National Drug Prevention Alliance & PPP

Nicotine

Abstract

Studies examining lifestyle and cognitive decline often use healthy lifestyle indices, making it difficult to understand implications for interventions. We examined associations of 16 lifestyles with cognitive decline. Data from 32,033 cognitively-healthy adults aged 50-104 years participating in prospective cohort studies of aging from 14 European countries were used to examine associations of lifestyle with memory and fluency decline over 10 years. The reference lifestyle comprised not smoking, no-to-moderate alcohol consumption, weekly moderate-plus-vigorous physical activity, and weekly social contact. We found that memory and fluency decline was generally similar for non-smoking lifestyles. By contrast, memory scores declined up to 0.17 standard deviations (95% confidence interval= 0.08 – 0.27) and fluency scores up to 0.16 standard deviations (0.07 – 0.25) more over 10 years for those reporting smoking lifestyles compared with the reference lifestyle. We thus show that differences in cognitive decline between lifestyles were primarily dependent on smoking status.

Source: https://www.nature.com/articles/s41467-024-49262-5 June 2024

Filed under: Brain and Behaviour,Health,Nicotine :

Cannabis is harmful to the lungs, but in a different way to tobacco, causing significant respiratory symptoms such as bronchitis with evidence to suggest it can result in destructive lung disease – sometimes referred to as ‘bong lung’ – in heavy cannabis users.

These are the key findings from a review of research on the effects of smoking cannabis on the lungs undertaken by respiratory specialists, Professor Bob Hancox, from the University of Otago’s Department of Preventive and Social Medicine and Dr Kathryn Gracie, from Waikato Hospital’s Respiratory Department.

Cannabis is the second-most commonly smoked substance after tobacco and the most widely-used illicit drug world-wide. Although cannabis remains illegal in most countries, many countries – like New Zealand – are considering decriminalising or legalising its use.

Professor Hancox explains that much of the debate about legalising cannabis appears to revolve around the social and mental health effects. Both he and Dr Gracie believe policies around the liberalisation of cannabis should consider the wider health effects of smoking cannabis.

“The potential for adverse effects on respiratory health from smoking cannabis has had much less attention than the social and mental health effects,” Professor Hancox says.

“We believe policies around the liberalisation of cannabis should consider the potential impacts on the lungs.

“Whether liberalising availability will lead to further increases in cannabis use remains to be seen, but it is likely that patterns of cannabis use will change, with resulting health consequences.”

Because cannabis has been an illegal and unregulated substance and the fact most cannabis users also smoke tobacco, making the effects difficult to separate, Dr Gracie explains that it has been difficult to carry out research on cannabis and its direct impact on the lungs.

“Perhaps, most importantly, the individuals who are extremely heavy users of cannabis may not be well represented in the existing epidemiological research. Most case reports of cannabis-related destructive lung disease document very heavy cannabis consumption.

“Despite these limitations there is sufficient evidence that cannabis causes respiratory symptoms and has the potential to damage both the airways and the lungs.”

“Cannabis may also increase the risk of lung cancer, but there is not enough evidence to be sure of this yet,” Dr Gracie says.

Professor Hancox says there is still a lot to learn about cannabis, but there is sufficient evidence to show that smoking cannabis is not harmless to the lungs.

A combination of smoking both cannabis and tobacco is likely to result in poorer health outcomes.

“Many people smoke both cannabis and tobacco and are likely to get the worst of both substances.”

Source: https://www.otago.ac.nz/news/news/smoking-cannabis-causes-bronchitis-and-changes-to-lung-function May 2020

Filed under: Cannabis/Marijuana,Health,Nicotine :

In 2017 Iceland received word-wide attention for having dramatically reversed the course of teenage substance use. From 1998 to 2018, the percentage of 15-16-year-old Icelandic youth who were drunk in the past 30 days declined from 42% to 5%; daily cigarette smoking dropped from 23% to 3%; and having used cannabis one or more times fell from 17% to 5%. The core elements of the model are: 1) long-term commitment by local communities; 2) emphasis on environmental rather than individual change; 3) perception of adolescents as social attributes. This presentation describes how the Iceland prevention model is built upon collaboration between policy makers, researchers, parent organizations, and youth practitioners. These groups have created a system whereby youth receive the necessary guidance and support to live fun and productive lives without reliance on psychoactive substances. The Model is being replicated in 35 municipalities within 17 countries around the globe. The Icelandic Model: Evidence Based Primary Prevention – 20 Years of Successful Primary Prevention Work was featured for the past two years at the Special Session of the United Nations General Assembly on the World Drug Problem.

Source: https://www.researchgate.net/publication/330347576_Perspective_Iceland_Succeeds_at_Preventing_Teenage_Substance_Use February 2019

Filed under: Alcohol,Cannabis/Marijuana,Methamphetamine/GHB/Hallucinogens/Oxycodone,Nicotine,Political Sector,Prevention and Intervention,Social Affairs,Youth :

Summary

Background

Adolescence represents a crucial developmental period in shaping mental health trajectories. In this study, we investigated the effect of the COVID-19 pandemic on mental health and substance use during this sensitive developmental stage.

Methods

In this longitudinal, population-based study, surveys were administered to a nationwide sample of 13–18-year-olds in Iceland in October or February in 2016 and 2018, and in October, 2020 (during the COVID-19 pandemic). The surveys assessed depressive symptoms with the Symptom Checklist-90, mental wellbeing with the Short Warwick Edinburgh Mental Wellbeing Scale, and the frequency of cigarette smoking, e-cigarette use, and alcohol intoxication. Demographic data were collected, which included language spoken at home although not ethnicity data. We used mixed effects models to study the effect of gender, age, and survey year on trends in mental health outcomes.

Findings

59 701 survey responses were included; response rates ranged from 63% to 86%. An increase in depressive symptoms (β 0·57, 95% CI 0·53 to 0·60) and worsened mental wellbeing (β −0·46, 95% CI −0·49 to −0·42) were observed across all age groups during the pandemic compared with same-aged peers before COVID-19. These outcomes were significantly worse in adolescent girls compared with boys (β 4·16, 95% CI 4·05 to 4·28, and β −1·13, 95% CI −1·23 to −1·03, respectively). Cigarette smoking (OR 2·61, 95% CI 2·59 to 2·66), e-cigarette use (OR 2·61, 95% CI 2·59 to 2·64), and alcohol intoxication (OR 2·59, 95% CI 2·56 to 2·64) declined among 15–18-year-olds during COVID-19, with no similar gender differences.

Interpretation

Our results suggest that COVID-19 has significantly impaired adolescent mental health. However, the decrease observed in substance use during the pandemic might be an unintended benefit of isolation, and might serve as a protective factor against future substance use disorders and dependence. Population-level prevention efforts, especially for girls, are warranted.

Funding

Icelandic Research Fund.

Source: Depressive symptoms, mental wellbeing, and substance use among adolescents before and during the COVID-19 pandemic in Iceland: a longitudinal, population-based study – The Lancet Psychiatry June 2021

Filed under: Alcohol,Brain and Behaviour,Drug use-various effects,Nicotine,Youth :

Abstract

Background:

Cardiovascular anomalies are the largest group of congenital anomalies and the major cause of death in young children, with various data linking rising atrial septal defect incidence (ASDI) with prenatal cannabis exposure.

Objectives / Hypotheses:

Is cannabis associated with ASDI in USA? Is this relationship causal?

Methods:

Geospatio/temporal cohort study, 1991–2016. Census populations of adults, babies, congenital anomalies, income and ethnicity.

Drug exposure data on cigarettes, alcohol abuse, past month cannabis use, analgesia abuse and cocaine taken from National Survey of Drug Use and Health (78.9% response rate). Cannabinoid concentrations from Drug Enforcement Agency. Inverse probability weighted (ipw) regressions.

Analysis conducted in R.

Results:

ASDI rose nationally three-fold from 27.4 to 82.8 / 10,000 births 1991–2014 during a period when tobacco and alcohol abuse were falling but cannabis was rising. States including Nevada, Kentucky, Mississippi and Tennessee had steeply rising epidemics (Time: Status β-estimate = 10.72 (95%C.I. 8.39–13.05), P < 2.0 × 10 − 16). ASDI was positively related to exposure to cannabis and most cannabinoids.

Drug exposure data was near-complete from 2006 thus restricting spatial modelling from 2006 to 2014, N = 282. In geospatial regression models cannabis: alcohol abuse term was significant (β-estimate = 19.44 (9.11, 29.77), P = 2.2 × 10 − 4 ); no ethnic or income factors survived model reduction.

Cannabis legalization was associated with a higher ASDI (Time: Status β-estimate = 0.03 (0.01, 0.05), P = 1.1 × 10 -3). Weighted panel regression interactive terms including cannabis significant (from β-estimate = 1418, (1080.6, 1755.4), P = 7.3 × 10 -15). Robust generalized linear models utilizing inverse probability weighting interactive terms including cannabis appear (from β-estimate = 78.88, (64.38, 93.38), P = 1.1 × 10 -8).

Marginal structural models with machine-aided Super Learning association of ASDI with high v. low cannabis exposure R.R. = 1.32 (1.28, 1.36). Model e-values mostly > 1.5.

Conclusions:

ASDI is associated with cannabis use, frequency, intensity and legalization in a spatiotemporally significant manner, robust to socioeconomic demographic adjustment and fulfilled causal criteria, consistent with multiple biological mechanisms and similar reports from Hawaii, Colorado, Canada and Australia. Not only are these results of concern in themselves, but they further imply that our list of the congenital teratology of cannabis is as yet incomplete, and highlight in particular cardiovascular toxicology of prenatal cannabinoid and drug exposure.

Albert Stuart Reece and Gary Kenneth Hulse

Source: BMC Pediatrics volume 20, Article number: 539 (2020) https://bmcpediatr.biomedcentral.com/articles/10.1186/s12887-020-02431-z November 2020

Filed under: Alcohol,Cannabis/Marijuana,Drug use-various effects on foetus, babies, children and youth,Global Drug Legalisation Efforts,Nicotine :

One way to deter harmful recreational drug use by teenagers is to treat them like adults. Rather than simply tell them to “Just Say No” to alcohol, tobacco or illicit drugs, it may be more helpful to explain how these substances create unique risks for them risks that arise due to the changing state of the adolescent brain.

It’s an approach recommended by Dr. Robert DuPont, the first director of the National Institute of Drug Abuse, the second White House “drug czar” and the current head of the Institute for Behavior and Health.

Scientists have long recognized that people who use alcohol, tobacco, marijuana and other drugs while adolescents are far more likely to use more dangerous drugs in their 30s and 40s. Back in 1984, researchers writing in the American Journal of Public Health reported that “the use of marijuana is a good predictor of the use of more serious drugs only if it begins early” and that early drinking is a similar “predictor of marijuana use.”

It should come as no surprise, then, that Americans in their 30s and 40s who used recreational drugs as teenagers are the group most severely affected by opioid overdoses today.

Unfortunately, neither the media nor popular culture adequately informs young people about the neurological damage alcohol, nicotine, and marijuana can inflict on the brain. On the contrary, despite strong evidence that early recreational drug use increases the likelihood of future drug addiction, the media and today’s culture often describe marijuana use as an “organic,” “natural” approach to anxiety and stress management. Indeed, Northern Michigan University launched the nation’s first medicinal plant chemistry major, offering students the chance to focus on marijuana-related studies. What message does that send to the still-developing minds of college students?

One group is taking a non-traditional approach to convincing students otherwise.

One Choice is a drug prevention campaign developed for teenagers by the Institute for Behavior and Health. It relies on cutting-edge neuroscience to encourage young Americans to make decisions that promote their brain health.

Pioneered by Dr. DuPont, One Choice specifically advocates that adolescents make “no use of any alcohol, nicotine, marijuana or other drugs” for health reasons. The theory is that adolescents who make the decision not to use alcohol, nicotine, or marijuana at all that make “One Choice” to avoid artificial, chemical brain stimulation are far less likely to wind up addicted to drugs such as opioids later on.

The One Choice approach is evidence-based. In 2017, scientists at Mclean Hospital and Harvard Medical School published their findings on the impact of early substance use on cognitive development. They explained that the brains of teenagers are still developing and can be negatively impacted by substance use. Adolescent brains are still forming the communication routes that regulate motivation, stress and habit-formation well into adulthood. As such, it is easier for substances to hijack and alter those routes in developing brains than in adult brains.

Hindering the vital attributes of habit formation, stress management and motivational behavior can drastically affect a young person’s academic performance. Collectively, and in the long run, that can impair the competitiveness of a national economy. Thus, it is crucial that young Americans learn to prioritize brain health.

The timing for the innovative One Choice approach is propitious. Today’s young Americans are more interested in biology, psychology and health sciences than ever before. According to the National Center for Education Statistics, the field of “health professions and related programs” is the second most popular major among college students, with psychology and biological or biomedical sciences following as the fourth and fifth most popular, respectively. By explaining developmental neuroscience to teenagers, One Choice engages young people on a topic of interest to them and presents the reality of a pressing public health issue, instead of throwing moral platitudes and statistics at them.

Pro-marijuana legalization organizations, such as the Drug Policy Alliance, agree: “The safest path for teens is to avoid drugs, doing alcohol, cigarettes, and prescription drugs outside of a doctor’s recommendations.” And certainly honesty, along with scientific accuracy, is critical if we are to persuade adolescents not to use drugs.

Brain health is critical to the pursuit of happiness. And leveraging scientifically accurate presentations and testimonies to convince young Americans to prioritize their own brain health early on can prevent future substance abuse.

Source: Using Neuroscience to Prevent Drug Addiction Among Teenagers | The Heritage Foundation January 2019

Filed under: Alcohol,Brain and Behaviour,Cannabis/Marijuana,Nicotine,Prevention and Intervention,Youth :

Abstract

Objectives: Many reports exist of the cardiovascular toxicity of smoked cannabis but none of arterial stiffness measures or vascular age (VA). In view of its diverse toxicology, the possibility that cannabis-exposed patients may be ageing more quickly requires investigation.

Design: Cross-sectional and longitudinal, observational. Prospective.

Setting: Single primary care addiction clinic in Brisbane, Australia.

Participants: 11 cannabis-only smokers, 504 tobacco-only smokers, 114 tobacco and cannabis smokers and 534 non-smokers.

Exclusions: known cardiovascular disease or therapy or acute exposure to alcohol, amphetamine, heroin or methadone.

Intervention: Radial arterial pulse wave tonometry (AtCor, SphygmoCor, Sydney) performed opportunistically and sequentially on patients between 2006 and 2011.

Main outcome measure: Algorithmically calculated VA.

Secondary outcomes: other central haemodynamic variables.

Results: Differences between group chronological ages (CA, 30.47±0.48 to 40.36±2.44, mean±SEM) were controlled with linear regression. Between-group sex differences were controlled by single-sex analysis. Mean cannabis exposure among patients was 37.67±7.16 g-years. In regression models controlling for CA, Body Mass Index (BMI), time and inhalant group, the effect of cannabis use on VA was significant in males (p=0.0156) and females (p=0.0084). The effect size in males was 11.84%. A dose-response relationship was demonstrated with lifetime exposure (p<0.002) additional to that of tobacco and opioids. In both sexes, the effect of cannabis was robust to adjustment and was unrelated to its acute effects. Significant power interactions between cannabis exposure and the square and cube of CA were demonstrated (from p<0.002).

Conclusions: Cannabis is an interactive cardiovascular risk factor (additional to tobacco and opioids), shows a prominent dose-response effect and is robust to adjustment. Cannabis use is associated with an acceleration of the cardiovascular age, which is a powerful surrogate for the organismal-biological age. This likely underlies and bi-directionally interacts with its diverse toxicological profile and is of considerable public health and regulatory importance.

Keywords: Accelerated aging; Biological age; Biomarkers of aging; Cannabis and aging.

Source: Cannabis exposure as an interactive cardiovascular risk factor and accelerant of organismal ageing: a longitudinal study – PubMed (nih.gov) November 2016

Filed under: Cannabis/Marijuana,Health,Nicotine :

A meta-analysis of all studies worldwide showing association between marijuana use and schizophrenia:

Moore TH, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370:319–328.
http://dirwww.colorado.edu/alcohol/downloads/Cannabis_and_behavior.pdf

“There was an increased risk of any psychotic outcome in individuals who had ever used cannabis…with greater risk in people who used cannabis most frequently. There is now sufficient evidence to warn young people that using cannabis could increase their risk of
developing a psychotic illness later in life.”

The most recent study conducted in the United States (Columbia University, New York), showing a high risk (odds ratio, “OR”) for schizophrenia spectrum disorders, particularly in those who become cannabis-dependent:

Davis GP, Compton MT, Wang S, Levin FR, Blanco C. Association between cannabis use, psychosis, and schizotypal personality disorder: findings from the National Epidemiologic Survey on Alcohol and Related Conditions. Schizophr Res. 2013 Dec;151(1-3):197-202.
“There was a similar dose-response relationship between the extent of cannabis use and schizotypal personality disorder (OR=2.02 for lifetime cannabis use, 95% CI 1.69-2.42; OR=2.83 for lifetime cannabis abuse, 95% CI 2.33-2.43; OR=7.32 for lifetime cannabis dependence, 95% CI 5.51-9.72). Likelihood of individual schizotypal features increased significantly with increased extent of cannabis use in a dose-dependent manner.”

Studies that corrected for general genetic background effects and many non-cannabis environmental variables by comparing siblings. The risk ratios are somewhat lower than general population studies, because genetic predisposition is more or less controlled for:

McGrath J, Welham J, Scott J, Varghese D, Degenhardt L, Hayatbakhsh MR, Alati R, Williams GM, Bor W, Najman JM. Association between cannabis use and psychosis-related outcomes using sibling pair analysis in a cohort of young adults. Arch Gen Psychiatry. 2010; 67(5):440-7.
“Longer duration since first cannabis use was associated with multiple psychosis-related outcomes in young adults… the longer the duration since first cannabis use, the higher the risk of psychosis-related outcomes…
Compared with those who had never used cannabis, young adults who had 6 or more years since first use of cannabis (i.e., who commenced use when around 15 years or younger) were twice as likely to develop a nonaffective psychosis…
This study provides further support for the hypothesis that early cannabis use is a risk-modifying factor for psychosis-related outcomes in young adults.”

Giordano GN, Ohlsson H, Sundquist K, Sundquist J, Kendler KS. The association between cannabis abuse and subsequent schizophrenia: a Swedish national co-relative control study.
Psychol Med. 2014 Jul 3:1-8. [Epub ahead of print]
http://journals.cambridge.org/download.php?file=%2FPSM%2FS0033291714001524a.pdf&code=79f795824a92c8eead870197ef071dd8

“Allowing 7 years from initial CA registration to later diagnosis, the risk for schizophrenia in discordant full sibling pairs remained almost twofold….The results of this study therefore lend support to the etiologic hypothesis, that CA is one direct cause of later schizophrenia.”

Those diagnosed with schizophrenia who also use recreational drugs are much more likely to be violent, including those who use cannabis:

Fazel S, Långström N, Hjern A, Grann M, Lichtenstein P. Schizophrenia, substance abuse, and violent crime. JAMA. 2009 May 20;301(19):2016-23.
“The risk was mostly confined to patients with substance abuse comorbidity (of whom 27.6% committed an offense), yielding an increased risk of violent crime among such patients (adjusted OR, 4.4; 95% CI,3.9-5.0), whereas the risk increase was small in schizophrenia patients without substance abuse comorbidity (8.5% of whom had at least 1 violent offense; adjusted OR,1.2; 95% CI, 1.1-1.4; P<0.001 for interaction).”

Fazel S, Gulati G, Linsell L, Geddes JR, Grann M. Schizophrenia and violence: systematic review and meta-analysis. PLoS Med. 2009 Aug;6(8):e1000120. doi: 10.1371/journal.pmed.1000120. Epub 2009 Aug 11.
“The effect of comorbid substance abuse was marked with….. an OR of 8.9” (as compared to the general population)

Arseneault L, Moffitt TE, Caspi A, Taylor PJ, Silva PA. Mental disorders and violence in a total birth cohort: results from the Dunedin Study. Arch Gen Psychiatry. 2000;57(10):979-86.
“for having more than two of these disorders at once…..the OR (odds ratio for violence) was, …..for marijuana dependence plus schizophrenia spectrum disorder, 18.4”

Harris AW, Large MM, Redoblado-Hodge A, Nielssen O, Anderson J, Brennan J. Clinical and cognitive associations with aggression in the first episode of psychosis. Aust N Z J Psychiatry. 2010 Jan;44(1):85-93.
‘The use of cannabis with a frequency of more than fourfold in the previous month was the only factor that was found to be associated with serious aggression’

Self-report of psychotic symptoms by otherwise healthy users (12% to 15%):

Thomas H. A community survey of adverse effects of cannabis use. Drug Alcohol Depend. 1996 Nov;42(3):201-7.
“This survey estimates the frequency of various adverse effects of the use of the drug cannabis. A sample of 1000 New Zealanders aged 18-35 years were asked to complete a self-administered questionnaire on cannabis use and associated problems. The questionnaire was derived from criteria for the identification of cannabis abuse which are analagous to criteria commonly used to diagnose alcoholism. Of those who responded 38% admitted to having used cannabis. The most common physical or mental health problems, experienced by 22% of users were acute anxiety or panic attacks following cannabis use. Fifteen percent reported psychotic symptoms following use.”

Barkus EJ, Stirling J, Hopkins RS, Lewis S.. Cannabis-induced psychosis-like experiences are associated with high schizotypy Psychopathology 2006;39(4):175-8.
“In the sample who reported ever using cannabis (72%) the means for the subscales from the CEQ were as follows: ……Psychotic-Like Experiences (12.98%).”

Rates of psychotic symptoms in those with cannabis dependence as compared to non-dependent users and nonusers:

Fergusson DM, Horwood LJ, Swain-Campbell NR. Cannabis dependence and psychotic symptoms in young people. Psychol Med. 2003 Jan;33(1):15-21.
“Young people meeting DSM-IV criteria for cannabis dependence had elevated rates of psychotic symptoms at ages 18 (rate ratio = 3.7; 95% CI 2.8-5.0; P < 0.0001) and 21 (rate ratio = 2.3; 95% CI 1.7-3.2; P < 0.0001).”

Smith MJ, Thirthalli J, Abdallah AB, Murray RM, Cottler LB. Prevalence of psychotic symptoms in substance users: a comparison across substances. Compr Psychiatry. 2009 May-Jun;50(3):245-50. doi: 10.1016/j.comppsych.2008.07.009. Epub 2008 Sep 23.
“more than half of the respondents who were dependent on cocaine (80%), cannabis (63.5%), amphetamines (56.1%), and opiates (53.1%) reported psychotic symptoms. Among all users of substances without a diagnosis of abuse or dependence, cannabis users reported the highest prevalence of psychotic symptoms (12.4%)……. There was also a marked increase in the risk for psychotic symptoms when dependence became moderate or severe for cannabis (OR=25.1, OR=26.8; respectively).”

