MarylandQuitter

Video highlights the fact that while the intensity and exact duration of physical withdrawals can vary widely when first quitting smoking, that any peak symptoms will ease up once the person gets through the first three days.

NEW VIDEO ADDED 7 FEB 2019 The importance of the first three days of your quit Video highlights the fact that while the intensity and exact duration of physical withdrawals can vary widely when first quitting smoking, that any peak symptoms will ease up once the person gets through the first three days.

February 4, 2019 Stanton A. Glantz, PhD https://tobacco.ucsf.edu/rct-comparing-e-cigs-nrt-shows-effectiveness-supervised-smoking-cessation-program-what-it-does-and-does-not-mean?fbclid=IwAR3BTV8SJ13deT_tMOiQFOhcidWO1jEkakN-ynQbJtIxNJ4gprzkn0OMZvY RCT comparing e-cigs to NRT shows effectiveness in a supervised smoking cessation program: what it does and does not mean February 4, 2019 Stanton A. Glantz, PhD RCT comparing e-cigs to NRT shows effectiveness in a supervised smoking cessation program: what it does and does not mean Peter Hajek and colleagues published “A Randomized Trial of E-cigarettes versus Nicotine-Replacement Therapy” in the New England Journal of Medicine. This is a well-done trial comparing e-cigarettes with nicotine replacement therapy among people enrolled in smoking cessation programs in England. In addition to being randomized to e-cigs or NRT, people in the study had at least 4 weeks of counseling. At one year the cigarette abstinence rate was 18.0% among patients randomized to e-cigs compared to 9.9% randomized to NRT, nearly a doubling of quitting. The study is thoughtfully designed and cautiously interpreted. The authors also did a nice set of sensitivity analyses to show that the results are robust to the usual kinds of problems one has in doing a randomized controlled trial. They conclude that “E-cigarettes were more effective for smoking cessation that nicotine-replacement therapy, when both products were accompanied by behavioral support.” I agree with that conclusion. Having said that, it is important to emphasize that this is not a study of e-cigarettes as most people use them, which is as recreational products not as part of a clinically supervised cessation attempt that, most important, includes intensive counseling. Thus, the results of the Hajek study do not contradict the overall result that, in the general population, smokers who use e-cigarettes are, on average, less likely to quit smoking. So, my bottom line is that if other well-done randomized controlled trials show that e-cigarettes improve smoking cessation, the manufacturers should submit the evidence to the appropriate authorities (the FDA in the USA) to get e-cigarettes approved as prescription medicines to be administered by physicians or other health professionals as part of supervised cessation efforts that include intensive counseling. The reason that I say they should be available by prescription is because of their high abuse potential, as evidenced by the run-away use of them by kids as well as the fact that when used unsupervised in the general population they depress smoking cessation. In addition to efficacy, the drug approval process needs to assess safety. Hajek and colleagues reported that after one year 80% of the e-cigarette group were still using e-cigarettes compared to just 9% of the NRT group were continuing to use NRT. This is of particular concern because of the evidence linking e-cigarette use to heart attacks and chronic obstructive pulmonary disease and is something that warrants serious consideration by regulatory authorities. The accompanying editorial by Belinda Borrelli and George T. O’Connor also raises several concerns about long-term safety of e-cigarette use and notes that varenicline -- which was not evaluated in the Hajek study -- outperforms NRT. Here is the abstract: BACKGROUND: E-cigarettes are commonly used in attempts to stop smoking, but evidence is limited regarding their effectiveness as compared with that of nicotine products approved as smoking-cessation treatments. METHODS: We randomly assigned adults attending U.K. National Health Service stop-smoking services to either nicotine-replacement products of their choice, including product combinations, provided for up to 3 months, or an e-cigarette starter pack (a second-generation refillable e-cigarette with one bottle of nicotine e-liquid [18 mg per milliliter]), with a recommendation to purchase further e-liquids of the flavor and strength of their choice. Treatment included weekly behavioral support for at least 4 weeks. The primary outcome was sustained abstinence for 1 year, which was validated biochemically at the final visit. Participants who were lost to follow-up or did not provide biochemical validation were considered to not be abstinent. Secondary outcomes included participant-reported treatment usage and respiratory symptoms. RESULTS: A total of 886 participants underwent randomization. The 1-year abstinence rate was 18.0% in the e-cigarette group, as compared with 9.9% in the nicotine-replacement group (relative risk, 1.83; 95% confidence interval [CI], 1.30 to 2.58; P<0.001). Among participants with 1-year abstinence, those in the e-cigarette group were more likely than those in the nicotine-replacement group to use their assigned product at 52 weeks (80% [63 of 79 participants] vs. 9% [4 of 44 participants]). Overall, throat or mouth irritation was reported more frequently in the e-cigarette group (65.3%, vs. 51.2% in the nicotine-replacement group) and nausea more frequently in the nicotine-replacement group (37.9%, vs. 31.3% in the e-cigarette group). The e-cigarette group reported greater declines in the incidence of cough and phlegm production from baseline to 52 weeks than did the nicotine-replacement group (relative risk for cough, 0.8; 95% CI, 0.6 to 0.9; relative risk for phlegm, 0.7; 95% CI, 0.6 to 0.9). There were no significant between-group differences in the incidence of wheezing or shortness of breath. CONCLUSIONS: E-cigarettes were more effective for smoking cessation than nicotine-replacement therapy, when both products were accompanied by behavioral support. (Funded by the National Institute for Health Research and Cancer Research UK; Current Controlled Trials number, ISRCTN60477608 .). The full citation is Hajek P, et al. A Randomized Trial of E-Cigarettes versus Nicotine-Replacement Therapy. N Engl J Med. 2019 Jan 30. doi: 10.1056/NEJMoa1808779. [Epub ahead of print]. The paper is available here.

