tobacco addiction
Recently Published Documents

Objectives: To determine the prevalence, patterns and behavioural attributes of tobacco abuse in patients of acute coronary syndrome (ACS). Furthermore, to assess the interaction of tobacco abuse with other conventional risk factors of cardiovascular disease (CVD). Methodology: This observational study included 230 consecutive patients with ACS. Data was collected regarding total duration and extent of tobacco consumption, “tobacco addiction” and various behavioural patterns related to it. Risk factors profile was acquired for hypertension, diabetes, obesity, family history of premature CVD and dyslipidemia. Odds ratios (OR) with 95% confidence intervals (CI) for these risk factors were calculated for tobacco abusers compared to non-abusers. Results: Among the study population, 63(27.4%) were active tobacco users. Urban residents had lesser odds of being tobacco abusers compared to non-urban residents (0.49, [0.27 – 0.89]). Tobacco abusers had a lower prevalence of hypertension compared to non-abusers (0.44 [0.24 – 0.81]). A similar trend was observed for diabetes, obesity and dyslipidemia, however, the differences could not reach significance thresholds. Cigarette smoking was the commonest mode of tobacco consumption (90.5%). “Tobacco addiction” could be attributed to 84.1% of abusers. Most (82.5%) were willing to give up tobacco abuse and 63.3% had already made attempts at quitting. Conclusion: About one-third of ACS patients were tobacco abusers with the majority being tobacco addicts. Tobacco abuse was observed to be independently implicated as a risk factor in ACS patients. Furthermore, tobacco abuse was inversely related to hypertension translating into a sub-multiplicative / additive impact of hypertension as a risk factor.

Despite rising acknowledgement of the onset of tobacco smoking in children and adolescents, foundational understanding about many elements of early-life smoking behavior, as well as statistics to advocate for specific treatment approaches among children and adolescents, is inadequate. Nicotine addiction and withdrawal have been linked to continued cigarette use and difficulty stopping. When adolescents first start smoking, few expect to have trouble quitting. However, more than half of smoking teens say they try to quit every year, and fewer than 20% of those who smoke ten or more cigarettes per day say they are successful for even a month. Treatment of tobacco addiction rely mainly on the behavioral interventions as medications safety are not assessed for those less than 18 years old, so more research should be encouraged to find about the safety and availability for alternatives as behavioral intervention is not suitable alone for moderate to severe cases, Tobacco products are used by youth in a variety of ways,When smoking cessation efforts are undertaken in developed and developing nations, the wide diversity of tobacco products must be taken into consideration. This research deals with the causes of tobacco dependence among young people, diagnosis and treatment methods.

Nicotine, the main psychoactive component in tobacco smoke, plays a major role in tobacco addiction, producing a high morbidity and mortality in the world. A great amount of research has been developed to elucidate the neural pathways and neurotransmitter systems involved in such a complex addictive behavior. The endocannabinoid system, which has been reported to participate in the addictive properties of most of the prototypical drugs of abuse, is also implicated in nicotine dependence. This review summarizes and updates the main behavioral and biochemical data involving the endocannabinoid system in the rewarding properties of nicotine as well as in nicotine withdrawal and relapse to nicotine-seeking behavior. Promising results from preclinical studies suggest that manipulation of the endocannabinoid system could be a potential therapeutic strategy for treating nicotine addiction.