Studies on the psychotomimetic properties of THC administered to healthy individuals in the clinic:

D’Souza DC, Perry E, MacDougall L, Ammerman Y, Cooper T, Wu YT, Braley G, Gueorguieva R, Krystal JH. The psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in healthy individuals: implications for psychosis. Neuropsychopharmacology. 2004 Aug;29(8):1558-72.
“∆-9-THC (1) produced schizophrenia-like positive and negative symptoms; (2) altered perception;(3) increased anxiety; (4) produced euphoria; (5) disrupted immediate and delayed word recall, sparing recognition recall; (6) impaired performance on tests of distractibility, verbal fluency, and working memory (7) did not impair orientation; (8) increased plasma cortisol. These data indicate that D-9-THC produces a broad range of transient symptoms, behaviors, and cognitive deficits in healthy individuals that resemble some aspects of endogenous psychoses.”

Morrison PD, Nottage J, Stone JM, Bhattacharyya S, Tunstall N, Brenneisen R, Holt D, Wilson D, Sumich A, McGuire P, Murray RM, Kapur S, Ffytche DH. Disruption of frontal θ coherence by ∆9-tetrahydrocannabinol is associated with positive psychotic symptoms. Neuropsychopharmacology. 2011;;36(4):827-36.
“Compared with placebo, THC evoked positive and negative psychotic symptoms, as measured by the positive and negative syndrome scale (p<0.001)…… The results reveal that the pro-psychotic effects of THC might be related to impaired network dynamics with impaired communication between the right and left frontal lobes.”

Bhattacharyya S, Crippa JA, Allen P, Martin-Santos R, Borgwardt S, Fusar-Poli P, Rubia K, Kambeitz J, O’Carroll C, Seal ML, Giampietro V, Brammer M, Zuardi AW, Atakan Z, McGuire PK. Induction of psychosis by ∆9-tetrahydrocannabinol reflects modulation of prefrontal and striatal function during attentional salience processing. Arch Gen Psychiatry. 2012 Jan;69(1):27-36. doi: 10.1001/archgenpsychiatry.2011.161.
“Pairwise comparisons revealed that 9-THC significantly increased the severity of psychotic symptoms compared with placebo (P<.001) and CBD (P<.001).”,

Freeman D, Dunn G, Murray RM, Evans N, Lister R, Antley A, Slater M, Godlewska B, Cornish R, Williams J, Di Simplicio M, Igoumenou A, Brenneisen R, Tunbridge EM, Harrison PJ, Harmer CJ, Cowen P, Morrison PD. How Cannabis Causes Paranoia: Using the Intravenous Administration of ∆9-Tetrahydrocannabinol (THC) to Identify Key Cognitive Mechanisms Leading to Paranoia. Schizophr Bull. 2014 Jul 15. pii: sbu098. [Epub ahead of print]
“THC significantly increased paranoia, negative affect (anxiety, worry, depression, negative thoughts about the self), and a range of anomalous experiences, and reduced working memory capacity.”

For data on dose-response (a very large study by Zammit et al., and another by van Os et al.) and the greater risk for psychosis posed by high strength marijuana (DiForti et al.):

Zammit S, Allebeck P, Andreasson S, Lundberg I, Lewis G, 2002, Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969: historical cohort study. BMJ. 2002 Nov 23;325(7374):1199. http://www.bmj.com/content/325/7374/1199.full.pdf
“We found a dose dependent relation between frequency of cannabis use and risk of schizophrenia, with an adjusted odds ratio for linear trend across the categories of frequency of cannabis use used in this study of 1.2 (1.1 to 1.4, P < 0.001). The adjusted odds ratio for subjects with a history of heaviest use of cannabis ( > 50 occasions) was 3.1 (1.7 to 5.5)………………Cannabis use is associated with an increased risk of
developing schizophrenia, consistent with a causal relation. This association is not explained by use of other psychoactive drugs or personality traits relating to social integration.”

van Os J, Bak M, Hanssen M, Bijl RV, de Graaf R, Verdoux H. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol. 2002 Aug 15;156(4):319-27.
“…..further evidence supporting the hypothesis of a causal relation is demonstrated by the existence of a dose-response relation.. between cumulative exposure to cannabis use and the psychosis outcome……. About 80 percent of the psychosis outcome associated with exposure to both cannabis and an established vulnerability to psychosis was attributable to the synergistic action of these two factors. This finding indicates that, of the subjects exposed to both a vulnerability to psychosis and cannabis use, approximately 80 percent had the psychosis outcome because of the combined action of the two risk factors and only about 20 percent because of the action of either factor alone.”

DiForti M, Morgan C, Dazzan P, Pariante C, Mondelli V, Marques TR, Handley R, Luzi S, Russo M, Paparelli A, Butt A, Stilo SA, Wiffen B, Powell J, Murray RM. High-potency cannabis and the risk of psychosis. Br J Psychiatry. 2009,195(6):488-91.
“78% (n = 125) of the cases group preferentially used sinsemilla (skunk) compared with only 31% (n = 41) of the control group (unadjusted OR= 8.1, 95% CI 4.6–13.5). This association was only slightly attenuated after controlling for potential confounders (adjusted OR= 6.8, 95% CI 2.6–25.4)………. Our most striking finding is that patients with a first episode of psychosis preferentially used high-potency cannabis preparations of the sinsemilla (skunk) variety…… our results suggest that the potency and frequency of cannabis use may interact in further increasing the risk of psychosis.”

DiForti M, Marconi A, Carra E, Fraietta S, Trotta A, Bonomo M, Bianconi F, Gardner-Sood P, O’Connor J, Russo M, Stilo SA, Marques TR, Mondelli V, Dazzan P, Pariante C, David AS, Gaughran F, Atakan Z, Iyegbe C, Powell J, Morgan C, Lynskey M, Murray RM. Proportion of
patients in south London with first-episode psychosis attributable to use of high potency cannabis: a case-control study. Lancet Psychiatry, online February 18, 2015, http://dx.doi.org/10.1016/S2215-0366(14)00117-5.
“In the present larger sample analysis, we replicated our previous report and showed that the highest probability to suffer a psychotic disorder is in those who are daily users of high potency cannabis. Indeed, skunk use appears to contribute to 24% of cases of first episode psychosis in south London. Our findings show the importance of raising awareness among young people of the risks associated with the use of high-potency cannabis. The need for such public education is emphasised by the worldwide trend of liberalisation of the legal constraints on cannabis and the fact that high potency varieties are becoming much more widely available.”

For data on percent of those with marijuana-induced psychosis who go on to receive a diagnosis of a schizophrenia spectrum disorder:

Arendt M, Mortensen PB, Rosenberg R, Pedersen CB, Waltoft BL. Familial predisposition for psychiatric disorder: comparison of subjects treated for cannabis-induced psychosis and schizophrenia. Arch Gen Psychiatry. 2008;65(11):1269-74. http://archpsyc.ama-assn.org/cgi/reprint/65/11/1269
“Approximately half of the subjects who received treatment of a cannabis induced psychosis developed a schizophrenia spectrum disorder within 9 years after treatment…… The risk of schizophrenia after a cannabis-induced psychosis is independent of familial predisposition……. cannabis-induced psychosis may not be a valid diagnosis but an early marker of schizophrenia……. Psychotic symptoms after cannabis
use should be taken extremely seriously.”

Niemi-Pynttäri JA, Sund R, Putkonen H, Vorma H, Wahlbeck K, Pirkola SP. Substance-induced psychoses converting into schizophrenia: a register-based study of 18,478 Finnish inpatient cases. J Clin Psychiatry. 2013 74(1):e94-9.
“Eight-year cumulative risk to receive a schizophrenia spectrum diagnosis was 46% for persons with a diagnosis of cannabis-induced psychosis ….. chances for amphetamine-, hallucinogen-, opioid-, sedative- and alcohol-induced (schizophrenia spectrum diagnoses) were 30%, 24%, 21%, and 5% respectively.”

For cause and effect (which comes first: psychosis or marijuana use):
Arseneault L, Cannon M, Poulton R, Murray R, Caspi A, Moffitt TE, 2002, Cannabis use in
adolescence and risk for adult psychosis: longitudinal prospective study.BMJ. 2002 Nov 23;325(7374):1212-3.
“Firstly, cannabis use is associated with an increased risk of experiencing schizophrenia symptoms, even after psychotic symptoms preceding the onset of cannabis use are controlled for, indicating that cannabis use is not secondary to a pre-existing psychosis. Secondly, early cannabis use (by age 15) confers greater risk for schizophrenia outcomes than later cannabis use (by age 18). Thirdly, risk was specific to cannabis use, as opposed to use of other drugs….”

Henquet C, Krabbendam L, Spauwen J, et al. Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. BMJ. 2005;330:11–15. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC539839/pdf/bmj33000011.pdf
“Exposure to cannabis during adolescence and young adulthood increases the risk of psychotic symptoms later in life. Cannabis use at baseline increased the cumulative incidence of psychotic symptoms at follow up four years later…but has a much stronger effect in those with evidence of predisposition for psychosis……….Predisposition for psychosis at baseline did not significantly predict cannabis use four years later..”

and also:

Kuepper R, van Os J, Lieb R, Wittchen HU, Höfler M, Henquet C. Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study.BMJ. 2011 Mar 1;342: d738 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047001/pdf/bmj.d738.pdf
“In individuals who had no reported lifetime psychotic symptoms and no reported lifetime cannabis use at baseline, incident cannabis use over the period from baseline to T2 increased the risk of later incident psychotic symptoms over the period from T2 to T3 (adjusted odds ratio 1.9, 95% confidence interval 1.1 to 3.1; P=0.021)…………There was no evidence for self medication effects, as psychotic experiences at T2 did not predict incident cannabis use between T2 and T3 (0.8, 0.6 to 1.2; P=0.3).”

For data on those who quit using when psychotic symptoms develop (further evidence against self-medication):

Fergusson DM, Horwood LJ, Ridder EM. Tests of causal linkages between cannabis use and psychotic symptoms. Addiction. 2005;100(3):354-66.

For degree of risk relative to other drugs:

Another angle on the potential confound of self-medication: genetic predisposition for schizophrenia does not predict cannabis use:

Veling W, Mackenbach JP, van Os J, Hoek HW. Cannabis use and genetic predisposition for schizophrenia: a case-control study. Psychol Med. 2008 Sep;38(9):1251-6. Epub 2008 May 19.
“BACKGROUND: Cannabis use may be a risk factor for schizophrenia. RESULTS: Cannabis use predicted schizophrenia [adjusted odds ratio (OR) cases compared to general hospital controls 7.8, 95% confidence interval (CI) 2.7-22.6; adjusted OR cases compared to siblings 15.9 (95% CI 1.5-167.1)], but genetic predisposition for schizophrenia did not predict cannabis use [adjusted OR intermediate predisposition
compared to lowest predisposition 1.2 (95% CI 0.4-3.8)].”

For data on potential benefits of cessation:

González-Pinto A, Alberich S, Barbeito S, Gutierrez M, Vega P, Ibáñez B, Haidar MK, Vieta E, Arango C. Cannabis and first-episode psychosis: different long-term outcomes depending on continued or discontinued use. Schizophr Bull. 2011 May;37(3):631-9. Epub 2009 Nov 13. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3080669/pdf/sbp126.pdf
“OBJECTIVE: To examine the influence of cannabis use on long-term outcome in patients with a first psychotic episode, comparing patients who have never used cannabis with (a) those who used cannabis before the first episode but stopped using it during follow-up and (b) those who used cannabis both before the first episode and during follow-up….. CONCLUSION: Cannabis has a deleterious effect, but stopping use after the first psychotic episode contributes to a clear improvement in outcome. The positive effects of stopping cannabis use can be seen more clearly in the long term.”

Kuepper R, van Os J, Lieb R, Wittchen HU, Höfler M, Henquet C. Continued cannabis use and risk of incidence and persistence of psychotic symptoms: 10 year follow-up cohort study.BMJ. 2011 Mar 1;342: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3047001/pdf/bmj.d738.pdf
“The finding that longer exposure to cannabis was associated with greater risk for persistence of psychotic experiences is in line with an earlier study showing that continued cannabis use over time increases the risk for psychosis in a dose-response fashion. This is also in agreement with the hypothesis that a process of sensitisation might underlie emergence and persistence of psychotic experiences as an indicator of liability to psychotic disorder.”

For data on marijuana use resulting in an earlier age of onset of schizophrenia (suggestive of causality), see Dragt et al. and a meta-analysis (see Large et al.,); also: a very extensive (676 schizophrena patients) and therefore more statistically powered analysis (see DeHert paper); two papers showing that the age-of-onset effect may be specific to those without a family history (see Scherr et al. and Leeson et al., papers); two studies that evaluate the age of onset specific to gender (Veen et al. and Compton et al. ) which is important because comparing across genders can be confounded by the greater tendency of males to engage in risky behavior (the conclusions are not the same in terms of gender; the gender distribution was slightly better in the Veen et al. study) and finally, two papers of relevance to specificity of age of onset effect to cannabis, a meta-analysis of published studies on age of onset that shows another drug of abuse (tobacco) is not associated with
a decreased age of onset (Myles et al.) and a study showing that ecstasy, LSD, stimulants, or sedatives did not have an effect to lower age of onset whereas cannabis use did (Barnes et al.) :

Large M, Sharma S, Compton MT, Slade T, Nielssen O. Cannabis Use and Earlier Onset of Psychosis: A Systematic Meta-analysis. Arch Gen Psychiatry. 2011 68(6):555-61. http://www.ncbi.nlm.nih.gov/pubmed/21300939
“The results of meta-analysis provide evidence for a relationship between cannabis use and earlier onset of psychotic illness, and they support the hypothesis that cannabis use plays a causal role in the development of psychosis in some patients. The results suggest the need for renewed warnings about the potentially harmful effects of cannabis.”

Dragt S, Nieman DH, Schultze-Lutter F, van der Meer F, Becker H, de Haan L, Dingemans PM, Birchwood M, Patterson P, Salokangas RK, Heinimaa M, Heinz A, Juckel G, Graf von Reventlow H, French P, Stevens H, Ruhrmann S, Klosterkötter J, Linszen DH; on behalf of the EPOS group.Cannabis use and age at onset of symptoms in subjects at clinical high risk for psychosis. Acta Psychiatr Scand. 2011 Aug 29. doi: 10.1111/j.1600-0447.2011.01763.x. [Epub ahead of print]
“Cannabis use and age at onset of symptoms in subjects at clinical high risk for psychosis. Objective: Numerous studies have found a robust association between cannabis use and the onset of psychosis. Nevertheless, the relationship between cannabis use and the onset of early (or, in retrospect, prodromal) symptoms of psychosis remains unclear. The study focused on investigating the relationship between cannabis
use and early and high-risk symptoms in subjects at clinical high risk for psychosis. Results: Younger age at onset of cannabis use or a cannabis use disorder was significantly related to younger age at onset of six symptoms (0.33 < r(s) < 0.83, 0.004 < P < 0.001). Onset of cannabis use preceded symptoms in most participants. Conclusion: Our results provide support that cannabis use plays an important role in the development of psychosis in vulnerable individuals.”

De Hert M, Wampers M, Jendricko T, Franic T, Vidovic D, De Vriendt N, Sweers K, Peuskens J, van Winkel R.Effects of cannabis use on age at onset in schizophrenia and bipolar disorder. Schizophr Res. 2011 Mar;126(1-3):270-6.

“BACKGROUND: Cannabis use may decrease age at onset in both schizophrenia and bipolar disorder, given the evidence for substantial phenotypic and genetic overlap between both disorders….RESULTS:… Both cannabis use and a schizophrenia diagnosis predicted earlier age at onset. There was a significant interaction between cannabis use and diagnosis, cannabis having a greater effect in bipolar patients….DISCUSSION:…. Our results suggest that cannabis use is associated with a reduction in age at onset in both schizophrenic and bipolar patients. This reduction seems more pronounced in the bipolar group than in the schizophrenia group: the use of cannabis reduced age at onset by on average 8.9 years in the bipolar group, as compared to an average predicted reduction of 1.5 years in the schizophrenia group.”

Scherr M, Hamann M, Schwerthöffer D, Froböse T, Vukovich R, Pit schel-Walz G, Bäuml J.. Environmental risk factors and their impact on the age of onset of schizophrenia: Comparing familial to non-familial schizophrenia. Nord J Psychiatry. 2011 Aug 31. [Epub ahead of print]
“Background and aims: Several risk factors for schizophrenia have yet been identified. The aim of our study was to investigate how certain childhood and adolescent risk factors predict the age of onset of psychosis in patients with and without a familial component (i.e. a relative with schizophrenia or schizoaffective disorder). Results: Birth complications and cannabis abuse are predictors for an earlier onset of schizophrenia in patients with non-familial schizophrenia. No environmental risk factors for an earlier age of onset in familial schizophrenia have been identified.”

Leeson VC, Harrison I, Ron MA, Barnes TR, Joyce EM. The Effect of Cannabis Use and Cognitive Reserve on Age at Onset and Psychosis Outcomes in First-Episode Schizophrenia. Schizophr Bull. 2011 Mar 9. [Epub ahead of print] http://schizophreniabulletin.oxfordjournals.org/content/early/2011/03/09/schbul.sbq153.full.pdf+html
“Objective: Cannabis use is associated with a younger age at onset of psychosis, an indicator of poor prognosis, but better cognitive function, a positive prognostic indicator. We aimed to clarify the role of age at onset and cognition on outcomes in cannabis users with first-episode schizophrenia as well as the effect of cannabis dose and cessation of use……Conclusions: Cannabis use brings forward the onset of psychosis in people who otherwise have good prognostic features indicating that an early age at onset can be due to a toxic action of cannabis rather than an intrinsically more severe illness. Many patients abstain over time, but in those who persist, psychosis is more difficult to treat.”

Veen ND, Selten JP, van der Tweel I, Feller WG, Hoek HW, Kahn RS. Cannabis use and age at onset of schizophrenia. Am J Psychiatry. 2004 Mar;161(3):501-6. http://ajp.psychiatryonline.org/cgi/reprint/161/3/501
“The results indicate a strong association between use of cannabis and earlier age at first psychotic episode in male schizophrenia patients.”

Compton MT, Kelley ME, Ramsay CE, Pringle M, Goulding SM, Esterberg ML, Stewart T, Walker EF. Association of pre-onset cannabis, alcohol, and tobacco use with age at onset of prodrome and age at onset of psychosis in first-episode patients. Am J Psychiatry. 2009 Nov;166(11):1251-7. Epub 2009 Oct 1. http://ajp.psychiatryonlie.org/cgi/reprint/166/11/1251
“Whereas classifying participants according to maximum frequency of use prior to onset (none, ever, weekly, or daily) revealed no significant effects of cannabis or tobacco use on risk of (editor’s note: “timing of”) onset, analysis of change in frequency of use prior to
onset indicated that progression to daily cannabis and tobacco use was associated with an increased risk of onset of psychotic symptoms. Similar or even stronger effects were observed when onset of illness or prodromal symptoms was the outcome. A gender-by-daily-cannabis use interaction was observed; progression to daily use resulted in a much larger increased relative risk of onset of psychosis in females than in males.”

Myles N, Newall H, Compton MT, Curtis J, Nielssen O, Large M. The age at onset of psychosis and tobacco use: a systematic meta-analysis. Soc Psychiatry Psychiatr Epidemiol. 2011 Sep 8. [Epub ahead of print]
“Unlike cannabis use, tobacco use is not associated with an earlier onset of psychosis.”

Barnes TR, Mutsatsa SH, Hutton SB, Watt HC, Joyce EM. Comorbid substance use and age at onset of schizophrenia. Br J Psychiatry. 2006 Mar;188:237-42. http://bjp.rcpsych.org/content/188/3/237.full.pdf+html
“Alcohol misuse and any substance use (other than cannabis use) were not significant in relation to age at onset….. those patients in the sample who reported that they had used cannabis had an earlier age at onset of psychosis than other patients who did not report cannabis use but who shared the same profile with regard to the other variables (e.g. comparing men who reported alcohol misuse and use of both cannabis and other drugs with men who had the same characteristics apart from the fact that they had not used cannabis).”

Data from other cultures

Sarkar J, Murthy P, Singh SP. Psychiatric morbidity of cannabis abuse. Indian J Psychiatry. 2003 Jul;45(3):182-8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2952166/pdf/IJPsy-45-182.pdf
“The paper evaluates the hypothesis that cannabis abuse is associated with a broad range of psychiatric disorders in India, an area with relatively high prevalence of cannabis use. Retrospective case-note review of all cases with cannabis related diagnosis over a 11 -year period, for subjects presenting to a tertiary psychiatric hospital in southern India was carried out. Information pertaining to sociodemographic, personal, social, substance-use related, psychiatric and treatment histories, was gathered. Standardized diagnoses were made according to Diagnostic Criteria for Research of the World Health Organization, on the basis of information available.Cannabis abuse is associated with
widespread psychiatric morbidity that spans the major categories of mental disorders under the ICD-10 system, although proportion of patients with psychotic disorders far outweighed those with non-psychotic disorders. Whilst paranoid psychoses were more prevalent, a significant number of patients with affective psychoses, particularly mania, was also noted.”

Rodrigo C, Welgama S, Gunawardana A, Maithripala C, Jayananda G, Rajapakse S. A retrospective analysis of cannabis use in a cohort of mentally ill patients in Sri Lanka and its implications on policy development. Subst Abuse Treat Prev Policy. 2010 Jul 8;5:16. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2910013/pdf/1747-597X-5-16.pdf
”BACKGROUND: Several epidemiological studies have shown that cannabis; the most widely used illegal drug in the world, is associated with schizophrenia spectrum disorders (SSD)……. CONCLUSIONS: Self reported LTC (editor’s note: life time cannabis) use was strongly associated with being diagnosed with SSD (editor’s note: schizophrenia spectrum disorders”.

Population study showing change in incidence rate in young when drug laws are eased

Ajdacic-Gross V, Lauber C, Warnke I, Haker H, Murray RM, Rössler W. Changing incidence of psychotic disorders among the young in Zurich. Schizophr Res. 2007 Sep;95(1-3):9-18. Epub 2007 Jul 16.
“There is controversy over whether the incidence rates of schizophrenia and psychotic disorders have changed in recent decades. To detect deviations from trends in incidence, we analysed admission data of patients with an ICD-8/9/10 diagnosis of psychotic disorders in the Canton Zurich / Switzerland, for the period 1977-2005. The data was derived from the central psychiatric register of the Canton Zurich. Ex-post forecasting with ARIMA (Autoregressive Integrated Moving Average) models was used to assess departures from existing trends. In addition, age-period-cohort analysis was applied to determine hidden birth cohort effects. First admission rates of patients with psychotic
disorders were constant in men and showed a downward trend in women. However, the rates in the youngest age groups showed a strong increase in the second half of the 1990’s. The trend reversal among the youngest age groups coincides with the increased
use of cannabis among young Swiss in the 1990’s.”