February 5, 2019 Stanton A. Glantz, PhD Another study ties e-cigs to strokes and confirms association with heart attacks https://tobacco.ucsf.edu/another-study-ties-e-cigs-strokes-and-confirms-association-heart-attacks?fbclid=IwAR2aK6T2Gkvb6wVPo8gJyahJt9Eqg8cna0T6xzaWatoNTxtTxskVoxPGc-8 Paul M Ndunda and Tabitha M Muutu just presented their paper “Electronic Cigarette Use is Associated With a Higher Risk of Stroke” at the International Stroke Conference. They conducted a cross-sectional analysis using the CDC’s Behavorial Risk Factor Surveillance System data from 2016 to assess the risks of stroke and myocardial infarction in e-cigarette users, controlling for cigarette smoking. They found compared with non-users, e-cigarette users had higher adjusted odds of stroke (OR 1.71 [1.64 - 1.8]), myocardial infarction (OR 1.59 [1.53 - 1.66]), angina or coronary heart disease (OR 1.4 [1.35 - 1.46]). These risks are similar to what we reported based on the National Health Interview Survey. The fact that two independent data sources yielded such similar results is strong evidence that the association is real. Farsalinos has already criticized the paper, mostly with linguistic challenges of what the word “risk factor” means. Had he checked Wikipedia he would have seen that the term “risk factor” is meant to be used when describing associations in cross-sectional studies. Here is an NPR story on the study that has a good description and puts it into context.

Feb 05 2019 An exploding vaporiser pen resulted in the death of a 24-year-old Texas man, a post-mortem examination has ruled. https://www.bbc.com/news/world-us-canada-47136678 The pen's battery blew up when William Brown tried to use it, sending shards of metal into his face and neck and severing an artery. He died two days later in hospital of a stroke, in what is at least the second such death in the US. Malfunctioning e-cigarette batteries have caused hundreds to thousands of similar injuries, US reports say. The Tarrant County Medical Examiner's Office found on Tuesday that shrapnel from the vape pen's exploding battery impacted Mr Brown's skull, severed his carotid artery and ultimately caused his death on 29 January. The incident took place in the parking lot of a vape shop in Fort Worth, Texas on 27 January. Mr Brown had visited the shop to seek help using a Mechanical Mod style pen - a model known to have issues, a local CBS News affiliate reported. He attempted to use the pen in the car when the battery exploded with enough force to melt plastic in the vehicle and fling metal debris into Mr Brown's face. E-cigarettes 'more harmful than we think' How likely is your e-cigarette to explode? The owners of the shop called an ambulance after seeing Mr Brown bleeding in the parking lot. "When they x-rayed him, they found the stem, the metal embedded to where the blood flows up to the brain," Mr Brown's grandmother, Alice Brown, told WFAA News. Doctors were apparently unable to remove the metal surgically. Mr Brown was placed in an induced coma, but eventually passed away. Mrs Brown, who raised Mr Brown, told the Star Telegram her grandson was just weeks away from his 25th birthday. "It just hurts so bad. Now he'll never see that birthday. It's a waste of the things he could have accomplished." The 24-year-old was a licensed electrician and not a regular smoker - he had been testing out the pen for the first time, his grandmother said. She hopes his death gives others pause before trying an e-cigarette. "If anything, I hope it stops someone," she said. "I don't know how many more people will have to die." How common is this? Last May, a 38-year-old Florida man was also killed by an exploding vape pen. Tallmadge D'Elia was burned on 80% of his body and died when metal pieces entered his skull. A US government report says there have been 195 documented cases of exploding e-cigarettes between 2009 and 2016. The National Fire Data Center found 29% of exploding vape pen incidents from January 2009 to December 2016 had caused severe injuries. Another report from the University of North Texas Health Science Center looked at US emergency room data from 2015 to 2017 and found 2,035 e-cigarette related explosion and burn injuries - far more than previous reports. The researchers said regulation and surveillance of e-cigarette devices "is urgently needed".