Background: The therapeutic options for neurobehavioral disorders are still limited, and in many cases, they lack a satisfactory balance between efficacy and side effects. Objective: This work aims to review current evidence regarding the potential contribution of psychedelics and hallucinogens to the discovery of new drugs for treating different psychiatric disorders. Discussion: Ayahuasca/N,N-dimethyltryptamine (DMT), lysergic acid diethylamide (LSD), and psilocybin have evidence supporting their use in depression, and psilocybin and ayahuasca have also shown good results in treatment-resistant depression. In randomized controlled trials (RCTs) conducted with anxious patients, there were symptomatic improvements with psilocybin and LSD. Psilocybin diminished Yale–Brown Obsessive Compulsive Scale (Y-BOCS) scores in a small obsessive–compulsive disorder (OCD) sample. The evidence is less robust regarding substance use disorders, but it suggests a possible role for LSD and psilocybin in alcohol use disorders and for psilocybin in tobacco addiction. In a clinical setting, these substances seem to be safe and well-tolerated. Their mechanisms of action are not fully elucidated, but there seems to be a preponderant role of 5-hydroxytryptamine (5HT) 2A agonism, as well as connectivity changes within the default mode network (DMN) and amygdala and some other molecular modifications. Conclusion: The studies underlying the conclusions have small samples and are heterogeneous in their methods. However, the results suggest that the use of psychedelics and hallucinogens could be considered in some disorders. More studies are needed to reinforce their evidence as potential new drugs.

<p>Schizophrenia as with most mental disorders develops due to an interaction of multiple genetic and environmental factors. Prenatal exposure to a maternal immuneactivation (MIA) is an environmental risk factor that can predispose offspring to develop schizophrenia later in life. The neurodevelopmental theory suggests that an immunechallenge during gestation can lead to long-lasting impairments such as in learning, memory,attention, or language (Brown & Patterson, 2012). Based on findings in human studies,prenatal exposure to a MIA has been utilized in preclinical research. Thus, the first aim of this study was to establish an animal model that generates subjects with schizophrenia-like cognitive impairments. To this end, a bacterial endotoxin, lipopolysaccharide (LPS) was used, which like most infectious agents, cannot cross the blood-placenta-barrier, yet reliably mimics an infection and initiates a MIA. Pregnant rats were subcutaneously (sc) injected with LPS (0.5 mg/kg) at one of three important neurodevelopmental time periods, gestation days (GD) 10/11, 15/16 or 18/19 (Fortier, Luheshi, & Boksa, 2007; Graciarena, Depino, & Pitossi, 2010). As individuals with schizophrenia commonly show deficits in multiple domains, three assessment paradigms were used to examine sensory and cognitive abilities in early and late adulthood. Tasks included prepulse inhibition to assess sensorimotor gating, latent inhibition to measure selective attention, and delayed non-matching to sample to evaluate working memory (WM).  Several theories have been suggested to explain high smoking incidence in schizophrenic patients (75-90%) compared to the general population (23%). The self-medication theory suggests high smoking rates amongst patients because nicotine, the primary addictive constituent in tobacco smoke, ameliorates some of the symptoms of the disorder such as cognitive deficits (D'Souza & Markou, 2012). Thus, the second aim of this study was to determine whether repeated experimenter and self-administered nicotine ameliorates or reduces schizophrenia-like cognitive deficits. Finally, the third aim was to investigate the common substrate theory, which suggests that shared underlying biological pathways may lead to increased susceptibility for an individual to develop both schizophrenia and tobacco addiction (Chambers, Krystal, & Self, 2001).  In conclusion, the findings of this study were coherently consistent and revealed that firstly, prenatal exposure to MIA early during foetal development led to long-lasting deficits in cognitive domains such as selective attention and WM. Secondly, supporting the self-medication theory, nicotine reversed MIA-induced cognitive impairments independent of the administration paradigm. Thirdly, increased responding rates for nicotine during self-administration acquisition in animals prenatally exposed to MIA were observed, yet there was no effect of prenatal treatment in dose response or progressive ratio testing. Thus, these findings only offer weak support for the common substrate theory.  Importantly, the findings of this study revealed that animals can be repeatedly assessed in these paradigms to examine the therapeutic efficacy of drugs and other treatments. This is of particular importance considering the lack of effective pharmacological treatments for cognitive deficits in schizophrenic patients.</p>