Estimates of how many men aged 20-40 would have to avoid regular marijuana use for one year in order to prevent one case of schizophrenia in that same year (but for number relevant to a 20 year avoidance of schizophrenia by avoiding regular marijuana use during
20 years, divide by 20):

Hickman M, Vickerman P, Macleod J, Lewis G, Zammit S, Kirkbride J, Jones P. If cannabis caused schizophrenia–how many cannabis users may need to be prevented in order to prevent one case of schizophrenia? England and Wales calculations. Addiction. 2009;104(11):1856-61.

“In men the annual mean NNP (number needed to prevent) for heavy cannabis and schizophrenia ranged from 2800 [90% confidence interval (CI) 2018–4530] in those aged 20–24 years to 4700 (90% CI 3114–8416) in those aged 35–39”.

Key studies interpreted to diminish the connection between marijuana and schizophrenia:

Proal AC, Fleming J, Galvez-Buccollini JA, Delisi LE. A controlled family study of cannabis users with and without psychosis. Schizophr Res. 2014 Jan;152(1):283-8.
“The results of the current study, both when analyzed using morbid risk and family frequency calculations, suggest that having an increased familial risk for schizophrenia is the underlying basis for schizophrenia in these samples and not the cannabis use. While cannabismay have an effect on theage of onset of schizophrenia it is unlikely to be the cause of illness.”

Rebuttal: Miller CL. Caution urged in interpreting a negative study of cannabis use and schizophrenia. Schizophr Res. 2014 Apr;154(1-3):119-20.
“The morbid risk reported for the relatives of the non-cannabis-using patients (Sample 3) was actually 1.4-fold higher than the cannabis using patients (Sample 4), but the study did not have enough power to statistically confirm or refute a less than 2-fold difference. An increase in sample size would be required to do so, and if the observed difference were to be confirmed, it would explain not only why the Sample 4 data fits poorly with a multigene/small environmental impact model but also would give weight to the premise that cannabis use significantly contributes to the development of this disease.”

Power RA, Verweij KJ, Zuhair M, Montgomery GW, Henders AK, Heath AC, Madden PA, Medland SE, Wray NR, Martin NG. Genetic predisposition to schizophrenia associated with increased use of cannabis. Mol Psychiatry. 2014 Jun 24. doi: 10.1038/mp.2014.51. [Epub ahead of print] http://emilkirkegaard.dk/en/wp-content/uploads/Genetic%20predisposition%20to%20schizophrenia%20associated%20with%20increased%20use%20of%20cannabis.pdf
“Our results show that to some extent the association between cannabis and schizophrenia is due to a shared genetic aetiology across common variants. They suggest that individuals with an increased genetic predisposition to schizophrenia are
both more likely to use cannabis and to use it in greater quantities.”

Rebuttal: Had this paper been titled “The causal genes for schizophrenia have been discovered” it would never have been published. In the absence of a consistent finding of genes of major effect size for schizophrenia, this study of inconsistently associated genes of low effect size is meaningless.

Buchy L, Perkins D, Woods SW, Liu L, Addington J. Impact of substance use on conversion to psychosis in youth at clinical high risk of psychosis. Schizophrenia Res 156 (2-3): 277–280.
“Results revealed that low use of alcohol, but neither cannabis use nor tobacco use at baseline, contributed to the prediction of psychosis in the CHR sample”.
Rebuttal: The study was small in size and the age range of their subjects at study onset was large (12 to 31) which included both subjects that had not reached the peak age of risk for schizophrenia even by the end of the study as well as subjects who were well past the peak age of onset of schizophrenia. The fact that the study screened out psychotic individuals was problematic for the latter group, in that those who were most vulnerable to the psychosis inducing effects of cannabis would already have converted to psychosis by that age.

Overview of Key Public Health Issues Regarding the Mental Health Effects of Marijuana

For the monetary cost of schizophrenia to the U.S. annually ($63 billion in 2002 dollars):

Wu EQ, Birnbaum HG, Shi L, Ball DE, Kessler RC, Moulis M, Aggarwal J. The economic burden of schizophrenia in the United States in 2002. J Clin Psychiatry. 2005 Sep;66(9):1122-9.

For the trends in adolescent drug, alcohol and cigarette use, showing an upward tick in marijuana use as medical marijuana has become more prevalent, and that the mind-altering drug legal for adults (alcohol) is still more commonly used by teens than is marijuana:

Johnston, L. D., O’Malley, P. M., Bachman, J. G., & Schulenberg, J. E. (2012). Monitoring the Future national results on adolescent drug use: Overview of key findings, 2011. Ann Arbor, MI: Institute for Social Research, The University of Michigan.

For a summary of Sweden’s drug law experience:
Hallam C., 2010, Briefing paper 20, The Beckley Foundation: What Can We Learn from Sweden’s Drug Policy Experience? www.beckleyfoundation.org/pdf/BriefingPaper_20.pdf
“in the case of Sweden, the clear association between a restrictive drug policy and low levels of drug use is striking. In his foreword to the article on Sweden’s Successful Drug Policy, Antonio Maria Costa is frank enough to confess that, “It is my firm belief that the generally positive situation of Sweden is a result of the policy that has been applied to address the problem”.

For data showing the relationship between drug enforcement policies in Europe and drug use, such that Sweden has a zero tolerance policy on drugs and has one of the lowest rates of “last month use” in Europe (1%), 4-fold lower than the Netherlands and 7-fold lower than Spain and Italy, two countries that have liberalized their enforcement policies so that marijuana possession carries no substantive penalty.

European Monitoring Centre for Drugs and Addiction, 2012 Annual report
http://www.emcdda.europa.eu/attachements.cfm/att_190854_EN_TDAC12001ENC_.pdf

Source: Microsoft Word – 2015- Summary of literature on marijuana and psychosis.doc (momsstrong.org) January 2016

Filed under: Alcohol,Brain and Behaviour,Cannabis/Marijuana,Crime/Violence/Prison,Drug use-various effects,Effects of Drugs,Nicotine,Political Sector,Social Affairs :

In a study published this week, researchers asked tens of thousands of individuals over 12 years of age about their use of tobacco products, e-cigarettes, and their health, and conducted follow-up questions over three years.¹ They found the development of lung problems like emphysema, bronchitis, asthma, and chronic obstructive pulmonary disease in individuals who had used e-cigarettes in the past or currently use them. Combined use of e-cigarette and tobacco products dramatically increased lung disease risks by an incredible 330 percent. The researchers concluded that, “Use of e-cigarettes is an independent risk factor for respiratory disease in addition to combustible tobacco smoking.” The study’s senior author, Stanton Glantz, told CNN, “I was a little surprised that we could find evidence on incident lung disease in the longitudinal study, because three years is a while but most studies that look at the development of lung disease go over 10 to 20 years.”

The Centers for Disease Control (CDC) reports that, as of December 10, 2019, there are 2,409 hospitalization cases of vaping-related lung injuries in the U.S., resulting in 52 deaths across 26 states and Washington, D.C.² The FDA has found THC in most of the samples it’s studying from these cases and has highlighted Vitamin E acetate as a chemical linked to some of the lung injuries. But the CDC warns that it still does not know how many other chemicals and products may be involved, and says that, “the best way for people to ensure that they are not at risk while the investigation continues is to consider refraining from the use of all e-cigarette, or vaping, products.” NIDA just reported that 3.5 percent of 12th graders and 3 percent of 10th graders say they vape on a daily basis, with 14 percent of 12th graders also saying that they vaped marijuana in the previous month. That figure is twice as large as it was last year.

Though federal officials have reportedly backed away from banning flavored vaping products³, some states have implemented such restrictions. And other national lawmakers are still considering similar options to confront the vaping epidemic.⁴ Dr. Scott Gottlieb, the former FDA Commissioner, has now recommended banning all cartridge-based e-cigarette products, which would include popular devices like Juul.⁵ Gottlieb, along with other experts, is worried about the epidemic of youth vaping, nicotine use and dependence which can lead to the use of tobacco-based products, the number one cause of preventable death, and other substances later in life.

Stories about vaping-related severe lung diseases, the epidemic of youth use, and public policy responses are important for patients, families, medical professionals, and consumers to follow. But we should also continue to monitor research that paints an even more distressing picture of e-cigarette products. In a recent study, researchers looked at the association between e-cigarette use and cancer.

What did this study find about e-cigarette use and cancer in mice?

This study found that exposure to e-cigarettes led to tumors and precancerous growths in the lungs and bladders of mice. The nicotine vapor from e-cigarettes damaged DNA in the exposed mice’s organs.

When tobacco burns, it can change nicotine into carcinogens called nitrosamine ketone. In individuals who use electronic cigarettes, these carcinogens in saliva and urine are 95 percent lower than they are individuals who smoke tobacco. That’s why the UK government says that electronic cigarettes are 95 percent safer than tobacco products. But it’s not as certain that nicotine from e-cigarettes gets turned into these carcinogens, so it’s also not clear if their levels in saliva and urine of individuals using e-cigarettes are a good guide to possible damage. The body can also absorb these carcinogens in other ways, as harmful to DNA. This study looked at DNA damage in mice to see if e-cigarettes might cause lung and bladder cancer, instead of carcinogenic impact in blood and urine. It’s also important to note that no experts suggest that vaping or smoking is good for you.

Researchers exposed the full bodies of 40 mice to e-cigarette vapor for 54 weeks. 22.5 percent of these mice developed lung tumors and, in their bladders, 57.5% ended up with precancerous growths. 20 mice in a control group, subjected to e-cigarette vapor but not nicotine, did not develop tumors. E-cigarette exposure in this study is comparable to human e-cigarette use over three to six years. The study’s authors believe that the results probably indicate e-cigarette aerosol nicotine reaching far into lung tissue and causing DNA damage. They also say that, “The public should not equate the risk of ECS [e-cigarette smoke] with that of TS [tobacco smoke]. Our data simply suggest, on the basis of experimental data in model systems, that this issue warrants in-depth study in the future.” This study also had limitations. It used a small sample size and did not focus on the inhalation of e-cigarette nicotine vapor. And animal studies are not necessarily clear guides for related effects in humans.

Why is this important?

This is the first study finding an association between e-cigarette use and cancer. Though the authors are careful to offer caveats about the research’s limitations, not drawing inferences about the relative safety of e-cigarettes and tobacco products, and the need for more extensive studies, this is still a significant and troubling result. It took many decades for experts to agree that tobacco smoke caused cancer. It seems more logical to assume that smoking and vaping are dangerous until proven otherwise. Some countries have seen enough and banned e-cigarettes completely, such as Argentina, Saudi Arabia, and Singapore. Others do not think it is safe but consider e-cigarettes as part of a harm reduction strategy. The study’s lead, New York University’s Dr. Moon-Shong Tang told CNBC, “It’s foreseeable that if you smoke e-cigarettes, all kinds of disease comes out. Long term, some cancer will come out, probably. E-cigarettes are bad news.” He also suggested that because e-cigarette products have only existed for a relatively short period of time, it may take a while for more research to measure their health effects more comprehensively—possibly up to a decade.

It’s always appropriate for researchers to be cautious about their findings and to point to countervailing factors and the need for supplemental work and corroborating studies. Even experts can be surprised. But more studies continue to indicate the dangers of e-cigarette use. It’s also worth pointing out that there are dangers beyond these studies: inhaling nicotine vapors is likely to stimulate its own continued use, while costing time, energy and money. The cost of a pack of cigarettes is quite cheap even with current taxes. Actual costs are difficult to understand. In general, we assume smoking two packs of cigarettes a day for 20 years is more expensive than the $75,000 for the cost of the cigarettes. The long-term costs are closer to $2 million, after factoring in treatments for tobacco-related cancer, lung and heart disease, and the reduction in lifespan and productivity of the individual using cigarettes.

Prevention of adolescent smoking initiation is a very important health goal, one that we were much closer to attaining before vaping. Experts warn that vaping is causing a new nicotine addiction epidemic.⁶ They estimate, for example, that, because of vaping, almost 500,000 individuals between the ages of 12 and 29 who used e-cigarettes also end up using tobacco products.⁷ Use of e-cigarettes paves the way for use of tobacco-based cigarettes, as research suggests.⁸ If the full costs to society were included at the point of purchase, each pack of cigarettes would cost at least $75. Very few people would choose to spend $75/pack. Similarly, we could find a price at which vaping is less attractive to consumers. The science, in other words, is clear about the risks, and tobacco-like public health-related tax initiatives may be appropriate. Vermont recently passed a 92% wholesale tax on vaping and e-cigarette products. Federal lawmakers are also considering tax changes.

Keeping in mind that it took decades, if not centuries, to prove that cigarette smoking causes cancer, these new e-cigarette studies suggest that the products aren’t just understudied and possibly dangerous, but increasingly just dangerous, associated more frequently with chronic disease, heart problems, and even cancer.⁹ This study is also interesting in its full-body exposure of mice to e-cigarette vapor, which suggests that secondhand vaping may be dangerous, too. Other reports are coming out suggesting that e-cigarette inhalation is dangerous for everyone, include individuals who do not use the products but may be exposed to them. Mounting evidence shows that e-cigarette use is a highly risky proposition for current and potential consumers and that officials and experts are justified in pursuing ways to curb use. Reversing use trends will require a great deal of work given the near exponential increases in youth vaping.

References:

Bhatta, D.N., Glantz, S.A. (2019) Association of E-Cigarette Use With Respiratory Disease Among Adults: A Longitudinal Analysis. American Journal of Preventive Medicine
Centers for Disease Control and Prevention (CDC). (2019) Outbreak of Lung Injury Associated with the Use of E-Cigarette, or Vaping, Products. Retrieved from https://www.cdc.gov/tobacco/basic_information/e-cigarettes/severe-lung-disease.html
Karni, A., Kaplan, S. (2019) Trump Warns a Flavor Ban Would Spawn Counterfeit Vaping Products. New York Times. Retrieved from https://www.nytimes.com/2019/11/22/health/trump-vaping.html
Hellmann, J. (2019) House Democrats to vote on flavored e-cigarettes ban next year. The Hill. Retrieved from https://thehill.com/policy/healthcare/474184-house-democrats-to-vote-on-flavored-e-cigarettes-ban-next-year
Florko, N. (2019) Former FDA commissioner calls for a full ban on pod-based e-cigarettes. Stat. Retrieved from https://www.statnews.com/2019/11/12/gottlieb-ban-pod-based-e-cigarettes/
Dinardo, P., Rome, E.S. (2019) Vaping: The new wave of nicotine addiction. Cleve Clin J Med.
Soneji, S., Wills, T.A. (2019) Challenges and Opportunities for Tobacco Control Policies in the 21st Century. JAMA Pediatr
National Academies of Sciences, Engineering, and Medicine. (2018) Public health consequences of e-cigarettes. The National Academies Press, Washington, DC
Proctor, R.N. (2012) The history of the discovery of the cigarette-lung cancer link: evidentiary traditions, corporate denial, global toll. Tob Control

Citation:

1. Tang, M., et al. (2019) Electronic-cigarette smoke induces lung adenocarcinoma and bladder urothelial hyperplasia in mice. PNAS

Source: We know vaping can cause serious lung problems. A new study says it might also cause cancer (addictionpolicy.org) December 2019

Filed under: Economic,Health,Nicotine,Social Affairs :

The 2018 Monitoring the Future College Students and Young Adults survey shows trends in the use of marijuana, alcohol, nicotine, and synthetic drugs in college students and non-college peers.

Marijuana Use

Annual Marijuana Use at Historic Highs among College and Non-College Peers*
Marijuana use is nearly the same for college students and their non-college peers at about 43%. This is approximately a 7% increase over five-years for college students. These rates for both groups are the highest in 35 years.

Daily/Near Daily Use** of Marijuana Twice as High among Non-College Group
Approximately one in nine non-college respondents reporting daily or near daily use, (11.1%) compared to about one in 17 college students (5.9%).

** Used on 20 or more occasions in the past 30 days

Past Month Nicotine Vaping Doubles Among College Students

This jump is among the greatest one-year increase seen for any substance in the history of the survey.
Between 2017 and 2018, nicotine vaping increased in college students from 6.1% to 15.5% and from 7.9% to 12.5% in non-college adults.

Rx Drug Misuse has Mixed Results

Rx Opioid Misuse: Significant Five Year Drop in Both Groups
Past year misuse of prescriptions opioids dropped from 5.4% in 2013 to 2.7% among college students and from 9.6% in 2013 to 3.2% among non-college adults.

Adderall® Misuse: Significant Gender Differences
Past year misuse rates of Adderall® were 14.6% among college men and 8.8% among college women. Rates were higher, however, in non-college women than in non-college men (10.1% and 5.3% respectively).

Overall Adderall® misuse is higher among college students (11.1%) than their non-college peers (8.1%)

Binge Drinking (five or more drinks in a row in the past two weeks) Fell Below 30% for the First Time among College Students

In 2018, binge drinking declined among college students (28%) and non-college adults (25%).

*Please note, the college-age adults are ages 19-22.

Source: Drug and Alcohol Use in College-Age Adults in 2018 | National Institute on Drug Abuse (NIDA) (nih.gov) September 2019

Filed under: Alcohol,Cannabis/Marijuana,Nicotine,Political Sector,Synthetics :

Researchers have found that even occasional cigarette use is enough to affect the volume and connectivity of developing brains

After decades of educational programming and advertising, regular cigarette smoking and sales in the United States have declined to their lowest levels in 50 years. But doctors and parents are now racing to deal with another health crisis that has popped up in its place: the meteoric rise of electronic cigarettes (or e-cigarettes) among adolescents.

This nicotine electronic delivery device was originally introduced to the market as a promising tool to aid smoking cessation among already current smokers. Yet, the lack of federal regulations, the appealing flavors available, and perceptions that these devices were less harmful than regular cigarettes have led to a worrying spike in use among U.S. adolescents. One in five U.S. high school students and one in 20 middle school students currently use e-cigarettes.

E-cigarette use among youth has skyrocketed in the past few years

U.S. Surgeon General Jerome Adams has declared e-cigarettes an epidemic among youth, stressing that e-cigarette aerosols containing nicotine increase the risk of addiction to nicotine and other drugs, and impact brain development which can induce mood disorders and lower impulse control. Now, new research led by Dr. Bader Chaarani of the University of Vermont and published in the journal Biological Psychiatry: Cognitive Neuroscience and Neuroimaging has found adolescents that smoked only a few cigarettes had smaller and less connected brain areas than their peers who never smoked. This could mean that adolescent smokers’ brains will develop and function differently, which may affect decision-making and self-control in adulthood.

Just like regular cigarettes, e-cigarettes contain nicotine, a neuroactive chemical and an addictive component whose main target is the brain. Nicotine acts upon receptors in our brains -through nicotinic acetylcholine receptors (nAChRs)- to promote the release of a neurotransmitter called dopamine. Dopamine is a feel-good chemical, triggering a pleasurable response in our brains. When linked with the action of smoking, it plays a fundamental role in nicotine addiction.

Adolescence is a vulnerable developmental period during which exposure to nicotine can fundamentally alter how the brain is wired

Nicotine exposure among adults presents lower risks compared to adolescents. This is because our brains develop throughout our first three decades of life. During this maturation period, the brain circuits are being remodeled, especially those involved in reward function (dopamine) and cognitive function (acetylcholine). Therefore, adolescence is a vulnerable developmental period during which exposure to nicotine can fundamentally alter how the brain is wired, making young people even more vulnerable to future addiction.

Previous studies have shown that adolescent smokers have reduced neural activity and show symptoms of nicotine dependency at lower nicotine levels than adults, and that individuals that begin smoking during adolescence are more likely to develop nicotine dependence than individuals that start in their late 20′s.

Studies of smoking’s effects on the brain have largely focused on adults, not youth – until now

One big gap in research observing the effects of cigarette smoking on brain volume, connectivity, and function to date is that such studies have been mostly performed on adult smokers rather than adolescent smokers. The majority have also focused on daily and heavy smokers, yet have overlooked occasional smokers, which is relevant due to common experimentation behaviors during adolescence.

The new research by Dr. Chaarani and their team finally addresses these gaps by looking at the brains of adolescent light smokers. They found that just a couple of cigarette puffs can potentially alter the development of adolescent brain.

The research team recruited over 600 14-year-old adolescents and calculated a cigarette-smoking score for each participant based on how many times, during their lifetime, they had smoked cigarettes. Participants ranged from young people who had never smoked to those who have smoked more than 40 times.

Smoking even a few times is significantly linked to a decreased volume of the gray matter and neuronal connectivity

The researchers also looked at the brain of each of the participants using functional magnetic resonance imaging (fMRI). These images were used to estimate the brain gray matter volume corresponding to the neuron bodies where synapses occur, and white matter connectivity, meaning the “telephone wires” that connect neurons and brain areas by carrying electrical signals.

Interestingly, Dr. Chaarani and their team found that smoking even a few times was significantly linked to a decreased volume of the gray matter and neuronal connectivity. And the more teens smoked, the more the gray matter volume at the ventromedial prefrontal cortex (vmPFC), and the connectivity at the corpus callosum of their brains was reduced. Scientists have previously linked alterations in the vmPFC volume with a reduction in reward and with an increased risk of anxiety disorders.

Moreover, reduction in the connectivity could indicate that nicotine induces axonal damage, meaning it may be altering the communication between brain areas. These alterations in brain connection have also been reported in individuals with substance addiction and alcohol dependence. While the research only showed a link between low doses of cigarette smoking and brain alterations, rather than a causal effect, these type of consequences have been consistently reported in many studies on brains of adult smokers.

E-cigarettes may look harmless, but they have lasting effects on developing brains

Although this study focused on adolescents who smoked traditional cigarettes, scientists have demonstrated that such risks are applicable to teenagers who vape using the popular JUUL brand of e-cigarettes since the two methods deliver similar amounts of nicotine.

Researchers are still working to understand the impact of nicotine in the brain of young smokers, particularly now that e-cigarette use among youth has increased rapidly. This new study could play a critical role in educational campaigns, and spur regulatory agencies, parents, and teachers to take an active role in preventing this newest addiction.

Source: https://massivesci.com/articles/smoking-vaping-risks-adolescent-brain-function-development-addiction-nicotine/ June 2019

Filed under: Brain and Behaviour,Nicotine,Youth :

The study by Sadananda et al published in the current issue of the IJMR highlights the neurophysiological basis of altered cognition in subjects with opioid addiction. The study demonstrated aberrant network activity between the default mode network (DMN) and fronto-parietal attentional network (FAN) as a major cause for working memory deficits in drug addiction. Working memory is an important to retain the cognitive information essential for goal directed behaviours. Human beings are endowed with an efficient cognitive faculty of working memory, essential for efficient functioning of the executive network system of the brain. As working memory is the key to carry out any cognitive process involving attention, volition, planning, goal directed behaviour, etc., consciousness is linked largely to working memory processing. The importance of integrating neuroscience knowledge especially the executive functions of human brain in leadership has been taught in neuro-leadership programs as a mean to maximize the human capabilities, productivity, creativity, leadership, wellness, positive attitude.

