Research has revealed that between 60% and
90% of people who have schizophrenia are heavy cigarette smokers, and that
smoking is likely the number one cause of premature death for people who
have schizophrenia. Schizophrenia.com has completed a special
report on cigarette smoking, schizophrenia and nicotine. Below is a
list of readings on this topic that we've come across while working on the
report.
Quitnet.com - The Web's original quit smoking site, operated in association with Boston University School of Public Health.
SmokeFree.gov - a good government-sponsored site on how to stop smoking
TrytoStop.org - A very good site focused on stopping smoking, by the Massachusetts Department of Public Health. Multiple language options (Spanish, French, Italian, etc.).
Scientific Research on Quiting Smoking for people who have Schizophrenia
'Unseen damage' smoke ad launched (BBC News) - "Today's survey is worrying in that it suggests smokers think nicotine is the killer in the cigarette - but it's the other constituents of cigarette smoke that damage arteries. "Nicotine replacement therapy is an ideal way to give up smoking because it satisfies the craving without causing the damage."
Articles on the Controversy of "Harm Reduction" vs. Quitting Smoking
Harm Reduction- An introduction to the Issues (Action on Smoking and Health) Estimates: "Smokeless tobacco in several forms is probably 10 to 100 times less hazardous than cigarettes, Medicinal nicotine ( for example Nicotine Replacement Therapy) harm is very small."
Should the European Union lift the ban on snus? Evidence from the Swedish experience. Recent data has found that among those starting tobacco use in the form of snus, 20% later go on to smoking while the same risk for those not starting with snus is 43%. On balance, there is reason to believe that having snus available to the Swedish population has been of benefit to public health. Repealing the ban on snus in the rest of the European Union might also have some positive effect, depending on the marketing
Evaluation of carcinogen exposure in people who used "reduced exposure" tobacco products - CONCLUSION: Switching to reduced-exposure tobacco products or medicinal nicotine can decrease levels of tobacco-associated carcinogens, with greater reductions being observed with medicinal nicotine. Medicinal nicotine is a safer alternative than modified tobacco products.
Influence of smoking and snus on the prevalence and incidence of type 2 diabetes amongst men: the northern Sweden - Conclusion: A negative effect of smoking on the risk of type 2 diabetes seems well established and was also found both in the present and in our study. Importantly, however, others and we found an increased risk only in subjects having consumed >20 cigarettes day. In line with the observed non-linear dose response for smoking, we found in our study an increased risk of diabetes only in snus-users who consumed three boxes of snus (50 g each) per week with no tendency for any increase at lower levels of exposure.
The burden of mortality from smoking: comparing Sweden with other countries in the European Union Almost 500,000 smoking-attributable deaths occur annually among men in the EU; about 200,000 would be avoided at Swedish smoking rates. In contrast, only 1100 deaths would be avoided if EU women smoked at Swedish rates. The low smoking-related mortality among Swedish men probably is due to their use of snus (Swedish smokeless tobacco).
Role of snus (oral moist snuff ) in smoking cessation and smoking reduction in Sweden Conclusion: Our study suggests that by using snus, Swedish male smokers may increase their overall chances of abstinence. However, 71% of the men in this sample who quit smoking did so without using snus and the duration of abstinence was not affected by snus use. This suggests that snus is not a necessary component of smoking cessation at the population level. Snus use was very rare among women.
Evolving patterns of tobacco use in northern Sweden CONCLUSIONS: The use of snus played a major role in the decline of smoking rates amongst men in northern Sweden. The evolution from smoking to snus use occurred in the absence of a specific public health policy encouraging such a transition and probably resulted from historical and societal influences.
Genotoxicity testing of extracts of a Swedish moist oral snuff. Based on these results, the carcinogenic potential of Swedish 'Snus' should be considered to be low, a conclusion in agreement with the low incidence of oral cancer in Sweden compared to other countries.
Evaluation of Carcinogen Exposure in People Who Used "Reduced Exposure" Tobacco Products CONCLUSION: Switching to reduced-exposure tobacco products or medicinal nicotine can decrease levels of tobacco-associated carcinogens, with greater reductions being observed with medicinal nicotine. Medicinal nicotine is a safer alternative than modified tobacco products
Smokeless tobacco use and risk of cancer of the pancreas and other organs The increase in the relative risk of pancreatic cancer was similar in former and current snus users and was restricted to current tobacco smokers. Our study suggests that smokeless tobacco products may be carcinogenic on the pancreas. Tobacco-specific N-nitrosamines are plausible candidates for the carcinogenicity of smokeless tobacco products in the pancreas.
Health risks of smoking compared to Swedish snus Although few in number, these seven studies do provide quantitative evidence that, for certain health outcomes, the health risks associated with snus are lower than those associated with smoking. Specifically, this is true for lung cancer (based on one study), for oral cancer (based on one study), for gastric cancer (based on one study), for cardiovascular disease (based on three of four studies), and for all-cause mortality (based on one study).
Adverse pregnancy outcomes in snuff users.Am J ObstetGynecol, (2003 Oct) Snuff use was associated with increased risk of preterm delivery and preeclampsia. Snuff does not appear to be a safe alternative to cigarettes during pregnancy
Smoking-health risks.(2005, Feb. 14). NetDoctor.co.uk. Retrieved August 1, 2005, from
Smokeless tobacco and oral cancer: A review of the risks and determinants.Crit Rev Oral Biol Med, (2004 Sep) In general, smokeless tobacco users are not exposed to significant levels of cadmium, lead, benzo(a)pyrene, polonium-210, and formaldehyde, when compared with concentrations of these compounds in foods. Finally, low oral cancer risk from smokeless tobacco use may be influenced by the presence of cancer inhibitors, mainly anti-oxidants, in smokeless tobacco products.