<p>Schizophrenia as with most mental disorders develops due to an interaction of multiple genetic and environmental factors. Prenatal exposure to a maternal immuneactivation (MIA) is an environmental risk factor that can predispose offspring to develop schizophrenia later in life. The neurodevelopmental theory suggests that an immunechallenge during gestation can lead to long-lasting impairments such as in learning, memory,attention, or language (Brown & Patterson, 2012). Based on findings in human studies,prenatal exposure to a MIA has been utilized in preclinical research. Thus, the first aim of this study was to establish an animal model that generates subjects with schizophrenia-like cognitive impairments. To this end, a bacterial endotoxin, lipopolysaccharide (LPS) was used, which like most infectious agents, cannot cross the blood-placenta-barrier, yet reliably mimics an infection and initiates a MIA. Pregnant rats were subcutaneously (sc) injected with LPS (0.5 mg/kg) at one of three important neurodevelopmental time periods, gestation days (GD) 10/11, 15/16 or 18/19 (Fortier, Luheshi, & Boksa, 2007; Graciarena, Depino, & Pitossi, 2010). As individuals with schizophrenia commonly show deficits in multiple domains, three assessment paradigms were used to examine sensory and cognitive abilities in early and late adulthood. Tasks included prepulse inhibition to assess sensorimotor gating, latent inhibition to measure selective attention, and delayed non-matching to sample to evaluate working memory (WM).  Several theories have been suggested to explain high smoking incidence in schizophrenic patients (75-90%) compared to the general population (23%). The self-medication theory suggests high smoking rates amongst patients because nicotine, the primary addictive constituent in tobacco smoke, ameliorates some of the symptoms of the disorder such as cognitive deficits (D'Souza & Markou, 2012). Thus, the second aim of this study was to determine whether repeated experimenter and self-administered nicotine ameliorates or reduces schizophrenia-like cognitive deficits. Finally, the third aim was to investigate the common substrate theory, which suggests that shared underlying biological pathways may lead to increased susceptibility for an individual to develop both schizophrenia and tobacco addiction (Chambers, Krystal, & Self, 2001).  In conclusion, the findings of this study were coherently consistent and revealed that firstly, prenatal exposure to MIA early during foetal development led to long-lasting deficits in cognitive domains such as selective attention and WM. Secondly, supporting the self-medication theory, nicotine reversed MIA-induced cognitive impairments independent of the administration paradigm. Thirdly, increased responding rates for nicotine during self-administration acquisition in animals prenatally exposed to MIA were observed, yet there was no effect of prenatal treatment in dose response or progressive ratio testing. Thus, these findings only offer weak support for the common substrate theory.  Importantly, the findings of this study revealed that animals can be repeatedly assessed in these paradigms to examine the therapeutic efficacy of drugs and other treatments. This is of particular importance considering the lack of effective pharmacological treatments for cognitive deficits in schizophrenic patients.</p>