Aberrant network activities and structural deficits in brain areas of executive functioning impede most of our intellect including mental flexibility, novel problem solving, behavioural inhibition, memory, learning, planning, judgement, emotion regulation, self-control and other social functioning. Deficits in working memory and attention owing to reduced fronto-parietal network (FPN) activity is reported in schizophrenia, autism, attention deficit hyperactive disorder (ADHD) and anxiety disorders. Opioid addiction is reported to impede such dynamicity of the executive system leading to a wide range of deficits in cognition. Opioid addiction alters the network integrity between DMN and FPN networks and weakens the cognitive information processing in cognitively challenging paradigms. Dysfunctional dynamics of DMN activity is believed to contribute to impaired self-awareness, negative emotions and addiction related ruminations. Aberrant DMN activity and reduced medial prefrontal cortical functions are common neural phenotypes of cognitive deficits in conditions like mental illness, drug addiction, sleep deprivation and neurodegenerative disorders. People with substance use disorders develop mental illnesses as a serious comorbidity that in turn, leads to severe behavioural impairments at the social, emotional and cognitive domains. Chronic sleep deprivation associated with drug addiction and substance abuse is another predisposing factor that worsen the behavioural impairments. Over all, drug addiction, substance abuse and the subsequent maladaptive behaviours including mental illness and sleep deprivation trigger a complex set of network instability in the domains of cognition and affect. The euphoria and hallucinating experience of drugs of abuse would soon lead to psychological distress and to cognitive and emotional behavioural impairments due to the disruption of various top down and bottom-up network dynamics.

Substance use disorders are an imminent socio-economic burden and have become a major public health concern worldwide. Despite knowing the harmful effects and consequences of drug use, reports say that the youth especially the adolescents have a tendency to continue the habit. There is a need to have effective measures in place such as educational programmes to improve the self-efficacy of parents and family members to help their children to develop the right behavioural attitude, enhance the capacity building in teachers to strengthen the self-esteem and wellness of students to organize substance use control awareness programmes in coordination with NGOs at educational institutions, involvement of television and other visual and social media platforms to organise substance abuse control programmes and for interactive opportunity for children/youth with educators, researchers and professionals, organization of knowledge dissemination programmes to the public/schools/colleges to highlight the adverse effects of drug abuse on mental health and cognition. Introduction to such knowledge sharing platforms such as the Virtual Knowledge Network (VKN) at NIMHANS, Bengaluru, provide interactive skill building opportunities to safeguard them from substance abuse and addiction. People should have easy access to such services and rehabilitation centers. Various behavioural intervention strategies such as cognitive retraining, psychotherapy, yoga therapy, mindfulness-based intervention programmes etc. are reported to improve cognitive abilities, regulation of negative emotions and restoration of motivational behaviours. A study on single night exposure to olfactory aversive conditioning during sleep helped to quit addiction to cigarette smoking temporarily. Such studies highlight the possibility of learning new behaviours during sleep and its positive impact on wake associated behaviours. Such approaches are quite useful, easily testable and cost-effective. Thanks to the incredible phenomenon of adult brain plasticity, it is possible to re-establish social intelligence, prosocial motivation among people with substance abuse.

Source: Drug addiction – How it hijacks our cognition & consciousness – PMC (nih.gov) October 2021

Filed under: Addiction,Brain and Behaviour,Drug use-various effects,Heroin/Methadone,Nicotine,Treatment and Addiction :

This article is distilled from a paper given at the Recovery Plus conference in London on 26^th June 2018 by Peter Stoker, Director of the National Drug Prevention Alliance.

References available on request.

Prevention, the word and meaning, comes from the Latin “praevenire” which means “to come before”. In other words, to act pre-the event – not during it or after it. Any action later than pre-the event is not prevention, it is repair. And both are required.

When it comes to funding, Prevention is the Cinderella service, and reasons why could include that Treatment has more workers with a resulting vigour; Treatment is easier to count, pleasing accountant-oriented funders; Prevention is (falsely) depicted as inhibiting Human Rights, and libertarian campaigners have always had deeper pockets that Prevention ever had.

INTERNATIONAL HISTORY

Early responses to the drug problem were characterised by being reactive rather than proactive, often with a legal or enforcement flavour.

There was also a tendency to focus on transmission of knowledge, sometimes coupled with a challenging of the users’ attitudes – unintended consequences could follow, for example:

if you give knowledge to a user you may produce a knowledgeable user, and
if you challenge a user’s attitude you may produce a knowledgeable user with an attitude.

In due course a more complete model was developed using the simple synonym – KAB, meaning you should address a mixture of Knowledge, Attitudes and Behaviour. (And focus on encouraging positive behaviour, rather than punishment).

Libertarians spotted the educational arena as fertile ground for their campaigns; their speculative allegation that the so-called ‘war on drugs’ was failing was the launchpad for harm reduction (HR1) – this was later augmented by inclusion of human rights (HR2). I witnessed all this being promoted vigorously at the 2009 UNGASS/CND conference in Vienna – we were emphasising ‘Whole Health’ as a goal, but throughout the proceedings there was an apparently innocuous and almost irresistible request from ACLU delegates that human rights should be included in all clauses. It wasn’t evident at this moment that they would later insist that using drugs was itself a “human right”, which therefore meant that prevention was, in effect, a breach of human rights. This activism was bankrolled by George Soros’ Open Society.

You can explore people’s thinking on this every day, in the Google Alerts, but remember what H.L.Mencken had to say: “For every complex problem there is a simple solution … and it doesn’t work”.

Exemplary practice can be observed in several initiatives. There are too many to cover them all, but here are some indicative examples and source materials:

DFAF – Drug Free America Foundation – www.dfaf.org – internationally active, establishing conferences in Europe and the Americas. Publishes a learned journal, and holds an enormous library.

NFIA – National Families In Action – Atlanta USA – www.nationalfamilies.org – countless years of detailed research and practice. Many learned papers. They have just published a very useful technical paper called ‘The MJ File’ – requires reading.

CADCA – www.cadca.org – Community Anti-Drug Coalitions of America – until recently under direction of Major General Arthur Dean, US Army retired. CADCA is well-resourced; in 2016 alone it trained over 8,000 youth.

A very useful publication by NIDA/CSAP www.drugabuse.gov (Center for Substance Abuse Prevention) is ‘Preventing Drug Abuse’ – a slim volume, its first edition in 1997, revised in 2003 … about due for an update, one might say!

DARE – www.dare.org – has suffered attacks in recent years but has survived, to the extent that it is signing new client organisations at the rate of about 200 a year even now.

DWI – Drug Watch International – www.drugwatch.org a long-standing forum of experts in America and abroad. Membership by invitation only.

Straight – peer-led youth rehab service, now closed. Featured in the movie ‘Not My Kid’ starring George Segal and Stockard Channing. Straight came in for criticism from the liberal left, and eventually closed, but not for this reason. I asked Bill Oliver, Chief Executive for many years, what caused the collapse of Straight. He told me “We were very good drug workers but lousy accountants”. A salutory comment!

SAM – Smart Approaches to Marijuana – www.sam.org . One of the most potent bodies in recent years, in the legalisation battle zone. Under the direction of Kevin Sabet, a former policy adviser in the US drug czar’s office. Senior staffers include former Congressman Patrick Kennedy. Their approach is soundly based on scientific evidence.

And NDPA – National Drug Prevention Alliance – based in Slough, near Heathrow, and almost 30 years old. NDPA has provided support and training for parents, young people, drugs professionals and teachers. It has provided counselling and referral for users, and has done a large amount of work in the broadcast and print media,. It runs two websites – one for drugs professionals www.drugprevent.org.uk and one – more accessible in its presentation – for parents – www.pinpoints.org.uk The websites include thousands of technical papers as well as other advisory publications. The websites are regularly visited internationally, several hundred thousand visits per year, and readers include our own Home Office.

EXAMPLES OF SUCCESS

Perhaps the earliest example was almost 40 years ago, in the late 1980s. Increased drug use sparked large numbers of parents to press academics into action, with the most memorable campaign being ‘Just Say No’ – under Ronald Regan’s wife Nancy. It was ridiculed by the left, but the campaign was very much more than a slogan, included detailed trainings for parents and youth, plus media activism, and the hard evidence is that it reduced prevalence by more than 60% – 11 million fewer users. Any other health-related campaign today would kill for such a result.

Perhaps the best example of this in recent years has been around the use of tobacco. Historically tobacco was used freely everywhere. Even doctors said it was good for you – it would soothe your throat, for example. Advertising sold it vigorously. Such protests as were made, were largely ignored. And if any people suggested that smoking had made them ill, the rest of us felt that that was their own fault and nothing to do with the us – they were getting what they deserved

Then, one day, the US Surgeon General announced that tobacco smoking by one person could give other persons cancer (through passive smoking). This was a game-changing announcement; we could no longer ignore what these drug users were doing – now it was affecting all of us. Anti-smoking articles and adverts appeared in the media; doctors advised strongly against it, schools told their pupils to avoid it, offices prohibited smoking in the premises, causing those who still were dependent on cigarettes to huddle in unpleasant external doorways, and the newly emerging Health and Safety brigade put in their six-pennorth. In due course the government reacted, producing new and influential legislation, banning smoking in many places. Before long the culture changed markedly, and in consequence so did the prevalence.

But if you want a bang up-to-date success, story you need look no further than Iceland. Comparing latest European figures with a couple of decades ago, teen drinkers have dropped from 42% to 5%, cannabis use has dropped from 17% to 7%, and tobacco smoking from 23% to 3%. The emphasis is on providing stimulating activities for youth, and on schooling parents in now to be more engaged with their families. Countries are following the Icelandic model, and research shows Risk factors and Protective Factors are pretty much the same everywhere.

There are localised examples of how to get ahead of the game – for example, one effective program was run in New York – called ‘Fixing Broken Windows’ the approach was to keep the streets and buildings clean and tidy – it reduced drug abuse and other social aspects.

In society as a whole, what promises the best results? In essence, the most effective strategy will come from changing the culture.

Balanced prevention policy and strategy

I have yet to find a better definition what we should do than that written by a leading expert in the prevention field, based in Arizona – William Lofquist:

“We need to get beyond the notion that prevention is stopping something happening, to a more positive approach which creates conditions which promote the well-being of people”.

Lofquist found the importance of treating youth as resources, rather than objects or recipients of project work. He also emphasised that it should engage the whole of society, not in some rigid formulaic way but in a fluid, proactive approach which is alive to changes in society and always works to stay ahead of the game.

An assembly of this co-ordinated strategy and policy might include the following:

Government

Health

Education

Higher ed

Youth peers

Parents

Religions

Pharmacists

Businesses

Media

Volunteers

Sport

Leisure

Drugs services

– specify, resource, oversee, evaluate and improve

– address all health elements

– focus on health promoting approaches

– train teachers and youth workers in prevention

– develop and utilise their potential

– de-marginalise, train, resource, support

– spiritual lead, network, interface working

– more proactive, preventing, reducing harm

– health promoting environments. EAPs, RDTs

– educate and support editorial staff, no mixed messages

– realise their potential, utilise more widely

– health promoting environments, health image

– widen education and training. Explore expansion

– encourage plurality, with more emphasis on recovery

We can also learn much from the science of ‘Behaviour Modification’ – as practised by, inter all, Professor Brian Sheldon of the Royal Holloway University.

Constructive selfishness …

The tobacco example above describes what I mean by this expression. We should not shrink from recognising that selfishness is a powerful driving force across society. And since it is a powerful driving force, we should seek to drive it to our advantage.

We have yet to wake up to the potential of defining and communicating to society at large the various ways in which one person’s drug misuse adversely affects the rest of us.

Establishing readiness for prevention – CULTURAL CHANGE

What influences culture?

Peer group influence
Personal perceptions
Income versus cost of any action
Health issues
Moral structure
Spiritual structure
Family values
Attraction of risk-taking
Media
Mental state
Legislation
Economy – the well-off or the poor
Employment – job or no job

CSAP found in their comparison of practices that the best prevention results come through co-ordinated prevention efforts, offering multiple strategies, and providing multiple points of access.

* * * * *

This is but a quick canter through the jungle of Prevention. There is much more to it, but I hope I have whetted your appetite – and you may even see the sense in building prevention into your work spectrum. (As co-operators rather than competitors with other agencies).

Don’t fear that prevention will reduce your treatment client base – as treatment workers, you are going to be in demand for a long time yet! Whilst some will be prevented from drug and alcohol abuse, and some will manage to cure themselves, most people need expert help.

We are, after all, working towards the same objective. I once saw a cartoon in which a drug worker was asking a guru how to solve the drug problem. ‘Why do people use drugs?’ asked the guru. ‘To escape reality’ said the worker. ‘Then the solution is obvious’. Said the guru. ‘Improve reality’

Filed under: Brain and Behaviour,Nicotine,Prevention and Intervention :

Abstract

Objectives:

E-cigarette use has increased dramatically among adolescents in the past 5 years alongside a steady increase in daily use of marijuana. This period coincides with a historic rise in depression and suicidal ideation among adolescents. In this study, we describe the associations between e-cigarette and marijuana use and depressive symptoms and suicidality in a large nationally representative sample of high school students.

Methods:

We used data from the 2 most recent waves (2015 and 2017) of the Youth Risk Behavior Survey. Our sample (n = 26,821) included only participants with complete information for age, sex, race/ethnicity, and exposure to e-cigarettes and marijuana (89.5% of survey respondents). We performed multivariate logistic regressions to explore the associations between single or dual use of e-cigarette and marijuana and depressive and suicidal symptoms in the past year adjusting for relevant confounders.

Results:

E-cigarette-only use was reported in 9.1% of participants, marijuana-only use in 9.7%, and dual e-cigarette/marijuana use in 10.2%. E-cigarette-only use (vs no use) was associated with increased odds of reporting suicidal ideation (adjusted odds ratio [AOR]:1.23, 95% CI 1.03–1.47) and depressive symptoms (AOR: 1.37, 95% CI 1.19–1.57), which was also observed with marijuana-only use (AOR: 1.25, 95% CI 1.04–1.50 and AOR: 1.49, 95% CI 1.27–1.75) and dual use (AOR: 1.28, 95% CI 1.06–1.54 and AOR: 1.62, 95% CI 1.39–1.88).

Conclusions:

Youth with single and dual e-cigarette and marijuana use had increased odds of reporting depressive symptoms and suicidality compared to youth who denied use. There is a need for effective prevention and intervention strategies to help mitigate adverse mental health outcomes in this population.

Source: Depressive Symptoms and Suicidality in Adolescents Using e-C… : Journal of Addiction Medicine (lww.com) Sept/Oct 2019

Filed under: Brain and Behaviour,Cannabis/Marijuana,Nicotine,Prevention and Intervention,Youth :

— Effect on sperm quality, testicular function worse than cigarettes

CHICAGO — Men who smoked marijuana had significantly degraded sperm quality and testicular function, worse than tobacco users and comparable to men with diagnosed infertility, according to a long-term Brazilian study.

As compared with smokers, marijuana users had lower median values for sperm concentration, motility, and morphology (P<0.01). Marijuana use also was associated with reduced testicular volume and an increased rate of nonobstructive azoospermia, clinical features often found in male infertility.

Marijuana’s deleterious effects on reproductive parameters resulted from increased production of reactive oxygen species (ROS), as seminal ROS concentrations were 20 times higher in marijuana users as compared with smokers, reported Jorge Hallak, MD, of the University of Sao Paulo, at the American Urological Association (AUA )annual meeting.

“Overall, the marijuana group had semen quality equivalent to the infertile group, with the exception of higher ROS and DNA damage than infertile men,” Hallak said during an AUA press briefing. “DNA damage is higher in all groups (marijuana users, smokers, and infertile men) as compared to controls, but higher levels were found in the marijuana group and infertile men. Basic semen parameters are not sufficient to identify changes of magnitude in sperm cell function.”

A second study summarized at the press briefing provided the first reported evidence of an association between marijuana use and development of benign prostatic hyperplasia/lower urinary tract symptoms (BPH/LUTS).

A recent international study showed a consistent and statistically significant decline in sperm quality (count and motility) over the past 40 years. The explanation for the decline remains elusive, but multiple factors have been proposed: environmental exposures, poor nutrition, genetics, and social/behavioral factors.

Over the past 2 decades, technologic advances allowed more detailed examination of sperm. Showed that sperm are highly vulnerable to oxidative stress, which has been implicated in a multitude of major human diseases and disorders. Subfertility and infertility almost almost always arise as a consequence of oxidative stress, said Hallak.

The rationale for evaluating marijuana’s effect on male fertility parameters included a lack of information on the topic and the worldwide use of the drug. With an estimated 200 million users worldwide, marijuana is the most widely used psychoactive drug, including more than 20 million regular users in the U.S.

Since 2000, Hallak and colleagues have studied the effects of marijuana and tobacco on spermatozoa and testicular function and relationships with male infertility, hypogonadism, and sexual dysfunction. Each study participant has two comprehensive semen analyses that go well beyond usual lab assessments and include ROS, sperm DNA integrity, creatinine kinase activity, and antisperm antibodies.

Unlike many prior studies, enrollment was limited to users of cannabis and excluded use of cannabinoid-containing products. The study population comprised 125 men with diagnosed infertility, 144 tobacco smokers, 74 marijuana users, and a control group of 279 men (prevasectomy with no clinical factors for testicular dysfunction).

Current marijuana use was ascertained by self-report at the time of enrollment. Median age at first use of marijuana was 18.6, and median duration of marijuana use was 8 years.

Clinical characteristics of the infertile men included increased levels of prolactin; decreased sperm concentration, motility, and morphology; and increased seminal pH and ROS. Tobacco smokers had decreased follicle-stimulating hormone, luteinizing hormone, and prolactin; decreased testicular volume; and decreased seminal volume.

Marijuana users had a significantly lower median estradiol level (10.04 ng/dL) as compared with all the other groups (P<0.001). Marijuana use was associated with the highest median seminal ROS: 14.31 x 104 cpm/20 x 10⁶ versus 5.66 for infertile men, 0.70 for smokers, and 0.68 for the fertile control group. Hallak noted that marijuana induces production of intracellular ROS whereas tobacco smoke creates extracellular oxidative stress.

The study of marijuana use and BPH/LUTS included 20,548 men (age >45) who had prescriptions for finasteride and or a super-selective alpha blocker during the period from January 2011 to October 2018. The primary objective was to identify factors significantly associated with BPH/LUTS, said Granville Lloyd, MD, of the University of Colorado Anschutz School of Medicine in Aurora.

A multivariable analysis identified marijuana use as a statistically significant player in the development of BPH/LUTS (odds ratio 1.253, P<0.001). Other significant predictors were depression (OR 2.015), erectile dysfunction (OR 1.847), metabolic syndrome/obesity (OR 1.586), hypertension (OR 1.576), hypogonadism (OR 1.392), and diabetes (OR 1.280, P<0.001 for all). Alcohol use did not have a significant association with BPH/LUTS (OR 0.982).

Noting that BPH/LUTS etiology is poorly understood, Lloyd said, “From this analysis we can conclude that BPH is associated with systemic diseases, depression, and marijuana use but not alcohol.”

“Men who use marijuana are more likely to be treated for BPH,” he stated. “This is a novel finding. Cannabinoids are pharmacologically active and influence voiding, which raises the question of whether marijuana is a risk factor or self-treatment?”

Source: Studies: Weed Degrades Sperm, Spurs LUTS | MedPage Today May 2019

Filed under: Cannabis/Marijuana,Drug use-various effects,Nicotine :

It is not all that long since people seriously tried to pretend that cigarettes were safe. Most of them were motivated by greed, and by fear that the truth would destroy their profits.

Everyone now agrees that cigarettes cause lung cancer and many other diseases. But we forget the struggle that doctors and scientists had to fight, against Big Tobacco, to get this accepted.

Sir Richard Doll and Sir Austin Bradford-Hill established in 1950 that there was a clear link between smoking and cancer. A wider study in 1954 absolutely confirmed this.

Yet such was the power and wealth of the tobacco giants that it was decades before anything serious was done to discourage smoking. It was not until 1971 that the first feeble warning was placed on cigarette packets in this country.

As late as 1962, the cigarette-makers were still pretending there hadn’t been enough research, and even that tobacco was good for you, claiming ‘smoking has pharmacological and psychological effects that are of real value to smokers’.

A Tory MP, Ted Leather, denounced the doctors’ warnings as ‘unscientific tosh’ and ‘hysterical nonsense’. Lung cancer was blamed on air pollution. The prominent journalist Chapman Pincher proclaimed ‘cigarette risks are being exaggerated’. It was seriously argued that restrictions on smoking were an attack on liberty.

I’d guess that many who made such claims lived to regret, bitterly and with some embarrassment, their part in covering up a terrible danger. Those who listened to them died, early and often horribly. They are still dying now, in cancer wards up and down the country.

Earlier, firmer action would have saved them and their families from much grief. Those tobacco apologists all have their parallels now.

I know, but will not name here, drug lobbyists, a Tory MP and several prominent journalists, who make the same excuses for marijuana, just as the evidence of its grave dangers piles up. They claim the evidence against it is exaggerated. They claim it has medical benefits. They claim its effects are caused by something else. May God forgive them. I cannot.

Our society, learning nothing from the tobacco disaster, has for years been appallingly complacent about this terribly dangerous drug, whose effect on the brains and minds of its users can be utterly devastating. Knowledge of its dangers does not show up in statistics which pay little attention to the sort of damage it does.

The victims of marijuana seldom die (though they increasingly frequently kill others, in mad car crashes and violent crime).

School failure, delinquency, delusional behaviour, persecution mania, young lives wholly blighted and continued only thanks to a devastating cocktails of antipsychotic drugs, do not register much in NHS figures. Nor do the special miseries of the families of these people, compelled to care, for life, for a husk of the person they once knew and had hopes for, and still love. Such families keep their grief to themselves. But there are many of them.

Look, I am right about this. But it is no good being right if you are not believed. I and my allies are roughly where the doctors who warned against lung cancer were in the mid-1950s. The evidence keeps on coming. Last week’s report linking marijuana use to depression and suicidal feelings among the young is just the latest in a great mountain of such studies. But the popular culture continues to act as if there’s nothing to worry about.

It is now seven years since I published a book which pointed out the truth – that the police and courts have given up prosecuting the major crime of marijuana possession. Back in 2012 I was denounced, snubbed, sneered at and told by distinguished academics that I was wrong and that there was a stern regime of cruel prohibition.

Now everybody recognises that what I said seven years ago is absolutely true. It is hard not to do so when so much of our country openly stinks of marijuana. Even if the Commissioner of the Metropolitan Police, Cressida Dick, cannot smell it, the rest of us can.

Sooner than seven years from now, I suspect that the connection between marijuana and severe mental illness will also be widely understood and accepted. But will it be too late?