Watts, G. (2003, August 4) Smoke signals: pure nicotine may help in certain bowel and mental disorders. Newspaper Publishing PLC: The Independent (London)
Effects of Nicotine Nasal Spray on Cognitive Function in SchizophreniaNeuropsychopharmacology. 2005 Sep 14 There were no effects of active nicotine nasal spray on verbal memory. Our results suggest that nicotine may modestly enhance attention and spatial working memory in schizophrenic patients who are cigarette smokers and have been abstinent overnight.
Subjective and physiological responses to smoking cues in smokers with schizophrenia.Nicotine Tob Res. 2005 Jun Results indicate that both exposure to smoking cues and brief abstinence increased urge levels, nicotine withdrawal symptom levels, and negative affect. Abstinence did not amplify the effects of cues on urges or other cue reactivity measures. These results indicate that smoking cue reactivity laboratory models may be useful for investigating potential smoking treatments for, or neurobiological contributions to, smoking behavior in smokers with schizophrenia.
Tobacco use in schizophrenia: a study of cotinine concentrations in the saliva of patients and controls Eur Psychiatry. (2005 Jan) The results indicate that the schizophrenic patients smoke cigarettes more intensely than other patients and healthy subjects. The correlation between high cotinine levels and negative symptomatology may reflect an attempt by schizophrenic patients to overcome the emotional withdrawal and thus the results may lend support to a self-medication hypothesis.
Nicotinic receptors and schizophrenia. Curr Med Res Opin. (2004 Jul) This review assesses the involvement of the nicotinic system in schizophrenia and suggests ways in which this system may participate in the pathophysiology of this disease.
General Articles on Antioxidants and tobacco or nicotine use
Vitamin C prevents cigarette smoke-induced oxidative damage in vivo Conclusion: Our recent in vitro results indicate that cigarette smoke induces oxidation of human plasma proteins and extensive oxidative degradation of the guinea pig lung, heart, and liver microsomal proteins, which is almost completely prevented by ascorbic acid. The results, if extrapolated to humans, indicate that comparatively large doses of vitamin C may protect the smokers from cigarette smoke-induced oxidative damage and associated degenerative diseases.
Antioxidant Vitamin Supplementation Reduces Benzo(a)pyrene-DNA Adducts and Potential Cancer Risk in Female Smokers Conclusion: Our primary hypothesis that the mean level of smoking-related B(a)P-DNA adducts would be lower in all subjects in the vitamin treatment group compared with all placebo-treated subjects was not substantiated. However, oursecondary gender-specific analysis found a significant reduction in B(a)P-DNA adducts in women with vitamin treatment, suggesting that antioxidant supplementation maymitigate some of the procarcinogenic effects of exposuretoB(a)P.
Effect of smoke shield-a herbal formulation on the mutagenicity and oxidative stress produced by cigarette smoke in rats . Conclusions: In vitro antioxidant potential of smoke shield was found to be comparable or better than known antioxidants such as vitamin C and vitamin E. These results indicated that Smoke Shield administration could effectively reduce the oxidative stress produced in rats by cigarette smoke and it could inhibit mutagenicity produced by smoke condensates and tobacco extract in Salmonella typhimurium.
Oxidative mechanisms contributing to the developmental neurotoxicity of nicotine and chlorpyrifos . Conclusion: Our results indicate that nicotine and chlorpyrifos elicit oxidative damage to developing neural cells both in vitro and in vivo, a mechanism that explains some of the neurodevelopmental endpoints that are common to the two agents. The balance between neuroprotectant and neurotoxicant actions of nicotine may be particularly important in situations where exposure to tobacco smoke is combined with other prooxidant insults
Vitamin C prevents the effects of prenatal nicotine on pulmonary function in newborn monkeys . Conclusion: Prenatal nicotine exposure significantly decreased levels of elastin content in the lungs of offspring, and these effects were slightly attenuated by vitamin C. These findings suggest that vitamin C supplementation may potentially be clinically useful to limit the deleterious effects of maternal smoking during pregnancy on offspring's lung function.
Chronic nicotine toxicity is prevented by aqueous garlic extract . Conclusion: Treatment of rats with AGE restored the reduced GSH levels while it decreased MDA levels as well as MPO activity. Increased collagen contents of the tissues by chronic nicotine were reversed back to the control levels with AGE. Since AGE administration reversed these oxidant responses, improved renal function and histological damage, it seems likely that AGE protects the tissues against nicotine-induced oxidative damage.
Effects of nicotine and vitamin E on carbonic anhydrase activity in some rat tissues in vivo and in vitro Conclusion: Nicotine + HRe-1 inhibited the heart and stomach CA enzyme activities by approximately 51% (p < 0.001), and approximately 32% (p < 0.002), respectively, and activated the muscle and brain CA activities, but had no effects on the lung, testicle, kidney, and liver CA activities. In vitro CA inhibition results for similar experiments correlated well with the in vivo experimental results in lungs, testicles, kidney, stomach, brain and liver tissues.