotion and nociception were evaluated after acute nicotine administration in prodynorphin knockout mice. In addition, nicotine rewarding properties were investigated in the place-conditioning and the intravenous self-administration paradigms. The somatic signs of nicotine withdrawal were also analysed after the injection of the nicotinic antagonist mecamylamine in nicotine-dependent mice. The hypolocomotor and antinociceptive effects induced by acute nicotine administration were not modified in knockout (KO) animals. Nicotine also produced similar conditioned place preference in both genotypes. However, a shift to the left in the percentage of acquisition of intravenous nicotine-self administration was observed in prodynorphin KO mice. Indeed, a significant increase in the number of KO mice acquiring this operant behaviour was revealed when low doses of nicotine were used. Nicotine physical dependence was similar in wild-type and KO animals. These findings reveal a specific role of endogenous peptides derived from prodynorphin in nicotine self-administration, probably through the modulation of its aversive effects.
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PMID:Prodynorphin gene disruption increases the sensitivity to nicotine self-administration in mice. 1893 81

The endogenous opioid system plays an important role in the behavioral effects of nicotine. Thus, micro-opioid receptor and the endogenous opioids derived from proenkephalin are involved in the central effects of nicotine. However, the role played by the different endogenous opioid peptides in the acute and chronic effects of nicotine remains to be fully established. Mice lacking beta-endorphin were acutely injected with nicotine at different doses to evaluate locomotor, anxiogenic and antinociceptive responses. The rewarding properties of nicotine were evaluated by using the conditioned place-preference paradigm. Mice chronically treated with nicotine were acutely injected with mecamylamine to study the behavioral expression of nicotine withdrawal. Mice lacking beta-endorphin exhibited a spontaneous hypoalgesia and hyperlocomotion and a reduction on the anxiogenic and rewarding effects induced by nicotine. Nicotine induced similar antinociception and hypolocomotion in both genotypes and no differences were found in the development of physical dependence. The dissociation between nicotine rewarding properties and physical dependence suggests a differential implication of beta-endorphin in these addictive related responses.
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PMID:Nicotine anxiogenic and rewarding effects are decreased in mice lacking beta-endorphin. 1937 43


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