Today’s Big Dope lobby wants to silence warnings about the dangers of marijuana until they have it legalised, and we can’t go back. They are like the Big Tobacco of the 1950s, a cynical greed campaign prepared to cause misery to others in the pursuit of riches.

This is the reason for its busy Trojan Horse operation to portray marijuana as a medicine, a claim for which there is very little evidence. And in any case, what use would a medicine be whose users risked irreversible mental illness?

Thalidomide was wonderful at treating morning sickness. But what does that matter compared with its terrible side effects?

Be on your guard. Make sure your MP isn’t fooled by Big Dope propaganda. Write to your MP when you see reports of crimes whose perpetrators were cannabis smokers. Your local papers will be full of them, if you look. Ask your MP to read the many reports linking this drug with mental illness.

And don’t be fooled. All of us sympathise with the mothers of very sick children who seek remedies for them. But beware of the shadowy figures who often stand behind such stories, and who use this suffering to promote a nasty cause.

It’s a race against time. If we lose it, the suffering which follows will be at least as bad as the suffering caused by cigarettes, and probably far worse.

Peter Hitchens Mail on Sunday

Source: Cigarettes are healthy! (And if you believe that, you’ll fall for Big Dope’s marijuana propaganda, too) – Mail Online – Peter Hitchens blog (mailonsunday.co.uk) February 2019

Filed under: Cannabis/Marijuana,Drug use-various effects,Nicotine,Political Sector :

Kevin Sabet was a drug control policy adviser in the White House for both Republicans and Democrats

When most people talk about Canada’s impending legalization of marijuana, they talk about the future. When Kevin Sabet talks about it, he worries about history repeating.

“There are huge misconceptions, I often feel like we’re living in 1918, not 2018,” he said.” When I say 1918, I mean 1918 for tobacco when everyone thought that smoking cigarettes was no problem and we had a new industry that was just starting.”

In 1918, soldiers returning home from the trenches of the First World War brought cigarettes home with them and unwittingly sowed the seeds of one of 20th century’s biggest health epidemics.

“We hadn’t had tobacco related deaths before the 20th century because we hadn’t had a lot of cigarettes, which actually gave us the most deadly form of tobacco we’ve ever seen. I feel like we’re like that with marijuana.”

Kevin Sabet is the president of Smart Approaches to Marijuana, or SAM, a non-profit agency in the United States devoted to ‘preventing another big tobacco.’ (Smart Approaches to Marijuana)

A former drug control policy adviser to the White House under both the Democrats and Republicans, Sabet is the President and CEO of Smart Approaches to Marijuana, a public health organization opposed to marijuana legalization and commercialization in the United States.

He said the sudden about-face by Ontario’s newly-elected Progressive Conservative government away from a public monopoly on marijuana sales to a mixed public-private is “a really bad move.”

“When I see the government monopoly being tossed out the window in favour of a private program that really puts private profit over public health.. I worry about that,” he said. “I think it’s a really bad move.”

“They are moving from a government monopoly to private retail and that’s going to open the door to all the marketing and promotion and normalization that already is a huge problem for our already legal drugs.”

“We’ve seen how that turned out for pharmaceuticals like opiates, which are highly dangerous and we’ve seen how that turned out for tobacco and alcohol.”

Big investors lining up to cash-in on pot

With legalization still months away, there are growing signs that marijuana and big business are starting to become best buds. (Nicolas Pham/Radio-Canada)

In fact, Sabet points out, some of the same players have already expressed their willingness to provide Canadians with legal marijuana on a massive scale.

Constellation Brands, the maker of some of the most popular wines and beers in the world, has already paid $5 billion for Canopy Growth, the world’s largest publicly traded licensed producer of marijuana in Smith Falls, Ont.

Several notable Canadian brands have also expressed an interest in legal bud, including Molson, which has mused publicly about a THC infused beer and Shopper’s Drug Mart, which hopes to branch out in sales of medical marijuana online.

“We’re already seeing the private market salivating in Canada, waiting to be that next addiction for profit substance and I don’t see how that helps us.”

‘Not your Woodstock weed’

Why that worries Sabet is the combination of savvy corporate marketing and increasingly intense levels of THC, or tetrahydrocannabinol, the active ingredient in marijuana.

“Today’s marijuana is not your Woodstock weed,” he said. “I think there’s a wild misperception about what today’s marijuana experience really is.”

There are signs too that marijuana sold on the street is stronger than it used to be. According to a 2017 report from the Hazelden Betty Ford Foundation, an American healthcare organization that helps people struggling with addiction, said the concentration of THC in marijuana has risen three-fold in the last two decades, from four per cent in 1994 to 12 per cent in 2014.

Sabet notes that marijuana sold commercially in some states goes even further and is available in highly concentrated forms, such as hash, wax, or shatter with no rules or limits on the concentration of marijuana’s active ingredient.

“It’s not four per cent THC, which is the ingredient that gets you high. It’s up to 99 per cent THC and there are no limits on THC,” he said. “I’m really concerned especially how today’s high potent marijuana is going to contribute to mental illness.”

Potent pot and drug-induced psychosis

Anecdotally, one only has to look as far as the story of Mark Phillips, a lawyer from a prominent Toronto family, who pleaded guilty to assault causing bodily harm in April, after he attacked a St. Thomas family with a baseball bat, calling them terrorists.

During Phillips’ court appearance, his lawyer and psychiatrist said he was suffering from a drug-induced psychosis.

His lawyer, Steve Kurka told Justice John Skowronski that Phillips, whose mental health had been declining in the months and weeks leading up to the December 2017 baseball bat attack, smoked three or four joints before driving to London and then nearby St. Thomas, getting into arguments with people he believed to be Muslims targeting him along the way.

“[It] doesn’t shock me,” Sabet said of the Phillips case. “Today’s highly potent THC can have an aggressive violent effect. I’m not going to say everybody is going to have a psychotic breakdown. We’re going to see stuff like this become more and more common.”

Despite his concerns about pot, Sabet said he doesn’t want to see Canada go back to the days of arresting people for simple pot possession, nor does he see a problem with people growing the plant at home on a small scale either.

“I don’t care about that,” he said. “The issue is when you make this a legal market and advertise it and throw it to the forces who are in the business of promotion. They are in the business of advertising and commercialization and pot shops next to your kid’s school and billboards and coupons and products, that’s my worry.”

Sabet believes the real Reefer Madness is giving private companies control of retail sales, where they can use marijuana as a tool in their pursuit of profit at the cost of public health.

“I worry that Canada is following the example of the United States in terms of this new industry which promotes, recklessly advertises, makes wild claims, ignores all harms and absolutely focuses on advertising to kids.”

Source: Ontario’s new retail pot plan ‘puts profit over public health’ says former Obama drug adviser | CBC News August 2018

Filed under: Brain and Behaviour,Canada,Cannabis/Marijuana,Economic,Global Drug Legalisation Efforts,Nicotine,Political Sector :

A handful of recent studies are beginning to reveal the possible health effects of e-cigarette use, and they are not all positive.
These findings and a reported uptick in teen vaping have spurred government regulators to act.
Researchers have found evidence of toxic metals like lead in e-cig vapor. Evidence also suggests that vaping may be linked to an increased risk of heart attacks.
Regulators and health experts are particularly concerned about a device called the Juul, which packs the same nicotine content per pod as a pack of cigarettes.

Smoking kills. No other habit has been so strongly tied to death.

In addition to inhaling burned tobacco and tar, smokers breathe in toxic metals like cadmium and beryllium, as well as metallic elements like nickel and chromium — all of which accumulate naturally in the leaves of the tobacco plant.

It’s no surprise, then, that much of the available evidence suggests that vaping, which involves puffing on vaporized liquid nicotine instead of inhaling burned tobacco, is at least somewhat healthier. Some limited studies have suggested that reaching for a vape pen instead of a conventional cigarette may also help people quit smoking regular cigarettes, but hard evidence of that remains elusive.

Very few studies, however, look at how vaping affects the body and brain. Even fewer specifically examine the Juul, a popular device that packs as much nicotine in each of its pods as a standard pack of cigarettes.

But a handful of studies published in the past few months have begun to illuminate some of the potential health effects tied to vaping. They are troubling.

With that in mind, the Food and Drug Administration outlined a new policy on Thursday morning designed to eventually curb the sale of e-cigs and reign in their appeal to young people.

Most recently, researchers at the Stanford University School of Medicine surveyed young people who vaped and found that those who said they used Juuls vaped more frequently than those who used other brands. The participants appeared to be insufficiently aware of how addictive the devices could be.

Most e-cigs contain toxic metals, and using them may increase the risk of a heart attack

Researchers took a look at the compounds in several popular brands of e-cigs (not the Juul) this spring and found some of the same toxic metals (such as lead) inside the device that they would normally find in conventional cigarettes. For another study published around the same time, researchers concluded that at least some of those toxins appeared to be making their way through vapers’ bodies, as evidenced by a urine analysis they ran on nearly 100 study participants.

In another study published this summer, scientists concluded that there was substantial evidence tying daily e-cig use to an increased risk of heart attack. And this week, a small study in rats suggested that vaping could have a negative effect on wound healing that’s similar to the effect of regular cigarettes.

In addition to these findings, of course, is a well-established body of evidence about the harms of nicotine. The highly addictive substance can have dramatic impacts on the developing brains of young adults.

Brain-imaging studies of adolescents who begin smoking traditional cigarettes (not e-cigs) at a young age suggest that those people have markedly reduced activity in the prefrontal cortex and perform less well on tasks related to memory and attention, compared with people who don’t smoke. Those consequences are believed to be a result of the nicotine in the cigarettes rather than other ingredients.

Nicholas Chadi, a clinical pediatrics fellow at Boston Children’s Hospital, spoke about the Juul at the American Society of Addiction Medicine’s annual conference this spring. He said these observed brain changes were also linked to increased sensitivity to other drugs as well as greater impulsivity. He described some anecdotal effects of nicotine vaping that he’d seen among teens in and around his hospital.

“After only a few months of using nicotine,” Chadi said, the teens “describe cravings, sometimes intense ones.” He continued: “Sometimes they also lose their hopes of being able to quit. And interestingly, they show less severe symptoms of withdrawal than adults, but they start to show them earlier on. After only a few hundred cigarettes — or whatever the equivalent amount of vaping pods — some start showing irritability or shakiness when they stop.”

A new survey suggests that teens who use Juul e-cigs aren’t aware of these risks

The Juul, which is made by the Silicon Valley startup Juul Labs, has captured more than 80% of the e-cig market and was recently valued at $15 billion. But the company is facing a growing backlash from the FDA and scientists who say the company intentionally marketed to teens.

On Tuesday, the company responded to some of these concerns — first by announcing that they’d be temporarily banning the sale of their flavored products at retailers and by deleting their social media accounts, which some research suggests has allured more young customers.

Yet very little research about e-cigs has homed in on the Juul specifically.

So for a study published this week, researchers from the Stanford University School of Medicine surveyed young people who vaped and asked them whether they used the Juul or another e-cigarette.

Their results can be found in a widely accessible version of the Journal of the American Medical Association called JAMA Open. Based on a sample of 445 high-school students whose average age was 19, the researchers observed that teens who used the Juul tended to say they vaped more frequently than those who used other devices. Juul users also appeared to be less aware of how addictive the devices could be compared with teens who vaped other e-cigs.

“I was surprised and concerned that so many youths were using Juul more frequently than other products,” Bonnie Halpern-Felsher, a professor of pediatrics who was a lead author of the study, said in a statement.

“We need to help them understand the risks of addiction,” she added. “This is not a combustible cigarette, but it still contains an enormous amount of nicotine — at least as much as a pack of cigarettes.”

Source: https://www.businessinsider.com/vaping-e-cigs-juul-health-effects-2018-10 October 2018

Filed under: Drug use-various effects,Health,Nicotine,Youth :

This Notice of Liability Memo and attached Affidavit of Harms give formal notification to all addressees that they are morally, if not legally liable in cases of harm caused by making toxic marijuana products legally available, or knowingly withholding accurate information about the multiple risks of hemp/marijuana products to the Canadian consumer. This memo further gives notice that those elected or appointed as representatives of the people of Canada, by voting affirmatively for Bill C45, do so with the knowledge that they are breaching international treaties, conventions and law. They do so also with the knowledge that Canadian law enforcement have declared that they are not ready for implementation of marijuana legalization, and as they will not be ready to protect the lives of Canadians, there may arise grounds for a Charter of Rights challenge as all Canadian citizens are afforded a the right to security of self.

Scientific researchers and health organizations raise serious questions about the safety of ingesting even small amounts of cannabinoids. Adverse effects include risk of harm to the cardio-vascular system, respiratory tract, immune system, reproductive and endocrine systems, gastrointestinal system and the liver, hyperemesis, cognition, psychomotor performance, psychiatric effects including depression, anxiety and bipolar disorder, schizophrenia and psychosis, a-motivational syndrome, and addiction. The scientific literature also warns of teratogenicity (causing birth deformities) and epigenetic damage (affecting genetic development) and clearly establishes the need for further study. The attached affidavit cites statements made by Health Canada that are grounded in scientific evidence that documents many harms caused by smoking or ingesting marijuana.

Putting innocent citizens in “harm’s way” has been a costly bureaucratic mistake as evidenced by the 2015 Canadian $168 million payout to victims of exposure to the drug thalidomide. Health Canada approved thalidomide in 1961 to treat morning sickness in pregnant women but it caused catastrophic birth defects and death.

It would be instructive to reflect on “big tobacco” and their multi-billion-dollar liability in cases of misinformed sick and dead tobacco cigarette smokers. Litigants won lawsuits for harm done by smoking cigarettes even when it was the user’s own choice to obtain and smoke tobacco. In Minnesota during the 1930’s and up to the 1970’s tobacco cigarettes were given to generally healthy “juvenile delinquents’ incarcerated in a facility run by the state. One of the juveniles, now an adult, who received the state’s tobacco cigarettes, sued the state for addicting him. He won.

The marijuana industry, in making public, unsubstantiated claims of marijuana safety, is placing itself in the same position, in terms of liability, as the tobacco companies.
In 1954, the tobacco industry published a statement that came to be known during Minnesota’s tobacco trial as the “Frank Statement.” Tobacco companies then formed an industry group for the purposes of deceiving and confusing the public.

In the Frank Statement, tobacco industry spokesmen asserted that experiments linking smoking with lung cancer were “inconclusive,” and that there was no proof that cigarette smoking was one of the causes of lung cancer. They stated, “We believe the products we make are not injurious to health.” Judge Kenneth Fitzpatrick instructed the Minnesota jurors: “Jurors should assume in their deliberations that tobacco companies assumed a “special duty” by publishing the ad (Frank Statement), and that jurors will have to determine whether the industry fulfilled that duty.” The verdict ruled against the tobacco industry.

Effective June 19, 2009, marijuana smoke was added to the California Prop 65 list of chemicals known to cause cancer. The Carcinogen Identification Committee (CIC) of the Office of Environmental Health Hazard Assessment (OEHHA) “determined that marijuana smoke was clearly shown, through scientifically valid testing according to generally accepted principles, to cause cancer.”

Products liability and its application to marijuana businesses is a topic that was not discussed in the Senate committee hearings. Proposition 65, requires the State to publish a list of chemicals known to cause cancer, birth defects or other types of reproductive harm. Proposition 65 requires businesses to provide their customers with notice of these cancerous causing chemicals when present in consumer products and provides for both a public and private right of action.

The similarities between the tactics of “Big Tobacco” and the “Canadian Cannabis Trade Alliance Institute” and individual marijuana producers would seem to demand very close scrutiny. On May 23, a witness testified before the Canadian Senate claimed that marijuana is not carcinogenic. This evidence was not challenged.

The International Narcotics Control Board Report for 2017 reads: “Bill C-45, introduced by the Minister of Justice and Attorney General of Canada on 13 April 2017, would permit the non-medical use of cannabis. If the bill is enacted, adults aged 18 years or older will legally be allowed to possess up to 30 grams of dried cannabis or an equivalent amount in non-dried form. It will also become legal to grow a maximum of four cannabis plants, simultaneously for personal use, buy cannabis from licensed retailers, and produce edible cannabis products. The Board wishes to reiterate that article 4 (c) of the 1961 Convention restricts the use of controlled narcotic drugs to medical and scientific purposes and that legislative measures providing for non-medical use are in contravention of that Convention….

The situation pertaining to cannabis cultivation and trafficking in North America continues to be in flux owing to the widening scope of personal non-medical use schemes in force in certain constituent states of the United States. The decriminalization of cannabis has apparently led organized criminal groups to focus on manufacturing and trafficking other illegal drugs, such as heroin. This could explain why, for example, Canada saw a 32 per cent increase from 2015 to 2016 in criminal incidents involving heroin possession….The Canadian Research Initiative in Substance Misuse issued “Lower-risk cannabis use guidelines” in 2017. The document is a health education and prevention tool that acknowledges that cannabis use carries both immediate and long-term health risks.”

https://www.incb.org/documents/Publications/AnnualReports/AR2017/Annual_Report_chapters/Chapter_3_Americas_2017.pdf

Upon receipt of this Memo and Affidavit, the addressees can no longer say they are ignorant or unaware that promoting and/or distributing marijuana cigarettes for recreational purposes is an endangerment to citizens. Receipt of this Memo and Affidavit removes from the addressees any claim of ignorance as a defense in potential, future litigation.

Pamela McColl www.cleartheairnow.org

pam.mccoll@cleartheairnow.org

AFFIDAVIT May 27, 2018

I, Pamela McColl, wish to inform agencies and individuals of known and potential harm done/caused by the use of marijuana (especially marijuana cigarettes) and of the acknowledgement the risk of harm by Health Canada.

Marijuana is a complex, unstable mixture of over four hundred chemicals that, when smoked, produces over two thousand chemicals. Among those two thousand chemicals are many pollutants and cancer-causing substances. Some cannabinoids are psychoactive, all are bioactive, and all may remain in the body’s fatty tissues for long periods of times with unknown consequences. Marijuana smoke contains carcinogenic (cancer-causing) substances such as benzo(a)pyrene, benz(a)anthracene, and benzene in higher concentrations than are present in tobacco smoke. The mechanism by which benzo(a)pyrene causes cancer in smokers was demonstrated scientifically by Denissenko MF et al. Science 274:430-432, 1996.

Health Canada Consumer Information on Cannabis reads as follows: “The courts in Canada have ruled that the federal government must provide reasonable access to a legal source of marijuana for medical purposes.”

“Cannabis is not an approved therapeutic product and the provision of this information should not be interpreted as an endorsement of the use of cannabis for therapeutic purposes, or of marijuana generally, by Health Canada.”

“Serious Warnings and Precautions: Cannabis (marihuana, marijuana) contains hundreds of substances, some of which can affect the proper functioning of the brain and central nervous system.”

“The use of this product involves risks to health, some of which may not be known or fully understood. Studies supporting the safety and efficacy of cannabis for therapeutic purposes are limited and do not meet the standard required by the Food and Drug Regulations for marketed drugs in Canada.”

Health Canada – “When the product should not be used: Cannabis should not be used if you:-are under the age of 25 -are allergic to any cannabinoid or to smoke-have serious liver, kidney, heart or lung disease -have a personal or family history of serious mental disorders such as schizophrenia, psychosis, depression, or bipolar disorder-are pregnant, are planning to get pregnant, or are breast-feeding -are a man who wishes to start a family-have a history of alcohol or drug abuse or substance dependence Talk to your health care practitioner if you have any of these conditions. There may be other conditions where this product should not be used, but which are unknown due to limited scientific information.

Cannabis is not an approved therapeutic product and the provision of this information should not be interpreted as an endorsement of the use of this product, or cannabis generally, by Health Canada.”

Prepared by Health Canada Date of latest version: February 2013, accessed May 2018. https://www.canada.ca/en/health-canada/services/drugs-health-products/medical-use-marijuana/information-medical-practitioners/information-health-care-professionals-cannabis-marihuana-marijuana-cannabinoids.html

A report published by survey company RIWI Corp. (RIWI.com) can be found at: https://riwi.com/case-study/measuringcanadians-awareness-of-marijuanas-health-effects-may-2018

The report measures Canadians’ awareness of marijuana’s health effects as determined by Health Canada and published on Health Canada’s website. RIWI data indicates: 1. More than 40% of those under age 25 are unaware that marijuana impacts safe driving. Further, 21% of respondents are not aware that marijuana can negatively impact one’s ability to drive safely. Health Canada: “Using cannabis can impair your concentration, your ability to make decisions, and your reaction time and coordination. This can affect your motor skills, including your ability to drive.” 2. One in five women aged 25-34 believes marijuana is safe during pregnancy, while trying to get pregnant, or breastfeeding. • RIWI: “For women of prime childbearing age (25-34), roughly one in five believe smoking marijuana is safe during pregnancy, planning to get pregnant, and breastfeeding.” • Health Canada: “Marijuana should not be used if you are pregnant, are planning to get pregnant, or are breastfeeding. … Long-term use may negatively impact the behavioural and cognitive development of children born to mothers who used cannabis during pregnancy.” 3. One in three Canadians do not think that marijuana is addictive. • Health Canada: “Long term use may result in psychological dependence (addiction).” 4. One in three Canadians believe marijuana aids mental health. • Health Canada: “Long term use may increase the risk of triggering or aggravating psychiatric and/or mood disorders (schizophrenia, psychosis, anxiety, depression, bipolar disorder).” 5. One in two males were unaware that marijuana could harm a man’s fertility • “Marijuana should not be used if you are a man who wishes to start a family.”

ClearTheAirNow.org, a coalition of concerned Canadians commissioned the survey.

Affiant is willing to provide further sources of information about the toxicity of marijuana.

Pamela McColl

www.cleartheairnow.org

pam.mccoll@cleartheairnow.org

Source: From email sent to Drug Watch International May 2018

Filed under: Brain and Behaviour,Cannabis/Marijuana,Drug use-various effects,Drug use-various effects on foetus, babies, children and youth,Global Drug Legalisation Efforts,Health,Legal Sector,Marijuana and Medicine,Nicotine,Social Affairs :

Abstract

Background: Inconsistent findings exist regarding long-term substance use (SU) risk for children diagnosed with attention-deficit/hyperactivity disorder (ADHD). The observational follow-up of the Multimodal Treatment Study of Children with ADHD (MTA) provides an opportunity to assess long-term outcomes in a large, diverse sample.

Methods: Five hundred forty-seven children, mean age 8.5, diagnosed with DSM-IV combined-type ADHD and 258 classmates without ADHD (local normative comparison group; LNCG) completed the Substance Use Questionnaire up to eight times from mean age 10 to mean age 25.

Results: In adulthood, weekly marijuana use (32.8% ADHD vs. 21.3% LNCG) and daily cigarette smoking (35.9% vs. 17.5%) were more prevalent in the ADHD group than the LNCG. The cumulative record also revealed more early substance users in adolescence for ADHD (57.9%) than LNCG (41.9%), including younger first use of alcohol, cigarettes, marijuana, and illicit drugs. Alcohol and nonmarijuana illicit drug use escalated slightly faster in the ADHD group in early adolescence. Early SU predicted quicker SU escalation and more SU in adulthood for both groups.