<p>Tobacco addiction is a major public health concern and is responsible for approximately five million deaths globally each year. Although most current smokers express a desire to quit, few are successful in their attempts. Nicotine is the primary neurobiologically active component in tobacco smoke and acts through the nicotinic acetylcholine receptor (nAChR) to sustain addiction. However, nicotine replacement therapies have proven to be remarkably ineffective at helping smokers quit. This indicates that nicotine alone cannot fully account for the intense and enduring nature of tobacco addiction. Previous research has provided strong evidence that monoamine oxidase (MAO) enzymes and the endogenous opioid system may also play a role in tobacco dependence. The present study compared and contrasted the influence of nicotine and the non-nicotine components of tobacco smoke on the enzyme activity of MAO-A and MAO-B. Gene expression of MAO and the mu opioid receptor (MOR) in SH-SY5Y human neuroblastoma and U-118 MG glioma cell lines was also investigated. Using a kynuramine-based enzymatic assay adapted and optimised for this study, the MAO inhibitory activity of tobacco-based samples were tested, including total particulate matter (TPM) extracts from a range of New Zealand tobacco products, Quest(R) nicotine-free cigarettes, and fluid from the RUYAN(R) Electronic cigarette. TPM from both standard tobacco and Quest(R) significantly inhibited MAO-A and MAO-B activity in vitro and in cultured cells. Differences between the types and brands of tobacco products were observed. TPM derived from loose-leaf tobacco inhibited MAO enzymes more potently than samples from manufactured cigarettes. This difference was attributed to a significantly higher tar:nicotine ratio in loose-leaf tobacco. Standard TPM and Quest(R) TPM also inhibited total MAO activity in SH-SY5Y cells treated for 24 hours; whereas the weak activity in U-118 MG remained unchanged. However, MAO activity was highly dependent on the cell culture conditions, with activity increasing in SH-SY5Y cells when treated with a 5-day exposure regimen. This finding was unique to the present study. The gene expression of MAO-A, MAO-B, and MOR was examined using a qRT-PCR assay. All three genes were significantly up-regulated by standard and denicotinized TPM extracts after a 5-day treatment regimen. This finding was correlated with an increase in protein abundance for MOR, but not MAO-A or MAO-B, as assayed by Western blot. Up-regulation of MAO and MOR gene expression was abolished when cells were treated with TPM extracts in conjunction with the nAChR antagonist mecamylamine, suggesting that up-regulation of MAO and MOR genes was dependent, at least in part, on nAChR signalling. Both standard TPM and TPM from denicotinized Quest(R) cigarettes induced inhibition of MAO and up-regulation of MAO and MOR gene expression. This demonstrates that non-nicotine compounds within tobacco smoke can significantly influence the behaviour of cultured neuronal cells. Further research is required to fully elucidate the mechanisms behind the MAO and MOR gene response, and a better understanding of these mechanisms may provide a framework for the development of novel smoking cessation therapies.</p>

<p>Tobacco addiction is a major public health concern and is responsible for approximately five million deaths globally each year. Although most current smokers express a desire to quit, few are successful in their attempts. Nicotine is the primary neurobiologically active component in tobacco smoke and acts through the nicotinic acetylcholine receptor (nAChR) to sustain addiction. However, nicotine replacement therapies have proven to be remarkably ineffective at helping smokers quit. This indicates that nicotine alone cannot fully account for the intense and enduring nature of tobacco addiction. Previous research has provided strong evidence that monoamine oxidase (MAO) enzymes and the endogenous opioid system may also play a role in tobacco dependence. The present study compared and contrasted the influence of nicotine and the non-nicotine components of tobacco smoke on the enzyme activity of MAO-A and MAO-B. Gene expression of MAO and the mu opioid receptor (MOR) in SH-SY5Y human neuroblastoma and U-118 MG glioma cell lines was also investigated. Using a kynuramine-based enzymatic assay adapted and optimised for this study, the MAO inhibitory activity of tobacco-based samples were tested, including total particulate matter (TPM) extracts from a range of New Zealand tobacco products, Quest(R) nicotine-free cigarettes, and fluid from the RUYAN(R) Electronic cigarette. TPM from both standard tobacco and Quest(R) significantly inhibited MAO-A and MAO-B activity in vitro and in cultured cells. Differences between the types and brands of tobacco products were observed. TPM derived from loose-leaf tobacco inhibited MAO enzymes more potently than samples from manufactured cigarettes. This difference was attributed to a significantly higher tar:nicotine ratio in loose-leaf tobacco. Standard TPM and Quest(R) TPM also inhibited total MAO activity in SH-SY5Y cells treated for 24 hours; whereas the weak activity in U-118 MG remained unchanged. However, MAO activity was highly dependent on the cell culture conditions, with activity increasing in SH-SY5Y cells when treated with a 5-day exposure regimen. This finding was unique to the present study. The gene expression of MAO-A, MAO-B, and MOR was examined using a qRT-PCR assay. All three genes were significantly up-regulated by standard and denicotinized TPM extracts after a 5-day treatment regimen. This finding was correlated with an increase in protein abundance for MOR, but not MAO-A or MAO-B, as assayed by Western blot. Up-regulation of MAO and MOR gene expression was abolished when cells were treated with TPM extracts in conjunction with the nAChR antagonist mecamylamine, suggesting that up-regulation of MAO and MOR genes was dependent, at least in part, on nAChR signalling. Both standard TPM and TPM from denicotinized Quest(R) cigarettes induced inhibition of MAO and up-regulation of MAO and MOR gene expression. This demonstrates that non-nicotine compounds within tobacco smoke can significantly influence the behaviour of cultured neuronal cells. Further research is required to fully elucidate the mechanisms behind the MAO and MOR gene response, and a better understanding of these mechanisms may provide a framework for the development of novel smoking cessation therapies.</p>