Vaping linked to increased risk for stroke, heart attack By Dennis Thompson, HealthDay News https://www.upi.com/Vaping-linked-to-increased-risk-for-stroke-heart-attack/7431548880951/ People who vape might increase their odds of suffering a stroke, heart attack or heart disease, a new study suggests. Federal survey data revealed that compared with nonusers, people who use e-cigarettes have a: 71 percent higher risk of stroke. 59 percent higher risk of heart attack or angina. 40 percent higher risk of heart disease. E-cigarette users also have a doubled rate of smoking traditional tobacco cigarettes, the researchers noted. "Even as we consider electronic cigarettes as a means of aiding in smoking cessation, we need to be careful about the impact this may have on the health of folks," said lead researcher Dr. Paul Ndunda. He is an assistant professor with the University of Kansas School of Medicine, in Wichita. The increased health risks linked to e-cigarette use held strong even after Ndunda and his colleagues accounted for other potential risk factors, such as age, excess weight, diabetes and smoking. Dr. Larry Goldstein is chairman of neurology and co-director of the Kentucky Neuroscience Institute in Lexington. He said, "This is the first real data that we're seeing associating e-cigarette use with hard cardiovascular events." Goldstein added that "it's quite a concern, especially since nationwide now we've seen a leveling off in and, in many instances, an increase in the risk of stroke-related mortality in the country. It's hard to know what contribution this has to that, but it doesn't appear to be safer, or safe right now, from the data that's available." About 3 percent of adults and 11 percent of high school students reported using e-cigarettes within the previous month in 2016, the study authors noted. In addition, vaping among young people increased by 900 percent between 2011 and 2015. For the new study, researchers gathered data on over 400,000 participants in the 2016 Behavioral Risk Factor Surveillance System, a survey regularly conducted by the U.S. Centers for Disease Control and Prevention. The researchers included nearly 66,800 people who said they had ever regularly used e-cigarettes, comparing them with about 344,000 people who'd never tried the devices. Ndunda pointed out that the nicotine in e-cigarettes probably isn't directly causing the strokes or heart health problems, since previous studies have not linked the addictive substance to plaque formation in blood vessels. "But there are other chemicals found in electronic cigarettes that could increase inflammation of the lining of the blood vessels. That could lead to clot formation, clogging the artery and causing a stroke," Ndunda said. "The vapor is not innocuous," he concluded. However, because this is survey data, it cannot draw a direct cause-and-effect relationship between vaping and stroke or heart attack, Ndunda added. "This study has some limitations that do not allow us to make very firm conclusions and be able to change policy around e-cigarettes. I would look at this as a call for larger and longer studies into this issue," Ndunda said. Goldstein, a spokesman for the American Stroke Association, agreed. "In studies of this type, it's a common problem with all of them, is that the adjustment for potential confounders is limited," Goldstein said. "They adjust it for age, sex, smoking status, diabetes and body mass index, but there are obviously other factors that can increase the risk of cardiovascular disease that weren't measured." Gregory Conley is president of the American Vaping Association, a nonprofit that advocates for sensible regulation of vaping products. He took issue with the new findings. "Nearly all regular adult users of vaping products are current smokers or ex-smokers," Conley said. "It is not exactly breaking news that [tobacco] smokers are at a far higher risk of suffering serious medical conditions, and that it takes years for some risks to subside once a smoker has quit." The study findings were to be presented Feb. 6 at the American Stroke Association's annual meeting in Honolulu. Such research is considered preliminary until published in a peer-reviewed journal. More information Harvard Medical School has more about the health effects of e-cigarettes. Copyright © 2019 HealthDay. All rights reserved.