Conclusions: Frequent SU for young adults with childhood ADHD is accompanied by greater initial exposure at a young age and slightly faster progression. Early SU prevention and screening is critical before escalation to intractable levels.

Keywords: ADHD; Attention deficit disorder; adolescence; drug abuse.

Conflict of interest statement

Conflict of Interest Disclosures: J.M.S. acknowledges research support, advisory board/speaker’s bureau and/or consulting for Alza, Richwood, Shire, Celgene, Novartis, Celltech, Gliatech, Cephalon, Watson, CIBA, UCB, Janssen, McNeil, Noven, NLS, Medice, and Lilly. J.T.M. received royalties from New Harbinger Press. L.E.A. received research funding from Curemark, Forest, Lilly, Neuropharm, Novartis, Noven, Shire, Supernus, and YoungLiving and consulted with or was on advisory boards for Gowlings, Neuropharm, Novartis, Noven, Organon, Otsuka, Pfizer, Roche, Seaside Therapeutics, Sigma Tau, Shire, and Tris Pharma and received travel support from Noven. L.H. received research support, served on advisory boards and was speaker for Eli Lilly, Glaxo/Smith/Kline, Ortho Janssen, Purdue, Shire and Ironshore. Other authors have no disclosures.

Source: https://www.ncbi.nlm.nih.gov/pubmed/29315559 June 2018

Filed under: Addiction,Brain and Behaviour,Cannabis/Marijuana,Drug use-various effects,Nicotine,Youth :

Proportion of young people who tried cigarettes as their first drug fell over the same period, US study says

The proportion of young people using marijuana as their first drug doubled in the 10 years from 2004, a US-based study has found.

The government study reveals that among people aged between 12 and 21, the proportion of those who tried cigarettes as their first drug fell from about 21% to just under 9% between 2004 and 2014. However, the proportion who turned first to marijuana almost doubled from 4.4% to 8%.

While some studies have suggested that, overall, use and abuse of marijuana has fallen among teenagers in the US, the latest research sought to look at trends in which drug, if any, young people turned to first.

“We have, particularly in the US, done prevention programmes that are really focused on alcohol and tobacco – and they are relatively easy arguments to make to young people,” said Dr Renee Johnson, a co-author of the study from Johns Hopkins Bloomberg School of Public Health.

But she said the “fear factor” is less likely to work for marijuana, noting that public programmes need instead to educate young people so they can make good decisions around drugs, and offer support to help them cope with difficulties in life and think about their life plans. “Once we teach young people about that, that will address the unhealthy marijuana use,” she said.

The study, published in the journal Prevention Science, is based on an analysis of data from more than 275,000 participants aged between 12 and 21 collected as part of the US national survey on drug use and health – an annual study that involves participants across all 50 states who are interviewed in person.

Among the findings, the team found that between 2004 and 2014, reported age at first use of each of the substances rose. What’s more, the proportion of young people reporting no drug use increased from 35.5% to just over 46%, while the proportion reporting cigarettes as their first substance fell. The proportion reporting alcohol as the first drug remained fairly constant at about 30%.Males were more likely than females to report using marijuana first. Ethnicity was also a factor, with almost 12% of American Indian and Alaskan native participants and over 9% of black participants reporting marijuana as their first drug – compared to under 5% of white participants and 2.5% of Asian participants.

Once age, sex and ethnicity were taken into account, the team found that those who smoked marijuana first were more likely to be current heavy marijuana users and have cannabis use disorder than those who used other substances first.

They were also as likely as those who used cigarettes first to have a nicotine dependancy if a smoker. “One concern about marijuana and tobacco use is [if] it increases tobacco use later in life,” said Johnson.

In addition, those who reported marijuana or alcohol as their first substance were more likely to report use of other drugs, such as heroin, than those who first used cigarettes or other tobacco products.

Prof Terrie Moffitt, a clinical psychologist at King’s College London who was not involved in the study, said the data was robust.

“The finding might arise because in the past decade, there have been major public campaigns warning of the dangers of tobacco and alcohol, whereas in contrast the media coverage of American states legalising cannabis creates the public impression that cannabis has no risks or dangers,” she said.

Sir Robin Murray, professor of psychiatric research at King’s College London, agreed, saying the findings are highly predictable. “It’s a pity that so many young people appear to be swopping one set of health risks with another,” he said.

The impact of cannabis on the brains of young people, mental health and life prospects has received much scrutiny. Moffitt noted the latest study shows it is young people who are already living in socially disadvantaged circumstances who tend to turn to marijuana as their first drug.

“If indeed it is not safe for teens, then cannabis use could compound the life challenges they already have to surmount to make their way in the world as adults,” she said.

Source: Surge in young Americans using marijuana as first drug | Science | The Guardian May 2018

Filed under: Alcohol,Cannabis/Marijuana,Drug use-various effects,Nicotine,Youth :

Smoking during pregnancy has well-documented negative effects on birth weight in infants and is linked to several childhood health problems. Now, researchers at the University at Buffalo Research Institute on Addictions have found that prenatal marijuana use also can have consequences on infants’ weight and can influence behavior problems, especially when combined with tobacco use.

“Nearly 30 percent of women who smoke cigarettes during pregnancy also report using marijuana,” says Rina Das Eiden, PhD, RIA senior research scientist. “That number is likely to increase with many states moving toward marijuana legalization, so it’s imperative we know what effects prenatal marijuana use may have on infants.”

Through a grant from the National Institute on Drug Abuse, Eiden studied nearly 250 infants and their mothers. Of these, 173 of the infants had been exposed to tobacco and/or marijuana during their mothers’ pregnancies. None were exposed to significant amounts of alcohol.

Eiden found that infants who had been exposed to both tobacco and marijuana, especially into the third trimester, were smaller in length, weight and head size, and were more likely to be born earlier, compared to babies who were not exposed to anything. They also were more likely to be smaller in length and weight compared to babies exposed only to tobacco in the third trimester. The results were stronger for boys compared to girls.

“We also found that lower birth weight and size predicted a baby’s behavior in later infancy,” Eiden says. “Babies who were smaller were reported by their mothers to be more irritable, more easily frustrated and had greater difficulty calming themselves when frustrated. Thus, there was an indirect association between co-exposure to tobacco and marijuana and infant behavior via poor growth at delivery.”

Furthermore, women who showed symptoms of anger, hostility and aggression reported more stress in pregnancy and were more likely to continue using tobacco and marijuana throughout pregnancy. Therefore, due to the co-exposure, they were more likely to give birth to infants smaller in size and who were more irritable and easily frustrated. The infants’ irritability and frustration is also linked to mothers who experienced higher levels of stress while pregnant.

“Our results suggest that interventions with women who smoke cigarettes or use marijuana while pregnant should also focus on reducing stress and helping them cope with negative emotions,” Eiden says. “This may help reduce prenatal substance exposure and subsequent behavior problems in infants.”

The study appeared in the March/April issue of Child Development and was authored by Pamela Schuetze, PhD, Department of Psychology, Buffalo State College, with co-authors Eiden; Craig R. Colder, PhD, UB Department of Psychology; Marilyn A. Huestis, PhD, Institute of Emerging Health Professions, Thomas Jefferson University, Philadelphia; and Kenneth E. Leonard, PhD, RIA director.

Source: Prenatal marijuana use can affect infant size, behavior, study finds — ScienceDaily May 2018

Filed under: Brain and Behaviour,Cannabis/Marijuana,Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

Study finds combined use of cigarettes and marijuana may increase children’s exposure to second-hand smoke

Cannabis use increased among parents who smoke cigarettes, as well as among non-smoking parents, according to a latest study from researchers at Columbia University’s Mailman School of Public Health and City University of New York. Cannabis use was nearly four times more common among cigarette smokers compared with non-smokers. Until now, little had been known about current trends in the use of cannabis among parents with children in the home, the prevalence of exposure to both tobacco and cannabis, and which populations might be at greatest risk. The findings will be published online in the June issue of Pediatrics.

“While great strides have been made to reduce children’s exposure to second-hand cigarette smoke, those efforts may be undermined by increasing use of cannabis among parents with children living at home,” said Renee Goodwin, PhD, in the Department of Epidemiology at the Mailman School of Public Health, and corresponding author.

Analyzing data from the National Survey on Drug Use and Health from 2002 to 2015, the researchers found past-month cannabis use among parents with children at home increased from 5 percent in 2002 to 7 percent in 2015, whereas cigarette smoking declined from 28 percent to 20 percent. Cannabis use increased from 11 percent in 2002 to over 17 percent in 2015 among cigarette-smoking parents and from slightly over 2 percent to 4 percent among non-cigarette-smoking parents. Cannabis use was nearly 4 times more common among cigarette smokers versus nonsmokers (17 percent vs 4 percent), as was daily cannabis use (5 percent vs 1 percent). The overall percentage of parents who used cigarettes and/or cannabis decreased from 30 percent in 2002 to 24 percent in 2015.

“While use of either cigarettes or cannabis in homes with children has declined, there was an increase in the percent of homes with both. Therefore, the increase in cannabis use may be compromising progress in curbing exposure to secondhand smoke,” noted Goodwin, who is also at the Graduate School of Public Health and Health Policy at CUNY.

Cannabis use was also more prevalent among men who also smoked compared to women (10 percent vs 6 percent) and among younger parents with children in the home (11 percent) compared with those 50 and older (4 percent). The strength of the relationship between current cannabis use and cigarette smoking was significant and similar for all income levels.

“The results of our study support the public health gains in reducing overall child secondhand tobacco smoke but raise other public health concerns about child exposure to secondhand cannabis smoke and especially high risk for combined exposures in certain subpopulations,” observed Goodwin.

Noteworthy, according to Goodwin, is that there remains a lack of information on the location of smoking, whether it occurs in the house or in the proximity of children. Unlike cigarettes, smoking cannabis outdoors and in a range of public areas is illegal in most places. Therefore, there is reason to believe that cannabis use is even more likely to occur in the home than cigarette smoking given their differences in legal status.

“Efforts to decrease secondhand smoke exposure via cigarette smoking cessation may be complicated by increases in cannabis use,” said Goodwin. “Educating parents about secondhand cannabis smoke exposure should be integrated into public health education programs on secondhand smoke exposure.”

The study was funded by the National Institutes of Health and National Institute on Drug Abuse (DA20892).

Co-authors are Melanie Wall, Deborah Hasin, and Samantha Santoscoy, Mailman School of Public Health; Keely Cheslack-Postava, Columbia University College of Physicians and Surgeons; Nina Bakoyiannis, CUNY; and Bradley Collins and Stephen Lepore, Temple University.

Source: Cannabis use up among parents with children in the home: Study finds combined use of cigarettes and marijuana may increase children’s exposure to second-hand smoke — ScienceDaily May 2018

Filed under: Cannabis/Marijuana,Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

The popularity of electronic cigarettes continues to grow worldwide, as many people view them as a safer alternative to smoking. But the long-term effects of e-cigarette usage, commonly called “vaping,” are unknown. Today, researchers report that vaping may modify the genetic material, or DNA, in the oral cells of users, which could increase their cancer risk.

The researchers will present their results today at the 256th National Meeting & Exposition of the American Chemical Society (ACS).

“E-cigarettes are a popular trend, but the long-term health effects are unknown,” says Romel Dator, Ph.D., who is presenting the work at the meeting. “We want to characterize the chemicals that vapers are exposed to, as well as any DNA damage they may cause.”

Introduced to the market in 2004, e-cigarettes are handheld electronic devices that heat a liquid, usually containing nicotine, into an aerosol that the user inhales. Different flavors of liquids are available, including many that appeal to youth, such as fruit, chocolate and candy. According to a 2016 report by the U.S. Surgeon General, 13.5 percent of middle school students, 37.7 percent of high school students and 35.8 percent of young adults (18 to 24 years of age) have used e-cigarettes, compared with 16.4 percent of older adults (25 years and up).

“It’s clear that more carcinogens arise from the combustion of tobacco in regular cigarettes than from the vapor of e-cigarettes,” says Silvia Balbo, Ph.D., the project’s lead investigator, who is at the Masonic Cancer Center at the University of Minnesota. “However, we don’t really know the impact of inhaling the combination of compounds produced by this device. Just because the threats are different doesn’t mean that e-cigarettes are completely safe.”

To characterize chemical exposures during vaping, the researchers recruited five e-cigarette users. They collected saliva samples before and after a 15-minute vaping session and analyzed the samples for chemicals that are known to damage DNA. To evaluate possible long-term effects of vaping, the team assessed DNA damage in the cells of the volunteers’ mouths. The researchers used mass-spectrometry-based methods they had developed previously for a different study in which they evaluated oral DNA damage caused by alcohol consumption.

Dator and Balbo identified three DNA-damaging compounds, formaldehyde, acrolein and methylglyoxal, whose levels increased in the saliva after vaping. Compared with people who don’t vape, four of the five e-cigarette users showed increased DNA damage related to acrolein exposure. The type of damage, called a DNA adduct, occurs when toxic chemicals, such as acrolein, react with DNA. If the cell does not repair the damage so that normal DNA replication can take place, cancer could result.

The researchers plan to follow up this preliminary study with a larger one involving more e-cigarette users and controls. They also want to see how the level of DNA adducts differs between e-cigarette users and regular cigarette smokers. “Comparing e-cigarettes and tobacco cigarettes is really like comparing apples and oranges. The exposures are completely different,” Balbo says. “We still don’t know exactly what these e-cigarette devices are doing and what kinds of effects they may have on health, but our findings suggest that a closer look is warranted.”

Source: E-cigarettes can damage DNA — ScienceDaily August 2018

Filed under: Drug use-various effects,Health,Nicotine :

Source:Drug Use in Colorado 2000 – 2013 SAMHSA NSDUH data

Filed under: Cannabis/Marijuana,Cocaine,Drug Specifics,Nicotine,USA,Youth :

The Centers for Disease Control and Prevention’s Vital Signs addresses a single, important public health topic each month. This month’s edition presents their latest findings on youth exposure to e-cigarette advertising. They also highlight strategies to prevent youth exposure to e-cigarette advertising and youth e-cigarette use.

The use of e-cigarettes among U.S. youth has increased considerably since 2011. Exposure to advertisements depicting e-cigarettes might contribute to increased e-cigarette use among youth. CDC analyzed nationally representative data to estimate the prevalence of e-cigarette advertisements among middle school and high school students in the U.S. Four sources of exposure were assessed: retail stores, Internet, TV and movies, and newspapers and magazines.

Key points in the Vital Signs report include:

Approximately 18.3 million U.S. middle school and high school students were exposed to at least one source of e-cigarette advertising in 2014.
Approximately half of all middle school and high school students (an estimated 14.4 million students) were exposed to e-cigarette advertisements in retail stores.
Approximately one third of middle school and high school students were exposed to e-cigarette advertisements on the Internet (10.5 million), on TV or at the movies (9.6 million), or while reading newspapers or magazines (8.0 million).

Source: https://www.cadca.org/resources/e-cigarette-advertising-found-be-pervasive-youth-cdc-says 2016

Filed under: Nicotine,Youth :

The Centers for Disease Control (CDC) recently issued a warning about vaping following a multistate outbreak of severe lung problems linked to the use of electronic cigarettes. According to the CDC, there are, as of September 6, 450 reported cases of possible vaping-linked lung problems across 33 states and 1 territory, resulting in 6 deaths. Officials have not identified a specific e-cigarette product as a cause of the illnesses, meaning that various devices on the market could be contributing to this alarming pattern. Patients admitted for lung problems report difficulty breathing, fatigue, fever, nausea, and vomiting. Somehow, to proponents and purveyors of e-cigarettes, the very idea that vaping could be dangerous seems to have come as a surprise.

The CDC updated its warning to suggest that e-cigarette and vaping device users refrain from using the products at all during the course of its investigation. It has also warned against buying counterfeit or street vaping products, including those with THC or other cannabinoids, and against modifying e-cigarette products. Moreover, the CDC urges youth, pregnant women, and adults who do not currently use tobacco products to refrain from using e-cigarette products, and encourages individuals who smoke and want to quit to use FDA-approved medications instead of e-cigarettes. Some health officials and experts believe that street vaping products with illicit or tainted substances may be behind the outbreak of lung problems, but no one can be certain at this point. Some patients have reported using vaping cartridges with THC or cannabinoids, but others have reported using different vaping cartridges without such substances. Most contain ingredients not generally tested for chronic inhalation in humans, and, to make matters worse, they can become contaminated in ways detrimental to respiratory and heart health. It is unlikely that any substance you inhale has been tested for safety for weeks, months, or over the long haul. But inhalation from vaping has effects on the lungs that are dramatic, can be easily seen on imaging, and do not seem easy to reverse.

Tobacco smoking in the English colonies of North America started early and peaked in the U.S. in the 1960s and 1970s, credible evidence proving its causal links to cancer, emphysema, and bronchitis emerging only over a century after its explosive growth and wild popularity. Why would boosters and defenders of today’s e-cigarettes, looking back at this history, believe that research would come to indicate the product’s benefits for the lungs, or for the respiratory health of those they may expose to vaping?

While experts and officials will continue to study this outbreak and may identify particular illicit substances as the culprit, the headlines have naturally raised questions for individuals who vape about long term consequences. What we know about cigarette smoking is bad enough, but there are few surprises. Here, we’re in uncharted territory. Yes, the FDA and other agencies will look at the broader health and safety of e-cigarette products and devices, but in the meantime, users will need to be evaluated and hope that their own lungs are not compromised in ways that only become clearly understood after they stop, or years down the line. While receiving considerably less media coverage, journalists recently found that the FDA began investigating vaping-associated seizures after some users of JUUL, the top-selling vaping product in the U.S., submitted claims of seizures to the administration’s safety portal.

It is important to note that Research You Can Use previously observed that there is not yet enough evidence to conclude whether e-cigarettes are suitable for smoking cessation. Some researchers now suggest that vaping nicotine may not be safer than smoking tobacco cigarettes. More recently, the FDA has agreed that JUUL’s claims of comparative safety are unproven. Other new studies have looked at the relative health of ingredients in some e-cigarette products, and the effects of vaping on the vascular system. The truth is that it’s risky and scientifically invalid to start from the premise that drugs are safe until proven dangerous. It reminds me of cocaine being touted as safe, or non-addicting, or even as “the champagne of drugs” until the aftermath of widespread use in the 1970s and 80s demonstrated that it was highly addictive and led to heart problems, brain damage, and other diseases.

What did these studies find?

One study, led by Yale’s Julie Zimmerman, found that chemical interactions in some of JUUL’s inhaled liquid nicotine mixtures yield unanticipated new chemicals that can cause breathing problems. In this study, researchers created a machine to trap JUUL aerosol and investigate its chemical composition. They found that the alcohols hosting flavors and nicotine in JUUL’s e-liquid react with vanillin, a flavor prohibited in tobacco cigarettes, to produce acetals. The effects of inhaling acetal chemicals are unknown, but the study notes that they can cause inflammation and lung irritation. The study found acetals in JUUL’s ‘Crème Brulée’ flavor. One researcher told Yale in an interview that the team was surprised to find such high vanillin chemical levels, pointing out that the detected levels reached those established for health limits on vanillin in bakeries and flavoring businesses.

This study also found menthol in 4 of the 8 JUUL flavors it tested. Menthol, the researchers note, can expand nicotine intake. This could be concerning in part because JUUL pods already have high nicotine content relative to other nicotine products—individuals absorb from one JUUL pod as much nicotine as an entire pack of cigarettes. The researchers also observe that the findings are notable because users of the product often believe that the ingredients and chemical makeup of e-liquids are stable, without realizing that the included chemicals can combine, alter each other, or produce potentially harmful new compounds. The study calls for vaping regulations that tackle the creation of new and possibly toxic chemical elements in e-liquids, exposure to flavorings, and menthol levels.

Another new study, this time from the University of Pennsylvania, examined the effects of vaping on the vascular system and found that e-cigarette use, even without nicotine, can damage blood flow. Researchers studied 31 nonsmokers between the ages of 18 and 35, with no prior history of cardiovascular problems, hypertension, asthma, respiratory tract infections, or cancer. Participants in the study inhaled from e-cigarette devices 16 times each, at three seconds per inhalation. The researchers then used MRIs to measure the participants’ blood vessel health, having evaluated it before and after the vaping exercises. In the participants’ post-vaping leg veins, oxygen levels fell 20 percent, and their peak blood flow velocity fell 17 percent. Their femoral arteries also dilated 34 percent less. The researchers call for additional research on the topic to corroborate their findings in larger groups, and their results focus only on the ECO e-cigarette device, but they nonetheless point to serious concerns about chronic use of vaping products, which may not give time for users’ blood vessel health to normalize or reset.

Why is this important?

Individuals who use vaping products can assume, on the basis consumer-focused “evidence,” that because e-cigarette makers claim that their products are a healthier alternative to tobacco products, they must be “healthy” overall. Some evidence does support the idea that vaping is preferable to smoking tobacco, which is why the United Kingdom’s government asserts that vaping is 95 percent less harmful than e-cigarette use and encourages e-cigarette users to switch to vaping. The dispute over this assertion may come down to the exact meaning of “less harmful,” but those with vaping-related lung disease would certainly argue that vaping is not safer than smoking tobacco. It’s also true that news reports on vaping can often overstate claims in the other direction, alleging or implying that e-cigarettes alone are responsible for severe lung distress. On this point, it may be useful to consider a similar research problem: attempting to determine whether smoking cannabis causes lung cancer when most cannabis smokers also smoke other drugs, and when many also smoke tobacco. By the time health officials and experts reach a definitive conclusion, it may be too late for those vaping. While exaggerations or misleading reports exist, they should not be used to support denial of mounting evidence, or instill confidence in vapers when new research shows obvious reasons to worry—and to worry about health more seriously than the “long-term effects are unknown” talking point.

The CDC’s overall position on vaping in recent years, subject to change, is that e-cigarettes “have the potential” to help adult smokers quit if they are not pregnant and can entirely substitute vaping for smoking tobacco products. Again, the CDC is now suggesting that individuals avoid vaping while investigations into the associated outbreak continue. It also says that scientists still have much to learn about e-cigarettes and warns that they are not safe for youth. The CDC, FDA, NIDA, and other authorities have recognized youth vaping as a growing epidemic, and have begun taking measures to confront it. Federal officials are now reportedly creating a plan to ban flavored e-cigarette products, which have a particular appeal to youth. Given the recent outbreak of severe lung problems and continued youth interest in e-cigarettes, additional action on this front will likely be required. Another recent study, for example, found 25 distinct “vape tricks” in 59 sample videos on YouTube with a median count of over 32,000 views. “Vape tricks” are stylized and playfully affected techniques for vaping, such as exhaling clouds in unique shapes, that attract the young. 48 percent of the videos were linked to industry posting accounts. This study recommended restrictions on e-cigarette social media marketing to help curb youth vaping, which sounds like a promising avenue for public health. Officials may also find it beneficial to take account of new studies about vaping’s effects on lung and blood vessel health as they deal with the increasingly apparent reality that e-cigarette use is not merely problematic in associated outbreaks, but in legal use, too.