<p>Tobacco addiction is a major public health concern and is responsible for approximately five million deaths globally each year. Although most current smokers express a desire to quit, few are successful in their attempts. Nicotine is the primary neurobiologically active component in tobacco smoke and acts through the nicotinic acetylcholine receptor (nAChR) to sustain addiction. However, nicotine replacement therapies have proven to be remarkably ineffective at helping smokers quit. This indicates that nicotine alone cannot fully account for the intense and enduring nature of tobacco addiction. Previous research has provided strong evidence that monoamine oxidase (MAO) enzymes and the endogenous opioid system may also play a role in tobacco dependence. The present study compared and contrasted the influence of nicotine and the non-nicotine components of tobacco smoke on the enzyme activity of MAO-A and MAO-B. Gene expression of MAO and the mu opioid receptor (MOR) in SH-SY5Y human neuroblastoma and U-118 MG glioma cell lines was also investigated. Using a kynuramine-based enzymatic assay adapted and optimised for this study, the MAO inhibitory activity of tobacco-based samples were tested, including total particulate matter (TPM) extracts from a range of New Zealand tobacco products, Quest(R) nicotine-free cigarettes, and fluid from the RUYAN(R) Electronic cigarette. TPM from both standard tobacco and Quest(R) significantly inhibited MAO-A and MAO-B activity in vitro and in cultured cells. Differences between the types and brands of tobacco products were observed. TPM derived from loose-leaf tobacco inhibited MAO enzymes more potently than samples from manufactured cigarettes. This difference was attributed to a significantly higher tar:nicotine ratio in loose-leaf tobacco. Standard TPM and Quest(R) TPM also inhibited total MAO activity in SH-SY5Y cells treated for 24 hours; whereas the weak activity in U-118 MG remained unchanged. However, MAO activity was highly dependent on the cell culture conditions, with activity increasing in SH-SY5Y cells when treated with a 5-day exposure regimen. This finding was unique to the present study. The gene expression of MAO-A, MAO-B, and MOR was examined using a qRT-PCR assay. All three genes were significantly up-regulated by standard and denicotinized TPM extracts after a 5-day treatment regimen. This finding was correlated with an increase in protein abundance for MOR, but not MAO-A or MAO-B, as assayed by Western blot. Up-regulation of MAO and MOR gene expression was abolished when cells were treated with TPM extracts in conjunction with the nAChR antagonist mecamylamine, suggesting that up-regulation of MAO and MOR genes was dependent, at least in part, on nAChR signalling. Both standard TPM and TPM from denicotinized Quest(R) cigarettes induced inhibition of MAO and up-regulation of MAO and MOR gene expression. This demonstrates that non-nicotine compounds within tobacco smoke can significantly influence the behaviour of cultured neuronal cells. Further research is required to fully elucidate the mechanisms behind the MAO and MOR gene response, and a better understanding of these mechanisms may provide a framework for the development of novel smoking cessation therapies.</p>