Evidence of a Causal Relationship Between Smoking Tobacco and Schizophrenia Spectrum Disorders James G. Scott, Lori Matuschka, Solja Niemelä, Jouko Miettunen, Brett Emmerson and Antti Mustonen 1Faculty of Medicine, The University of Queensland, Herston, QLD, Australia 2Queensland Centre for Mental Health Research, Wacol, QLD, Australia 3Metro North Mental Health, Royal Brisbane and Women's Hospital, Herston, QLD, Australia 4Faculty of Medicine, University of Turku, Turku, Finland 5Department of Psychiatry, South-Western Hospital District, Turku, Finland 6Center for Life Course Health Research, University of Oulu, Oulu, Finland 7Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland https://www.frontiersin.org/articles/10.3389/fpsyt.2018.00607/full?utm_source=AD&amp;utm_medium=FB&amp;utm_campaign=BLG_FPSYT_20180123 There has been emerging evidence of an association between tobacco smoking and schizophrenia spectrum disorders (SSD). Two meta-analyses have reported that people who smoke tobacco have an ~2-fold increased risk of incident schizophrenia or psychosis, even after adjusting for confounding factors. This study aimed to critically appraise the research which has examined the association between tobacco smoking and SSD against the Bradford Hill criteria for causality, to determine the strength of the evidence for a causal relationship. Eight longitudinal studies (seven cohort studies and one case control study) were identified which examined tobacco smoking as an exposure and psychosis as an outcome. All seven cohort studies were assessed as being of high quality using the Newcastle-Ottawa Scale. Six of the eight studies found a statistically significant positive association between tobacco smoking and onset of SSD. These studies reported a consistent association with a moderate to large effect size and a dose response relationship. The studies adjusted for multiple potential confounders including age, sex, socioeconomic status, shared genetic risk, prodromal symptoms, and comorbid cannabis and other substance use. The studies did not adjust for exposure to childhood trauma or prenatal tobacco. There was substantial though inconclusive evidence supporting a causal relationship between tobacco smoking and increased risk of SSD. If a causal relationship does exist, nicotine is most likely responsible for this association. This raises serious public health concerns about the increasing use of e-cigarettes and other products, particularly by adolescents whose nicotine use may increase their risk of SSD. Research is urgently needed to examine the association between e-cigarette use and incident psychosis, particularly in adolescents and young adults. Introduction Schizophrenia spectrum disorders (SSD) are heterogeneous syndromes with well-established risk factors including exposure to childhood adversity, cannabis use during adolescence, a history of obstetric complications, stressful events during adulthood, and low maternal serum folate level (1). In recent years, there has been a growing interest in tobacco smoking as a risk factor for SSD (2, 3). Tobacco smoking is known to cause a wide range of physical health problems. It is the leading cause of preventable death, through increasing the risk of lung and other malignancies, chronic obstructive pulmonary disease (COPD), coronary heart disease, cerebrovascular disease, asthma and diabetes (4). Two systematic reviews and meta-analyses have examined the association between tobacco smoking and psychotic disorders (2, 3). In pooling longitudinal studies (n = 5), Gurillo and colleagues reported a 2-fold increase in the risk of incident psychotic disorders in people who were daily tobacco smokers compared to those who were not (RR = 2.18; 95% CI 1.23–3.85). Similarly, Hunter et al. (3) who pooled data from studies identified using inclusion criteria with the outcome restricted to schizophrenia (N = 5) also reported smoking tobacco was associated with a 2-fold risk of schizophrenia (RR = 1.99; 95% CI 1.10–3.61). Both studies concluded that further research was needed to examine the potential causal role of tobacco smoking in the onset of SSD. The association between tobacco smoking and SSD is of growing significance. There is evidence that nicotine alters signaling in the dopaminergic, cholinergic, and glutamatergic neurotransmitter systems, particularly in adolescence (5). Whilst the smoking of tobacco by young people has declined in many high income countries, there has been an increase in exposure to nicotine by this demographic through the availability of e-cigarettes (6). It is therefore important to critically examine the evidence for a causal relationship between tobacco smoking and SSD. In this review we aimed to evaluate the relationship between tobacco smoking and SSD which we defined as any non-affective psychotic disorder against causal criteria based on the Bradford Hill Framework (7, 8). The Bradford Hill Framework provides nine criteria for establishing a causal relationship between an exposure and outcome. This review examined longitudinal studies identified from the two recent systematic reviews of tobacco smoking and incident SSD and other identified studies. The evidence for a causal relationship between tobacco smoking and SSD, alternative explanations for the association and the health implications are discussed. Methods Literature Search We used the results of the two recently conducted systematic reviews (2, 3) to identify studies which examined tobacco smoking as an exposure and SSD as an outcome. As the review by Hunter et al. (3) restricted the outcome to a diagnosis of schizophrenia, we used the broader search strategy of Gurillo et al. (2) to identify studies from January 2014 to May 2018 that included the broader outcome of psychosis. These psychosis outcomes included schizophrenia, schizophreniform