Source: https://www.addictionpolicy.org/blog/tag/research-you-can-use/vaping-and-lungs September 2019

Filed under: Cannabis/Marijuana,Health,Nicotine :

Abstract

Tobacco and alcohol use are leading causes of mortality that influence risk for many complex diseases and disorders1. They are heritable2,3 and etiologically related4,5 behaviors that have been resistant to gene discovery efforts6,7,8,9,10,11. In sample sizes up to 1.2 million individuals, we discovered 566 genetic variants in 406 loci associated with multiple stages of tobacco use (initiation, cessation, and heaviness) as well as alcohol use, with 150 loci evidencing pleiotropic association.
Smoking phenotypes were positively genetically correlated with many health conditions, whereas alcohol use was negatively correlated with these conditions, such that increased genetic risk for alcohol use is associated with lower disease risk. We report evidence for the involvement of many systems in tobacco and alcohol use, including genes involved in nicotinic, dopaminergic, and glutamatergic neurotransmission. The results provide a solid starting point to evaluate the effects of these loci in model organisms and more precise substance use measures.

Source: Nature Genetics (2019) 14th Jan.201

Filed under: Addiction,Nicotine :

Researchers have long known that there is a link between nicotine and alcohol consumption. But the nature of the connection—how long it lasts, which begets which—remains a mystery.

A new Tel Aviv University study finds that nicotine exposure during adolescence can predict increased alcohol intake in adulthood. This suggests that memories of smoking tobacco as a teenager alter the brain’s reaction to alcohol even after a prolonged nicotine withdrawal. The research indicates that these nicotine “memories” may even lead to a tendency toward heavier drinking later in life.

The research was led by Dr. Segev Barak and his research team at TAU’s School of Psychological Sciences and Sagol School of Neuroscience. It was published in Scientific Reports.

The influence of memory

“Previously, it was believed that the mere consumption of nicotine during adolescence could trigger the use of other drugs—cocaine, heroin and alcohol,” Dr. Barak said. “Our study shows that nicotine ‘memories’ from adolescence are the culprit, not the nicotine itself.”

The researchers found that nicotine “memories” caused long-lasting changes in the brain, long after the cessation of nicotine consumption. A brief exposure to the nicotine environment triggered a robust decrease in the expression of the growth factor GDNF in the brain’s pleasure center. “We have previously shown that GDNF serves as a brain regulator of alcohol consumption,” Dr. Barak said. “We assume that this drop in GDNF following the retrieval of nicotine memories leads to loss of control, thus boosting drinking.”

The researchers used rat models to test the link between nicotine and alcohol consumption. To study the effects on alcohol consumption, the researchers installed an experimental self-serve alcohol dispenser, operated by a lever press. When placed in this “bar,” rats were free to consume unlimited amounts of alcohol.

Group 1 received nicotine during adolescence in Chamber B, and then drank alcohol in adulthood in Chamber A—in other words, drinking alcohol in an environment different to that in which they used nicotine. Conversely, Group 2 received nicotine during adolescence in Chamber A, and then in adulthood drank alcohol in the same chamber (that is, in the nicotine-associated environment), triggering a reminder of the nicotine experience.

“The rats eagerly drink alcohol,” said Yossi Sadot-Sogrin, who contributed to the research. “During the daily one-hour sessions, most of them consumed the amount of alcohol equivalent to a glass or two of wine.”

But when the self-serve alcohol dispenser was installed in the same chamber in which rats received nicotine during their adolescence, the amount of alcohol consumed rose sharply.

“In the nicotine-associated environment, rats drank the amount of alcohol that corresponded to four glasses of wine, and even more,” said Koral Goltseker, who collaborated on the study.

The team is currently researching the specific changes to the brain caused by nicotine memories. “If we can prevent these brain changes, we hope we can prevent the long-term increase in alcohol consumption,” said Dr. Barak. “It will also teach us a lot about the brain mechanisms that lead to alcoholism.”

Source: https://medicalxpress.com/news/2017-11-consumption-nicotine-adolescence-alcohol-intake.html November 2017

Filed under: Alcohol,Brain and Behaviour,Nicotine :

Teens who use e-cigarettes may be more likely to try marijuana in the future, especially if they start vaping at a younger age, a new study shows.

More than 1 in 4 teenagers who reported e-cigarette use eventually progressed to smoking pot, according to the survey of more than 10,000 teens.

That compared with just 8 percent of non-vapers, said lead researcher Hongying Dai, senior biostatistician with Children’s Mercy Hospital in Kansas City, Mo.

Further, teens who started vaping early had a greater risk of subsequent marijuana use.

Kids aged 12 to 14 who used e-cigarettes were 2.7 times more likely to try marijuana than their peers, compared with a 1.6 times greater risk for teens who tried vaping between 15 and 17.

“Our findings suggest that the widespread use of e-cigarettes among youth may have implications for uptake of other drugs of abuse beyond nicotine and tobacco products,” Dai said.

For the study, Dai and her colleagues twice surveyed 10,364 kids aged 12 to 17—once in 2013-2014, and again a year later.

The researchers found that teens who’d reported using e-cigarettes in the first wave were more likely to have tried marijuana for the first time during the subsequent year.

Results also showed that 12- to 14-year-olds who had tried e-cigs were 2.5 times more likely to become heavy marijuana users, smoking pot at least once a week.

Worse still, the researchers found that the more often young teens used e-cigarettes, the more likely they were to either try marijuana or become a heavy pot smoker.

Dai said the nicotine contained in e-cigarette vapor could be altering the brain chemistry of young teens.

“The brain is still developing during the teen years; nicotine exposure might lead to changes in the central nervous system that predisposes teens to dependence on other drugs of abuse,” Dai said.

It’s also possible that experimenting with e-cigarettes might increase a teen’s curiosity about marijuana, and reduce any worries about marijuana use, Dai added.

Additionally, kids who use e-cigarettes could be more likely to run with a crowd that tries other substances, said Dai and Dr. Scott Krakower, assistant unit chief of psychiatry at Zucker Hillside Hospital in Glen Oaks, N.Y.

“E-cigarettes are going to be in the same drug culture as other things,” Krakower said.

These findings should be concerning to parents because kids might not stop at trying marijuana, he said.

“If you go to marijuana, is that going to lead to pills? Is that going to lead to something else?” Krakower said. “When we see progression to another substance, it’s like the ‘and then what’ cascade—they went to marijuana, and then what?”

Since this is a survey, it can’t prove a cause-and-effect relationship. And it’s possible that wild, risk-taking teens who try e-cigarettes are predisposed to be adventurous with other drugs, Dai and Krakower said.

“It could be that they have more of that sensation-seeking personality, and if they pick up one they’re going to pick up the other,” Krakower said.

But Dai said her team took that into account, and even after adjusting for sensation seeking, “ever e-cigarette use was still significantly associated with subsequent marijuana use.”

Krakower recommends that parents look for warning signs of e-cigarette use—marked irritability, hiding things, skirting the truth—and put their foot down hard.

“There should be zero tolerance for this kind of behavior,” Krakower said.

Gregory Conley, president of the American Vaping Association, agreed.

“E-cigarettes are adult products and are not intended for youth of any age,” Conley said. “We agree with the authors’ conclusion that more education is needed to help young people understand the consequences of using age-restricted products and illicit drugs.”

The new study was published online April 23 in the journal Pediatrics.

Source: https://medicalxpress.com/news/2018-04-vaping-teens-pot.html April 2018

Filed under: Cannabis/Marijuana,Nicotine,Youth :

When I was a kid, smoking was very common among adults but not kids. If you look at many of the television programs and movies from before 1970, you will see just how popular smoking was. In the evenings during prime-time television, there seemed to be as many cigarette commercials as there were for any other product. Magazines were filled with cigarette ads and billboards along the roads helped to glamorized having a lit cigarette protruding from your lips. The rugged and handsome looking cowboy known at the Marlboro Man helped to attract men and women to the nicotine habit.

However, at the time, most junior and senior high schools forbid smoking on campus and anyone even caught with cigarettes was disciplined. Many high school kids did smoke and thought they were hiding it but little did they know just how much the smell of cigarettes stayed on their breath and on their clothes.

Then came all of the health warnings that smoking causes cancer. Anti-smoking groups sprang up all over America and pushed to ban most cigarette and tobacco advertising from television and magazines. Many states began to pass legislation to add an extra sales tax on all tobacco products. The push behind those taxes is that it helped raise money to fight cancer and the other health problems associated with smoking and chewing.

Yet, the sales of cigarettes and other tobacco products didn’t seem to be hurt that much if at all by the anti-tobacco push. Millions of American adults and teens still lit up and puffed away.

Then someone thought they were really smart and developed the e-cigarette. It’s a battery-operated devise that heats up a special liquid to point of creating a vapor, much like smoking. It didn’t take long for the concept to catch on and become a billion-dollar industry.

What attracted so many at first was that e-cigarettes didn’t contain the tar products found in burning real tobacco, so many believed it to be a safer alternative. Then it became stylish and millions of teens wanted to look like one of the gang, so they bought their e-cigarettes and began puffing away.

In fact, e-cigarettes became so popular with teens that the use of them by high school students rose by 900% from 2011 to 2015.

New research has found a two-fold danger, especially with teens smoking e-cigarettes.

First, that liquid that is heated up and inhaled as a vapor not only contains nicotine but some of the other toxic chemicals found in smoking real cigarettes. In other words, there is still a significant increased risk of developing cancer, emphysema and/or heart disease from smoking e-cigarettes.

Secondly, the use of e-cigarettes has been found to increase the chance of a teen and young adult turning to real cigarettes within 18 months of starting. They can still get addicted to the nicotine and that addiction often drives them to smoking the real thing. Instead of e-cigarettes helping people to stop smoking, studies have been found to indicate that they may actually increase the chance of smoking real tobacco products.

The bottom line is that e-cigarettes really aren’t that much better than smoking real cigarettes and in some cases are even worse because they give a false sense of safety.

Source: http://www.healthylifestylearena.com/2-fold-danger-of-teens-using-e-cigarettes/ May 2018

Filed under: Nicotine,Youth :

Interviewed by Mark Gold, MD

FEATURED ADDICTION EXPERT:
Daniel M. Blumenthal, MD, MBA
Attending Physician, Division of Cardiology, Massachusetts General Hospital
Instructor of Medicine at Harvard Medical School
Associate Chief Medical Officer at Devoted Health

Do FDA-approved psychostimulants increase the risk of cardiovascular events?

There is no convincing evidence that FDA-approved psychostimulants (e.g. methylphenidate, dextroamphetamine, amphetamine salts, and atomoxatine) increase the risk for cardiovascular events among patients without pre-existing cardiovascular disease (CVD). However, among those with pre-existing heart disease, including arrhythmias, coronary artery disease, heart failure, or in patients for whom an increase in heart rate or blood pressure could be harmful, psychostimulants may increase the risk for cardiovascular events.

How does cocaine end up as the number two cause of drug deaths, just behind opioids? Excluding adulteration with opioids, how does cocaine kill you?
The effects of cocaine on the cardiovascular system can be grouped into acute and chronic processes. Cocaine use can cause one or more of several acute, life-threatening cardiovascular effects. The most common is myocardial ischemia or infarction (e.g. a heart attack). Cocaine can induce a heart attack through one of several mechanisms. First, cocaine causes arterial (including coronary artery) vasoconstriction, which can lead to coronary vasospasm. Second, cocaine activates platelets, which increases the risk of thrombosis (including coronary thrombosis). Third, cocaine use produces an adrenergic surge which induces tachycardia (high heart rate) and hypertension. High heart rate and hypertension both increase myocardial oxygen demand, which can cause supply-demand mismatch and precipitate myocardial ischemia or infarction. Fourth, vasospasm or stress associated with cocaine use can also precipitate coronary artery plaque rupture (the mechanism underlying most classic heart attacks).

Two thirds of heart attacks due to cocaine occur within three hours of cocaine use; the risk of a heart attack is 24-fold higher than normal in the first sixty minutes after using cocaine. Cocaine has several other potentially devastating acute effects, including stroke, aortic dissection (e.g. dissection of the major artery connecting the heart to the rest of the body), life threatening heart arrhythmias, and myocarditis which can also occur with chronic use. Chronic cocaine can result in accelerated atherogenesis (i.e. accelerated plaque buildup in the coronary arteries), hypertrophy of the left ventricle, dilated cardiomyopathy, aortic aneurysms, and coronary aneurysms.

Patients who are acutely intoxicated with cocaine and present with chest discomfort should be referred to an emergency room immediately for evaluation. They should undergo a chest-x-ray, an electrocardiogram, blood work to evaluate for evidence of a heart attack and non-myocardial muscle breakdown (e.g. rhabdomyolysis), and to assess kidney function, white and red blood cell counts, and liver function.

Cocaine intoxication is diagnosed if and when patients report recent cocaine use and through serum and urine toxicology screens (which should be performed immediately as well). If a clinician suspects that a patient is acutely intoxicated with cocaine, treatment should not be withheld while waiting for the results of the toxicology screen. Patients with acute cocaine intoxication and symptoms concerning for cerebrovascular or other cardiovascular sequelae of cocaine intoxication may also need additional imaging to assess for evidence of damage to the heart, aorta, or other blood vessels.

In terms of treatment, these patients should receive benzodiazepines to help mitigate the adrenergic surge. If chest pain due to myocardial ischemia is suspected, sublingual nitroglycerin should be administered. Ongoing ischemic symptoms, as well as hypertension and tachycardia (drivers of myocardial oxygen demand) should be treated with calcium channel blockers (i.e. diltiazem or verapamil). Beta blockers should ideally be avoided until there is no cocaine remaining in the patient’s system. If beta blockers must be used, we recommend using either labetalol or carvedilol, which are non-selective inhibitors of both alpha and beta receptors (note: other beta blockers that are selective for beta receptors are contraindicated due to a theoretical risk that selective beta blockade could lead to unopposed alpha-mediated arterial vasoconstriction, which could precipitate marked hypertension and even peripheral and splanchnic ischemia).

Alternative, and highly effective, agents for treatment of hypertension include IV nitroglycerin (which should also be used if the patient has chest pain) and IV nitroprusside. Phentolamine, an alpha blocker, can be used for refractory hypertension. Patients presenting with chest pain should also receive a full dose chewable aspirin (325 mg) and 80 mg of atorvastatin (if available). Patients with ECG changes consistent with myocardial ischemia or infarction and/or elevated blood levels of cardiac biomarkers should be managed identically to patients with non-cocaine induced myocardial ischemia and infarction.

Cocaine and methamphetamine addicts often have heart disease. Why? How is a diagnosis made?
Cardiac sequelae are the second most common cause of death (behind overdose) in patients who use methamphetamines (“meth”). Like cocaine use, use of methamphetamines can produce both acute and chronic cardiovascular disease. Acute intoxication with methamphetamines produces a hyperadrenergic state, not unlike having a pheochromocytoma. The hypertension and tachycardia that result can lead to myocardial ischemia and infarction, aortic dissection, malignant arrhythmias, Takotsubo’s (stressinduced) cardiomyopathy, and cardiac arrest.

Chronic methamphetamine use can lead to hypertrophic cardiomyopathy (due to persistent severe hypertension) or dilated cardiomyopathy (due to the drug’s toxic effects on myocardium), and the clinical syndrome of heart failure. In addition, chronic meth use can also cause pulmonary arterial hypertension (PAH). Meth-associated PAH is a devastating disease, with five year mortality rates above 50%.

Diagnosing and managing acute methamphetamine intoxication:

Patients who present with suspected acute methamphetamine intoxication should undergo a full physical exam, electrocardiogram, and basic lab work (including basic metabolic panel, blood counts, clotting times (prothrombin time and international normalized ratio), liver function tests, creatine phosphokinase (CPK), urinalysis, and urine and serum toxicology screens). Amphetamine intoxication or toxicity is ultimately diagnosed by confirming the presence of amphetamines in urine or serum. However, if patients present with signs and symptoms which raise concern for amphetamine intoxication—including hyperthermia, agitation, hypertension, and tachycardia—treatment should not be delayed while waiting for these test results to return.

If there is concern for myocardial ischemia or infarction (for example, if the patient complains of chest discomfort or shortness of breath or the ECG shows ischemic changes), then cardiac biomarkers should be checked as well (i.e. troponin I or T). Acute methamphetamine intoxication with secondary sequelae (i.e. agitation, hypertension, tachycardia) should be managed initially with sedatives (benzodiazepines and 2nd generation atypical antipsychotics).

Hyperthermia should be managed aggressively by controlling core body temperature with sedatives and, if necessary, with paralysis and intubation (but antipyretics should not be used).

Rhabdomyolysis is common, and a CPK level should always be checked in patients who are acutely intoxicated with meth. If the hypertension is refractory to treatment with an adequate trial of sedation, then nitrates and/or phentolamine should be used. Calcium channel blockers can also be used, and are effective agents for managing tachycardia that persists despite sedation. Beta-blockers should be avoided in the acute setting to avoid precipitating unopposed alpha-mediated vasoconstriction (via identical mechanisms to those described above).

If beta blockers are necessary for chronic management of a different disease process (e.g. cardiomyopathy or coronary artery disease), then labetalol or carvedilol are the preferred agents due to their partial alphaantagonism. Myocardial infarction in the setting of methamphetamine intoxication should be managed per evidence-based guidelines for the management of heart attacks, and as described above (for cocaine). The one exception is that, if heart rate control is needed, calcium channel blockers, not beta blockers, should be used. Interestingly, monoclonal antibodies against methamphetamine have been developed and are currently in clinical trials.

Chest pain in the setting of acute methamphetamine intoxication should raise concern not only for myocardial infarction, but also for acute aortic dissection. Methamphetamine abuse is the second most common cause of acute fatal aortic dissection in the US, after hypertension. Unlike chest discomfort due to myocardial ischemia, which often starts as mild or moderate discomfort and worsens progressively over minutes-hours, chest discomfort due to aortic dissection is typically extreme from the outset.

What does the patient PE and EKG look like if a patient has overdosed on opioids? What about when injected with Narcan and reversed? Does Methadone, when given as a MAT, have QT and other effects on the heart? What about Suboxone and the heart?
Opiate overdose can precipitate respiratory depression and coma. The pupils will be mioitic, or “pinpoint.” Patients commonly experience mild hypotension as well. The electrocardiogram classically shows sinus bradycardia with nonspecific changes. Approximately 20% of patients will have prolongation of the QT interval. Administration of an adequate dose of Narcan rapidly reverses the respiratory depression, miosis, and coma, and can also lead to improvements in blood pressure and an increase in heart rate.

However, Narcan is short acting and the reversal is temporary. Thus, patients must be monitored following Narcan administration to determine if they need subsequent doses, or even initiation of an IV naloxone drip. Methadone may also cause QT prolongation but is an uncommon cause of Torsades Des Pointes, the potentially fatal arrhythmia that can result from QT prolongation. Suboxone can also cause hypotension, including orthostatic hypotension, and should be used with caution in patients with established cardiovascular disease (e.g. coronary artery disease). However, I am unaware of any unique cardiovascular side effects associated with suboxone use.

Does smoking have effects on the heart?
Smoking is an extremely strong and independent risk factor for heart disease, stroke, and peripheral artery disease. Smoking increases the risk of these conditions in a dose dependent fashion, and no amount of smoking is safe. People who smoke less than five cigarettes per day are at increased risk for myocardial infarction relative to non-smokers. The incidence of myocardial infarction among men and women who have smoked at least twenty cigarettes per day for any period of time is three fold and six fold higher, respectively, than the incidence of myocardial infarction in never smokers.

More generally, smoking increases the risk of coronary artery disease, heart attack, arterial aneurysms, aortic dissection, blood clots, carotid artery stenosis, upper and lower extremity ischemic claudication, and death. Smoking’s deleterious cardiac, cerebrovascular, and peripheral vascular effects are the result of a variety of mechanisms that contribute to atherogenesis. Smoking is associated with insulin resistance and oxidization of low-density lipoprotein (LDL-c, or bad cholesterol). Oxidization of LDL-c makes it more proatherogenic. Smoking also activates the sympathetic nervous system which increases heart rate and blood pressure and leads to peripheral vasoconstriction.

Moreover, smoking increases inflammation, which activates platelets and creates a prothrombotic milieu. Furthermore, smoking damages blood vessel walls, rendering them less elastic and promoting premature arterial stiffening; in addition, smoking promotes endothelial dysfunction, which impairs the ability of coronary arteries to vasodilate. The risks of cardiovascular, cerebrovascular, and peripheral artery disease and associated events decrease significantly and relatively rapidly with smoking cessation.

What about cannabis addicts or chronic smokers and the cardiologist?
While we know relatively less about the effects of marijuana on the cardiovascular system, there is significant and growing interest in understanding how marijuana use impacts heart and blood vessel function. We do know that smoking marijuana leads to an acute, four- to five-fold increase in the risk of myocardial infarction in young men. This risk persists for approximately 60 minutes following inhalation. Daily cannabis use is associated with a 1.5%-3% annual increase in the risk of myocardial infarction. There is some evidence that the mechanism underlying this increased risk is a higher likelihood of experiencing coronary artery vasospasm (as opposed to accelerated atherogenesis).

The physiologic effects of marijuana may surprise some people. Marijuana intoxication typically leads to a slowing of the reflexes, and the appearance of a relaxed state. However, marijuana use actually stimulates the sympathetic nervous system, which leads to tachycardia, the release of systemic catecholamines, and increased myocardial oxygen demand. At the same time, marijuana use increases supine systolic and diastolic blood pressure, and increases the likelihood of experiencing orthostatic hypotension.

There is also some evidence that marijuana use activates platelets by modulating the endocannabinoid system. Longitudinal prospective studies of cannabis users have failed to reveal evidence that chronic cannabis use leads to significant alterations body mass index, blood pressure, total cholesterol, high density lipoprotein, triglycerides, or blood glucose levels. There is no consistent evidence that marijuana use increases cardiovascular mortality. We know relatively little about whether the mode of use (i.e. smoking vs. ingestion) modifies the effects of marijuana on the cardiovascular system.

Ketamine is being used off label for depression. What are the cardiovascular risks and concern when this is done?
This is an extremely interesting question. Ketamine is a sympathomimetic. Studies of the cardiovascular effects of Ketamine have found that the drug increases cardiac output by up to 50% in healthy subjects. However, among sicker patients, the drug’s effects appear to be more variable, with some patients experiencing augmented ventricular performance, and others demonstrating some impairment in left ventricular function due to Ketamine use (among coronary artery bypass graft patients, for example, induction of anesthesia with Ketamine has been shown to significantly reduce left ventricular stroke volume).