disorder, schizoaffective disorder, delusional disorder, non-affective psychotic disorder, atypical psychosis, psychotic depression, and bipolar mania with psychotic features. The inclusion criteria of the current review were: (a) longitudinal case control or cohort studies; (b) study populations of participants with psychosis or schizophrenia as the outcome (defined as those who meet the diagnostic criteria by structured interview or diagnosed by treating clinician); (c) presence of tobacco smoking prior to psychosis or schizophrenia diagnosis. Studies which were cross sectional in design or only provided sub-diagnostic outcomes of psychosis (e.g., psychotic symptoms, hallucinations, delusions) were excluded. Data Extraction Titles and abstracts of the articles were reviewed to identify studies that met the eligibility criteria. The following characteristics were extracted from each study when available: (a) study methodology (including author, publication year, location, study design, follow-up period, sample numbers, loss to follow-up, age at baseline, tobacco smoking measures, and assessment of psychosis or schizophrenia), and (b) study findings (effect size metrics, 95% CI, and confounders adjusted for). The quality or the studies assessing for risk of bias was evaluated using Newcastle–Ottawa Scale (NOS) (9) as shown in Supplementary Table 1. The NOS is a method recommended by the Cochrane Non-randomized Studies Methods Working Group to evaluate the quality of the study. Points are assigned based on the selection process of cohorts (0–4 points), the comparability of the cohorts (0–2 points) and the identification of the exposures and the outcomes of research participants (0–3 points). A score of 7 or greater out of 9 was defined as high quality. Studies were assessed independently by two reviewers (LM and JS). Assessment of Causality Studies that met inclusion and exclusion criteria were assessed using causal criteria based on the Bradford Hill Framework shown in Supplementary Table 2. Of the nine criteria, five were chosen as most relevant for the purposes of this study (strength of association, consistency, temporality, dose-response, and biological plausibility). Given that smoking is known to cause a wide range of health problems, the criteria of specificity was not applicable. No studies have performed experimental manipulation exposing adolescents to tobacco because of the known harmful effects therefore this criteria was not included. Coherence was not included because of the lack of homogenous pathology evident in psychosis. In relation to analogy, the association between cannabis use and psychosis, reported to be causal (1) has some analogy to that of tobacco and psychosis. However, it is widely recognized that adolescents who smoke tobacco are more likely to smoke cannabis (10–12). Thus, cannabis rather than being analogous to tobacco in its relationship with psychosis may in fact be an important confounder. Similarly there are other important environmental factors which might confound the relationship between tobacco smoking and incident psychotic disorder. To address this concern, for the purpose of assessing evidence of causality, we included an extra criteria “accounted for confounding.” These six criteria were deemed appropriate by the research team in order to grade the associations reported between adolescent tobacco smoking and future risk of SSD as a basis for causality discussion (7). Results Gurillo and colleagues (2) identified four studies which met the specified inclusion criteria (13–16). One of the longitudinal studies (17) which they included in their pooled analysis did not determine the presence of tobacco smoking before the schizophrenia diagnosis and was therefore excluded. Hunter et al. (3) included another study (18) and the updated search identified a further three studies which met inclusion criteria (13, 19–21). In total, eight studies (seven cohort and one case-control studies) were included for assessment of a causal relationship between tobacco smoking in adolescence and incident SSD. Using the NOS, all seven cohort studies scored 7/9 or greater demonstrating they were of high quality (Table 1). Study Characteristics Table 2 summarizes the study characteristics. They utilized birth cohort studies of offspring (19, 21) or mothers (15), cohorts of young male conscripts from defense forces (14, 16), two cohorts combined, the first consisting of mothers recruited from a birth cohort, the second were male conscripts Kendler et al. (13) and two general population cohorts to assess cardiovascular risk factors (18). The longitudinal case control study was of participants at clinical high risk of psychosis (20). All studies were from high income countries. The follow-up period of all cohort studies was adequate to ascertain incident cases of SSD, ranging from a minimum of 4 years (14) to a maximum of 48 years (15). Two of the studies were genetically informed with one examining psychosis risk in family members discordant for smoking (13), the other examining schizophrenia in people with different alleles of the rs1051730 genotype in the nicotinic acetylcholine receptor gene stratified by smoking status (18). Assessment of Studies Against Bradford Hill Criteria Using causal criteria, based on the Bradford Hill Framework Hill (8), of the eight studies examined, six reported a positive association between tobacco smoking and risk of schizophrenia spectrum disorder. The strength of the associations were robust ranging from an almost 50% increased risk (15) to a 6-fold increased risk of schizophrenia in heavy smokers (18). In these six studies, all reported a temporal association with appropriate adjustment for confounding variables, particularly comorbid substance use. All but one (19) demonstrated a dose response relationship between tobacco use and SSD. By contrast, one study (16) reported that smoking tobacco reduced the risk of schizophrenia and the case control study (20) found no association. Discussion Two meta-analyses have demonstrated that smoking tobacco is associated with a 2-fold increase in risk of incident schizophrenia (3) or broader psychosis (2). Based on these systematic reviews and our own literature search, we identified eight studies that examined the longitudinal association between tobacco smoking and incident SSD of which six demonstrated a positive association (13–15, 18, 19, 21), one a negative association (16) and the final study showed no association (20). Using the Bradford Hill framework, a causal association between tobacco smoking and onset of SSD is discussed on the basis of strength of association, temporality, dose-response, adjustment for confounding factors, biological plausibility, and consistency of the association. Strength Of the six studies that found a positive association (13–15, 18, 19, 21), five reported moderate to large effect sizes (22) (Tables 2, 3) consistent with a causal relationship (8). Sørensen et al. (15) reported a smaller effect size with a 42% increase in the odds of schizophrenia spectrum disorder in people who smoked cigarettes. Consistency Consistency of the association is assessed through multiple studies of independent cohorts confirming the same result. In the eight longitudinal studies, six reported a positive association between tobacco smoking and incident SSD. Of the two which did not report a positive association, one was a case-control study of participants at clinical high risk for psychosis which found that neither tobacco nor cannabis smoking were associated with transition to psychosis. The prevalence of tobacco and cannabis dependence in this cohort was low and the study may have been underpowered to examine the effects of these substances on transition to psychosis. Zammit et al. (16) reported that smoking tobacco was associated with a lower risk of future schizophrenia, and was therefore inconsistent with the main body of research. The overwhelming majority of studies showed a positive relationship fulfilling criteria for consistency. Temporality The six studies that reported a positive association demonstrated a clear temporal relationship with the exposure of tobacco smoking preceding the onset of SSD. Schizophrenia spectrum disorders frequently have an insidious onset with a long prodrome. In order to address this concern, (21), adjusted for prodromal psychotic symptoms at baseline and Kendler et al. (13) accounted for the possible prodrome by conducting a subanalysis restricting the onset of SSD to at least 5 years following initial exposure to tobacco. The relationship between tobacco smoking and onset of schizophrenia was largely attenuated after accounting for the prodrome rendering reverse causality an unlikely explanation for the association between tobacco use and SSD thus suggesting tobacco smoking precedes the illness. Dose-Response A dose response between tobacco smoking and incident SSD was reported in five of the six studies reporting a positive association. In three studies (14, 15, 21) a significant linear trend was demonstrated where the risk of SSD increased with the an increase in tobacco smoking. In two studies (13, 18), those who smoked more daily tobacco had an increase in the odds of developing SSD. Potential Confounders The relationship between tobacco use and SSD remained significant even after adjusting for factors that might confound the relationship including family socio-economic status, cannabis use (1), parental substance abuse and parental psychosis (23–27). A shared genetic liability was also accounted for in two genetically informed studies (13, 18). Adjustment for confounders attenuated the strength of the association but significance was maintained in all but one study (19), probably due to a lack of power for the analysis. None of the studies adjusted for childhood trauma (28). Biological Plausibility Tobacco and tobacco smoke contain almost 5,000 different chemicals. Nicotine is the most important pharmacologically active and psychotogenic compound in tobacco smoke because of its interaction with nicotinic acetylcholine receptors (29). Previous reports on tobacco smoking suggests that nicotine could alter signaling of dopaminergic, cholinergic, and glutamatergic neurotransmitter systems (5, 30) and thus could potentially influence brain development as suggested by studies of adolescent nicotine exposure and neurodevelopmental trajectories (5). Also, excess nicotine intake during early adolescence is associated with abnormal white matter maturation in adults (31), and chronic cigarette smoking has been linked to structural brain changes such as gray matter decreases in the prefrontal cortex, which correspond with areas where functional alterations occur from nicotine exposure (32). Furthermore, recent evidence suggest that adolescent nicotine use could have persistent effects on nicotine receptor responsiveness, which results in the strengthening of negative emotional changes and alterations in cognitive functioning (5). Alternative Explanations There are other explanations for the positive association between tobacco smoking and SSD. Individuals who develop schizophrenia are more likely to have externalizing symptoms in childhood and adolescence (33, 34) and children with externalizing symptoms are more likely to smoke tobacco during adolescence (35). There may be unmeasured confounding. None of the studies adjusted for childhood trauma, a well-established risk factor for SSD (1, 28) and for tobacco use (36). Similarly there was no adjustment for prenatal tobacco smoking exposure which is associated with both an increased risk of smoking in adolescence (37) and an increased risk of schizophrenia even after adjusting for life time smoking (3, 38). Furthermore, recent studies have suggested bidirectional associations by revealing single nucleotide polymorphisms associated with nicotine dependence (CHRNA5) that are also associated with schizophrenia (39, 40). Limitations Each study included in this review is observational in methodology, and the majority of cohort studies included had significant attrition. Participants who are most likely to be lost to follow up are more likely to be socioeconomically disadvantaged and be at increased risk of both tobacco smoking and mental illness. Therefore, it is unlikely that attrition would significantly affect reported associations. Measurement of tobacco smoking has been measured via self-report or by interview, generally at one point in time and often retrospectively recalled. Only one study measured the long-term smoking exposure prior the psychotic illness using pack-years (18) which provides a more precise measurement of tobacco smoke exposure. Further, no studies have used biological markers for tobacco smoking such as expired air carbon monoxide (41) or serum cotinine measurement (42). These limitations are inherent to large cohort and registry studies and are difficult to overcome. Finally, as two recent systematic reviews had been published on this topic, we relied on these to identify the studies included in this review rather than replicating the searches in these studies. Implications Given tobacco is known to have widespread adverse health outcomes and governments around the world are adopting policies to reduce tobacco smoking, why is it important to clarify if smoking tobacco has a causal role in the onset of SSD? The first reason is that better understanding the aetiopathogenesis of SSD will inform our knowledge of this syndrome which may lead to better treatments. The second, a much more urgent consideration is the growing availability of electronic (e) cigarettes. These have been developed as a safer alternative to cigarettes by enabling nicotine use without the exposure to carcinogenic chemicals associated with smoking tobacco. However, there is growing use of e-cigarettes and other nicotine products by adolescents (6) and it is acknowledged that the health effects of e-cigarettes on youth are not fully understood (43). In addition to tobacco and cannabis, there is now evidence that adolescents who use inhalants are at increased risk of psychotic disorders (44) suggesting that adolescence is the developmental period where adverse neuropsychiatric outcomes from psychoactive substances are most likely to occur. There is substantial though not conclusive evidence that the association between tobacco smoking and SSD is causal and may well be a result of the effects of nicotine on multiple neurotransmitter systems. Therefore, policy makers must be cautious when developing regulations for the availability of e-cigarettes, nicotine replacement therapy products and smokeless tobacco. Similarly, health practitioners who recommend e-cigarettes or smokeless tobacco products as a safe alternative to smoking need to consider the findings of the studies identified in this review, especially when providing advice to adolescents. It is essential that future well designed observational studies are undertaken examining the risk of SSDs in those who use e-cigarettes, particularly in adolescence. A major challenge is the low prevalence of SSD. Recruiting samples large enough to examine the association between e-cigarettes and SSD will take many years. Previous longitudinal research has shown positive associations between cannabis, tobacco and alcohol use and psychotic experiences (PE) which are proxy markers for psychosis risk. PE have the advantage of being higher in prevalence compared to SSD thereby reducing the required sample size to identify associations. Schizophrenia endophenotypes may also have a role to inform the association between nicotine exposure through e-cigarettes and risk of SSD. Previous research has shown that smoking tobacco modulates the association between polymorphisms of transcription factor 4 and reduced sensory gating, an endophenotype of schizophrenia suggesting that the smoking of tobacco might play a role in early information processing deficits in schizophrenia (45). Use of research paradigms such as PE and endophenotypes PE would expedite research into the association between e-cigarette use and SSD risk. Further research is urgently needed to determine if nicotine is causally associated with incident SSD. In the interim, it is important that policy makers consider the available evidence between tobacco smoking and risk of schizophrenia when evaluating the potential health consequences that might arise from community access to e-cigarettes. Author Contributions JS and AM planned the review. LM conducted the initial literature search and JS and LM assessed papers for suitability for inclusion. JS and LM reviewed all the papers and assessed them for quality. JS, LM, and AM wrote the first draft of the manuscript and all authors contributed to further drafts. All authors reviewed and approved the final draft. Funding JS is supported by a National Health and Medical Research Council Practitioner Fellowship Grant APP1105807 and employed by The Queensland Centre for Mental Health Research which receives core funding from the Queensland Health. AM is supported by Juho Vainio Foundation, Scholarship Fund of the University of Oulu, Oulun Lääketieteellinen tutkimussäätiö and The Hospital District of South Ostrobothnia, Finland. JM is supported by Academy of Finland (#268336). Conflict of Interest Statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Supplementary Material The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fpsyt.2018.00607/full#supplementary-material References 1. Belbasis L, Köhler CA, Stefanis N, Stubbs B, Os Jv, Vieta E, et al. Risk factors and peripheral biomarkers for schizophrenia spectrum disorders: an umbrella review of meta-analyses. Acta Psychiatr Scand. (2018) 137:88–97. doi: 10.1111/acps.12847 PubMed Abstract | CrossRef Full Text | Google Scholar 2. Gurillo P, Jauhar S, Murray RM, MacCabe JH. 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I think everybody is looking at the same forest but the trees are getting in the way. The bottom line is, whether NRT is used or not, the goal is to get off of nicotine completely and for good. The use of NRT delays nicotine withdrawal but again, that's okay so long as the goal is to stop nicotine for good, and much sooner than later. There is no one right way to quit but there is only one way to stay quit and that is to NEVER TAKE ANOTHER PUFF, EVER. I used Wellbutrin to quit and it worked for me. No need for anybody to look in the past because as long as we're not smoking and not using nicotine in any form, we've succeeded at stomping nicotine addiction out of lives and much, much less of a chance of relapse. Our philosophy on quitting smoking: Quit Train®, a quit smoking support community, was created by former smokers who have a deep desire to help people quit smoking and to help keep those quits intact. This place should be a safe haven to escape the daily grind and focus on protecting our quits. We don't believe that there is a "one size fits all" approach when it comes to quitting smoking. Each of us has our own unique set of circumstances which contributes to how we go about quitting and more importantly, how we keep our quits. This is not an environment where anybody will be judged as we only exist to offer education, support and acceptance. Through education and sharing experiences, we can all help each other to keep this nasty, deadly addiction out of our lives. We all want the same thing; to stay smoke-free and enjoy our lives of living as a non-smoker and all of the health benefits and freedom that it offers. Anybody can quit smoking and anybody can stay that way. It's a matter of finding a good combination of education and support to expose the lies of smoking in a comfortable, come as you are environment. We welcome all with open arms and hope that you can make this your safe haven to take your freedom back and get on with the business of living life as a non-smoker.

notsmokinjo, That's awesome! You had a conversation with those children that they probably won't ever forget. It's fantastic that you had the opportunity to talk to your daughter and a group of her friends about smoking and vaping. That's really paying it forward. Very cool that they were able to use QT for a research tool. I love it! Oh, you might have already seen article about nicotine found in vape liquids, despite it being illegal in AT, but in case you haven't...

mpower download from WHO mpower_english.pdf

I have a 9 year old daughter who remembers when I used to smoke. This is a conversation that has come up from time-to-time since I quit but even more so now, because I bring up smoking and vaping to her, which leads to a lot of questions from her. The superintendent of her school system sent an email to all of the parents about the kids vaping. I talked to her about this and explained to her about the nasty things that come along with vaping. Things like heavy metals, how the heavy metals get into the vapor and how dangerous it actually is and of course the dangers of nicotine addiction. I want her to not even be tempted to try any of this but if she ever is, I want her to know the truth behind all of the clever marketing targeting our children. This is 1970's tobacco advertising all over again. As former smokers who are educated about addiction and how to beat it, there is nobody more qualified to reach kids and stop this epidemic from going any further. Moreover, there also is nobody better than us to talk to kids who are already vaping (or smoking) and addicted and help them to quit. We're experts in this field and talk about paying it forward, this is our chance. Do any members here have school age children, nieces, nephews, grandchildren etc. and if so, have you talked to them about this? There are lots if educational articles and videos about the dangers of vaping and juuling on the new board: Vaping & Juuling: Unquestionable Addiction, Reckless Aftermath The concerted efforts of big tobacco corporations - same drug, new package, new demographic; our youth.

My 9 year old daughter asked me the other day if my lungs were more black or pink. I talk to her about smoking, vaping etc. so she knows the truth about this stuff. My Mom and my Aunt have never taken a single puff of a cigarette, despite growing up with both parents who smoked, all her brothers, uncles, aunts etc. My goal is to teach my daughter now so she knows the consequences of smoking, vaping etc. so she doesn't even want to try any of it.

Some members here are still smoking, trying to quit. That's okay. This is where they need to be. Some are using NRT products. However, that is fine so long as the NRT is short-term, very short-term because the goal is to get off of nicotine completely. The sooner the better which is why the cold turkey method have the most success. It's not the only method that works, but it is the method of quitting that has best success rates, hands down. Anybody who is vaping any amount of nicotine is not quit. This is not even worth debating because the person is still putting nicotine into their body and keeping the drug addiction alive and well; they're only lying to themselves, as all using drug addicts do. See this board for everything you need to know about vaping. Vaping & Juuling: Unquestionable Addiction, Reckless Aftermath

Congratulations! Glad to see you're celebrating! You deserve it because staying quit for two weeks is no small feat! 😎

NOPE!