Ketamine does consistently produce tachycardia and this simple fact should lead us to be cautious about using it to treat depression in patients with obstructive coronary artery disease or congestive heart failure. The cardiovascular effects of Ketamine remain incompletely characterized, and the prospect of widespread use to treat chronic illnesses like depression heightens the need to more clearly elucidate how Ketamine effects the cardiovascular system.

Withdrawal from opioids is associated with hypertension and tachycardia. Is this a concern?
Yes—the hypertension and tachycardia which occur during opioid withdrawal can undoubtedly stress the cardiovascular system. Patients with a history of coronary artery disease (particularly those with a history of angina), patients with congestive heart failure, and those with aortic aneurysms should be monitored closely during the withdrawal period for new or worsening cardiovascular symptoms. In addition, patients’ home cardiovascular medication regimens, including beta blockers, antihypertensives, and anti-anginals (i.e. nitrates) should ideally be continued during the withdrawal period if possible in order to blunt the physiologic effects of opioid withdrawal.

Are any drug withdrawal syndromes a concern to a cardiologist?
In general, most withdrawal syndromes result in some degree of heightened sympathetic tone, which can produce hypertension and tachycardia. In patients with serious chronic cardiovascular illness, including coronary artery disease, congestive heart failure, valvular disease (i.e. aortic stenosis, mitral stenosis, or mitral regurgitation), or arrhythmias, including atrial fibrillation or paroxysmal supraventricular tachycardia, this sympathetic surge can precipitate symptoms or even acute decompensations. So, and this is a key point, it is the patient substrate which matters more than the specific withdrawal syndrome. Put another way, if the patient has significant cardiovascular comorbidities, any withdrawal syndrome may be dangerous.

In general, I worry most about alcohol withdrawal for a few reasons. First, alcoholics regularly live with multiple comorbidities, including cardiovascular comorbidities like atrial fibrillation and heart failure (which may be due to an alcoholic cardiomyopathy). I have seen alcohol withdrawal precipitate new or recurrent atrial fibrillation, and lead to acute heart failure decompensations in patients with underlying alcoholic cardiomyopathies.

Second, alcohol withdrawal is by far the most mortal withdrawal syndrome; seizures due to withdrawal, or delirium tremens, carry a significant risk of mortality in patients without underlying cardiovascular illness, and may be even more dangerous in patients who are suffering from concomitant cardiovascular disease. Third, many alcoholics are poorly nourished, and have significant electrolyte disturbances, including hypokalemia (which is a risk factor for ventricular arrhythmias).

The wasting of magnesium that occurs in alcoholics is particularly concerning, because potassium repletion is ineffective in the absence of adequate serum magnesium levels. Thus, when checking basic electrolytes in an alcoholic (e.g. sodium, potassium, bicarbonate, chloride, etc.), be sure to also check magnesium levels. And, if an alcoholic is hypokalemic and you don’t have a serum magnesium level, replete the magnesium before giving potassium (or alongside the potassium). A little extra magnesium won’t have any adverse consequences, but failing to replete magnesium could result in failure to correct the low potassium level, which could have serious consequences.

Which patients should an addiction rehab send to a cardiologist for evaluation?
This is a difficult question to answer with high specificity. First, any patient with new or concerning cardiovascular symptoms or confirmed cardiovascular disease, including 1) exertional chest discomfort; 2) documentation of a new or recurrent arrhythmia; 3) new exertional shortness of breath; and/or 4) new signs or symptoms of congestive heart failure, including exertional shortness of breath, new or progressive lower extremity edema, and/or paroxysmal nocturnal dyspnea or orthopnea, should be evaluated by a cardiologist. In addition, anyone with a syncopal event without a prodrome (i.e. sudden, unexplained, and unheralded syncope) or with a history of complex congenital heart disease should be referred to see a cardiologist.

Patients with chronic, stable cardiovascular comorbidities, including coronary artery disease (with or without angina), congestive heart failure, peripheral artery disease (with or without claudication), valvular disease (i.e. aortic stenosis or mitral regurgitation), and/or cerebrovascular disease do not necessarily need to be seen by a cardiologist while they are in Rehab, and provided they remain stable and are able to continue their long term outpatient treatment regimens for these conditions. However, a rehab should generally have a low threshold to engage a cardiologist in the management of any patient with complex, chronic cardiovascular disease.

What are the CVD effects of alcohol use, abuse, and addiction? Alcohol users have a variety of CV effects including noticing that their heart skips a beat or so…is this related to alcohol abusers or alcoholics heart blocks?
Modest alcohol consumption—two or fewer drinks per night for a man, and one drink per night for a woman— has been shown to be healthy, and may even reduce all-cause mortality and mortality due to cardiovascular disease. However, when consumed in greater quantities, alcohol is a cardiotoxin. People who abuse or are dependent on alcohol have a heightened risk of arrhythmias—including atrial fibrillation, atrial flutter, and ventricular arrhythmias (due to electrolyte abnormalities or an alcoholic cardiomyopathy)—and alcoholic cardiomyopathy.

Alcoholic cardiomyopathies can be profound; I have taken care of daily drinkers who present with severe, bi-ventricular dysfunction and left ventricular ejection fractions (LVEF) of 10%-15% (normal is 52- 70%). Importantly, alcoholic cardiomyopathy is usually not this fulminant. Many daily drinkers may suffer from very mild, and even subclinical, forms of this cardiomyopathy, and their LVEF may be normal.

However, in these patients the cardiotoxic effects of alcohol may still predispose to premature atrial and ventricular beats—which they may experience, and describe, as “skipped beats.” As noted above, alcoholic cardiomyopathy increases the risk of both atrial and ventricular arrhythmias, and prior work shows that the risk of ventricular tachycardia in alcoholic cardiomyopathy is comparable to that seen in patients with idiopathic dilated cardiomyopathies. The electrolyte abnormalities commonly found in alcoholics—most notably hypomagnesemia and hypokalemia— further compound the risk for these arrhythmias.

Fortunately, alcoholic cardiomyopathy is usually a reversible process; I have multiple patients whose LVEF has improved from this 10%-15% range (while drinking daily) to 50% or more (essentially normal) after one-two years of abstinence from alcohol and adherence with traditional heart failure therapies. Alcoholic cardiomyopathy may at times reach a point of irreversibility, of course, but, broadly speaking, it has a very favorable prognosis if long term abstinence can be achieved.

Alcoholic abuse/dependence is also associated with a modestly increased risk for myocardial infarction, particularly in patients with pre-existing cardiovascular disease.

Source:

https://www.rivermendhealth.com/resources/qa-daniel-blumenthal-abuse-cardiovascular-disease May 2018

Filed under: Alcohol,Cannabis/Marijuana,Cocaine,Health,Heroin/Methadone,Ketamine,Nicotine :

Interviewed by Mark Gold, MD

FEATURED ADDICTION EXPERT:
Frederick S. Southwick, MD
Professor of Internal Medicine and Former Chief of Infectious Diseases at the University of Florida
2010 Harvard University Advanced Leadership Fellow
Expert in Medicine, Infectious Disease and Medical Errors

We see patients who smoke cigarettes, drink and/or abuse drugs. How does this affect their immune status or ability to fight common infections? Any association between a drug dependency like cigarettes and/or marijuana, smoking and/or alcohol drinking?

Smoking is a major risk factor for developing pneumonia. Those who smoke 20 or more cigarettes a day have three times the risk of developing pneumonia. Cigarette smoke damages the tracheal lining of the lungs, alters the consistency of the fluid that coats this lining, and destroys the cilia that move bacteria and other foreign substances out of the lung. When the fluid coating the tubes of the lung becomes thicker as a consequence of the inflammatory reaction to smoke, cilia can no longer transport this fluid, and the foreign particles, including bacteria, usually trapped by this fluid can no longer be transported out of the lungs. Damage to the cilia also interferes with this important protective mechanism.

Alcohol and other sedating drugs interfere with the function of the epiglottis. This large flap of tissue covers the trachea to prevent saliva, food and liquids from entering the lungs. We have all accidently choked on water when our epiglottis malfunctions and water enters the lung. We quickly cough it out. When drugs lead to sedation our epiglottis is more likely to malfunction and food, saliva and bacteria from the mouth can more easily enter the lungs. Sedation also interferes with our cough reflex, and as a consequence, severe aspiration pneumonia can follow an overdose or an episode of heavy drinking.

Drug abuse often leads to malnutrition and some drugs, particularly alcohol, can depress the body’s ability to produce white blood cells. Malnutrition and the loss of these cells can depress the normal acute immune response to infection, and as a consequence, infections are often more severe and life threatening in alcoholics and patients who suffer drug abuse.

Do substance abusers or addicts have more mono, flu, pneumonia, TB or other Infectious Diseases (ID)?

The incidence of mononucleosis is not known to be higher. Influenza is more severe in addicts with depressed immune responses. Tuberculosis may have a higher incidence in addicts because their depressed immune function allows the organism to more readily spread in the lungs and throughout the body.

What are some IDs associated with intravenous drug users?

Another major risk for infection is the use of intravenous drugs. Too often the drugs being injected into the blood stream are contaminated with bacteria, particularly Staphylococcus aureus (found on the skin) and Pseudomonas (found in tap water). These bacteria can infect the heart valves leading to endocarditis, a very serious and potentially fatal infection. Once bacteria enter the blood stream they can also lodge in small vessels of the bones, particularly the vertebral bodies or back bones resulting in bone infection or osteomyelitis. This infection is associated with chronic pain, fever and loss of energy. Osteomyelitis is very difficult to treat and requires six weeks of high dose intravenous antibiotics. Despite prolonged therapy, this infection often relapses resulting in years of pain and suffering.

In addition to bacteria contaminating intravenous drug preparations, shared needles can transmit viruses – Hepatitis B, Hepatitis C, and HIV virus. Hepatitis B and Hepatitis C both can lead to severe liver inflammation that causes scaring of the liver called cirrhosis. Eventually the liver fails resulting in ascites (filling of the abdominal cavity with fluid), dilatation and bleeding of the esophageal veins (esophageal varices) resulting in gastrointestinal bleeding, and difficulty detoxifying substances in the blood resulting in the loss of alertness and eventually coma (called Hepatic encephalopathy).

HIV is another dreaded and all too common complication of IV drug use.

What would you evaluate all IV addicts for?

All IV addicts should be screened for Hepatitis B, Hepatitis C and HIV. They should also be screened for STDs.

What vaccinations would you suggest for patients with substance use disorders?

They should receive the influenza vaccine annually and the two pneumococcal vaccines. Also, if they are Hepatitis B antibody negative, they should receive the Hepatitis B vaccine.

Can you explain Hepatitis C. What is it? Who gets it? Why do so many addicts and abusers have it? What can you do to prevent it? Diagnose it? Treat it?

Hepatitis C is a virus that specifically infects the liver. This virus is transmitted by blood and blood products. Before the virus was recognized in the early 1990s, it contaminated our blood supply. Risk factors associated with an increased risk of Hepatitis C include:

persons receiving blood transfusions or transplanted organs before July of 1992
those who received clotting factors before 1987
anyone born to a mother with Hepatitis C virus
anyone who shared needles to inject drugs, or who had tattoos or body piercing with unsterile equipment

Addicts who use intravenous drugs and share needles are at very high risk, because the virus is transmitted by needles contaminated with virally infected blood. Individuals infected with Hep C have very high numbers of viral particles in their blood, and when they share a needle with an uninfected person, that person is at high risk of inadvertently injecting those viral particles intotheir own blood stream and infecting their liver. The best way to prevent the spread of Hep C is to avoid IV drug use.

Another alternative is to use a clean needle, and never share needles. In some areas of the country, needle exchange programs have been instituted to prevent the spread of Hep C, Hep B, and HIV. The diagnosis can be readily made with a blood test that measures antibodies directed against the virus. This is a very sensitive and specific test and anyone who falls into the above risk groups should undergo testing because we now have excellent antiviral therapy for this infection. Direct acting antiviral therapy offers high cure rates of over 95% in most cases. Treatment usually takes 8-12 weeks of a single pill once per day. In more complicated cases, treatment may be continued for 24 weeks. The cost of treatment is very high ($1,000/ pill) usually costing between $80,000-100,000 to achieve a cure.

Is there a new epidemic of STDs. Which? Who gets which? Why do so many addicts and abusers have it? What can you do to prevent it? Diagnose it? Treat it?

Drug abuse is associated with increased sexual activity and the more sexual partners one has the greater the risk of STDs. The incidence of syphilis in the U.S. has increased among women by 36% from 2015 to 2016 and 15% in men during this same period. Also, the incidence of newborn syphilis has increased by 28% as a consequence of transmission from mother to child.

The group with the highest incidence of this infection is men having sex with men (MSM), and about ½ of MSM who have syphilis also have HIV. The incidence of gonorrhea has also increased during this time period by 22%. This is a particularly worrisome development because strains of gonorrhea are increasingly becoming drug resistant meaning that we are at risk of running out of antibiotic treatments for this infection in the future. Condoms prevent the spread of these diseases; and should always be used given the high risk of STDs among drug abusers.

Public health workers try to identify contacts when a STD case is reported so that these contacts can be tested and treated to prevent the further spread of infection. All patients who have more than one sexual partner or who use illicit drugs should be screened for syphilis, gonorrhea, chlamydia, Hepatitis B and HIV, particularly sexually active women under 25, pregnant women, and men having sex with men.

Syphilis, Hepatitis B and HIV are detected primarily through blood tests. Gonorrhea and chlamydia are tested using vaginal and urethral (opening of the penis) swabs. These tests are all very sensitive and specific. Syphilis, gonorrhea and chlamydia are treated with antibiotics and can be cured. Hepatitis B, like Hepatitis C, can now be cured using antiviral agents, but at great expense. HIV requires lifelong treatment.

Can you explain HIV? AIDS? What is it? Who gets it? Why do so many addicts and abusers have it? What can you do to prevent it? Diagnose it? Treat it?

HIV stands for Human Immunodeficiency Virus and is caused by a retrovirus that is transmitted primarily through blood and through sexual contact as an STD. HIV is a lifelong infection that over time destroys immune cells and results in opportunistic infections (infections by organisms that rarely infect people with normal immune systems) including cryptococcal (fungal) meningitis, pneumocystis pneumonia, and toxoplasmosis brain infections.

When the immune system deteriorates to the point of allowing these infections to develop, HIV infection is said to have progressed to AIDS or Acquired Immune Deficiency Syndrome. Anti-retroviral medications can lower the viral counts and reverse this immunodeficiency; however, these medications cannot completely eradicate the infection, and they must be taken for life. If anti-retroviral medications are discontinued, the infection reactivates.

Can you explain what is HPV? Is it just a woman’s problem? Who gets it? Why do so many addicts and abusers have it? What can you do to prevent it? Diagnose it? Treat it?

Human papilloma virus (HPV) is a wart causing virus that is transmitted by close skin to skin contact and is most commonly transmitted by vaginal or anal sex. A high percentage of people become infected but our immune system often clears the virus; however, when the virus remains active it can cause genital warts that have a cauliflower like appearance. This virus can cause mouth and throat, penis, anal, vaginal and cervical cancer. The diagnosis of HPV is usually made based on examination. Cervical pap smears are recommended periodically for women to look for atypical precancerous cells. Treatment consists of removing the precancerous cells through surgical procedures. When cancer develops, chemotherapy and surgical resection are required.

There is no medical treatment for HPV. However, a very effective vaccine is now available that can prevent HPV induced cancer. The vaccine is recommended for all children at age 11-12 years and can be given up to age 21 for women and up to age 26 for men. This vaccine is strongly recommended for men who intend to have sex with men, transgenders, and adolescents who are immunocompromised, including patients with HIV.

For many years, we treated cigarette-related cancers rather than identifying smokers and helping people stop smoking. Is that still happening today with alcohol and drugs? With no drug testing or limited in Pediatrics and Medicine, how can asking the patient if they use or inject drugs identify and help treat the primary disease or users?

The newspapers and television news are now publicizing the worsening drug epidemic in our country. This epidemic has spread to people in every socioeconomic class. Given the many health risks of drug addiction, physicians and nurses have an obligation to ask questions about this potentially life-threatening behavior. Drug addiction is a disease, and to identify and treat this disease, medical caregivers are obligated to inquire about this important health issue. And those who suffer from drug addiction need not be ashamed. They should be open to help. The infectious disease risks of continuing addiction are real and potentially life threatening. Therapy for addiction is available and can be effective. Why wait until the damage has been done?

Source:

https://www.rivermendhealth.com/resources/qa-frederick-southwick-infections-and-addiction/ May 2018

Filed under: Addiction,Alcohol,Health,HIV/Injecting-Drug-Users,Nicotine :

Submitted by Andy Travis

Much research on normative misconceptions among university students has been published in North America, but much less has surfaced in Europe. This cross-sectional study is based on 12 classes of second-year French college students in sociology, medicine, nursing or foreign language. Rather than focus on one substance the students were asked to estimate the proportion of tobacco, cannabis, alcohol use and heavy episodic drinking among their peers and to report their own use.

Researchers found that that substance use patterns and perceptions of the norms differ significantly across academic disciplines and that substance users are more likely to misjudge real peer use prevalence.

They conclude that social norms of substance use are an important factor among students personal use. Overestimating these norms is associated with increased levels of use. In addition to other strategies, the researchers recommend that prevention programs should consider changing use perception when it is overestimated.

“These results show that there are grounds for university level prevention campaigns based on local survey results.”

read more…

Source:

http://preventionhub.org/en/prevention-update/french-students-found-overestimate-their-peers-consumption-cannabis-tobacco-and-alcohol-pre

Filed under: Alcohol,Cannabis/Marijuana,Nicotine,Prevention and Intervention :

Submitted by Livia Edegger

Earlier this month Germany celebrated the results of the 2014 drug report which revealed a rapid decline in smoking, drinking and marijuana use among youth over the past ten years. Smoking among German teens aged 12 – 17 has halved in ten years (11.7%). Smoking rates have also dropped among 18 – 25 year olds, not as significantly though. Drinking rates have fallen from 17.9% in 2001 to 13.6% in 2012 among 12 – 17 year olds. In terms of gender differences, teenage boys are twice more likely to consume alcohol than their female counterparts. Little has changed among 18 – 25 year olds, the group that accounts for the highest alcohol consumption rate. Drinking in that age group was reported at 38.4% in 2012 which means it only dropped by a little over 1%. Cannabis ranks first among illicit drugs used with 5.6% of 12 – 17 year old teenagers using it compared to 9.2% in 2001. After years of steady consumption rates, cannabis use among 18 – 25 year olds is on the rise again and at 15.8% resembles figures of 2001.

Source:

http://preventionhub.org/en/prevention-update/germany-releases-drug-report

23rd July 2014

Filed under: Addiction,Alcohol,Cannabis/Marijuana,Nicotine,Youth :

Submitted by Livia Edegger

The findings of a report released by the Health and Social Care Information Centre (HSCIC) reveal a promising downward trend regarding drug use among secondary school students in England. Tobacco, alcohol and drug use among students have been cut in half in the past ten years. Smoking rates have dropped from 9% to 3% and alcohol rates have dropped from 25% to 9%. Illicit drug use has fallen by 50% between 2003 and 2013. The growing concern that e-cigarettes might fuel the uptake of smoking in teenagers was not supported by the report.

Links:

Smoking, Drinking and Drug Use Among Young People in England – 2013(link is external) – Health and Social Care Information Centre

Source:

http://preventionhub.org/en/prevention-update/drug-use-plunges-50-among-secondary-school-students-england

29th July 2014

Filed under: Alcohol,Nicotine,Youth :

Submitted by Livia Edegger

A new study found that children of smokers are not only more likely to take up smoking themselves, but are also at a higher risk of becoming addicted. The longer children are exposed to their parents’ smoking at home, the more likely they are to become nicotine-dependent themselves. Consistent with previous research, quitting smoking is not only crucial for the parents’ personal health, but also for their children’s well-being. Although the findings seem obvious, they do highlight the critical role parents play in preventing their children’s tobacco use.

Links:

Children of nicotine-addicted parents more likely to become heavy smokers(link is external)– Georgetown University Medical Center

Source:

http://preventionhub.org/prevention-update/parent-child-%E2%80%98vicious-cycle%E2%80%99-family-smoking

20th May 2014

Filed under: Drug use-various effects on foetus, babies, children and youth,Nicotine :

Submitted by Andy Travis

This study found that youth with more substance users in their networks reported greater alcohol, cigarette, and marijuana consumption regardless of whether these network members provided tangible or emotional support. The homeless setting was more significant in consumption than meeting network members in other contexts. Numbers of adults and school attendees in networks reduced consumption.

Links:
• One in three parents do not talk to their children about the risks associated with drinking alcohol(link is external) Full statement ,with further links.
• Alcohol. It’s no joke. | Why Let Drink Decide(link is external) The video campaign.

Source:

http://preventionhub.org/en/prevention-update/survey-uk-parents-suggests-parents-more-concerned-about-risks-drugs-alcohol-government-anno

11th January 2011

Filed under: Alcohol,Cannabis/Marijuana,Nicotine,Youth :

Submitted by Livia Edegger

As a country with a history of heavy smoking and drug use among youth, Ireland embraces the results of a new study indicating a substantial drop in teen smoking. Youth smoking rates fell from 21.1% in 1998 to 11.9% in 2010. Similarly, the percentage of teenagers that take their first puff at age 13 or younger has decreased significantly. While in 2002 more than 60% of Irish teenagers had their first cigarette at age 13 or younger, by 2010 that number had fallen to just under 50%. These positive developments were presented at the Irish Cancer Society’s X-Hale Film Festival in Dublin, which featured 43 short clips produced by youth groups that drew attention to the harms of smoking.

Links:

School-age smoking rate plunges 50% in 12 years(link is external)– Irish Examiner

Source:

http://preventionhub.org/en/prevention-update/teenage-smoking-cut-half-ireland

23rd July 2014

Filed under: Nicotine,Youth :

Click on the images to enlarge the detail.

Source:

https://www.intervenenow.com/breaking-the-stigma-of-recovery/

Filed under: Alcohol,Cannabis/Marijuana,Nicotine,Prescription Drugs,Treatment and Addiction :

It’s a question often raised in today’s heated discussion about the efficacy of drug policy in America: Do regulations outlawing certain drugs actually work?

Let’s go to the data. Here’s what the Nation’s largest, longest-running, and most comprehensive source on the state of drug use in America shows:

As you can see, the use of legal drugs like alcohol and tobacco far outpaces the use of illegal drugs. It is clear, then, that laws discouraging drug use do have an effect in keeping rates relatively low compared to rates for other drugs that are legal and therefore more available. Even beyond this one-year snapshot, we know that significant progress has been made in the long term. Since 1979, there has been a roughly 30 percent decline in the overall use of illicit drugs in America.

So our challenge is not that we’re powerless against the problem of substance use in America. The challenge is that rates of drug use – a behavior that harms too many of our fellow citizens — are still too high. That’s why the President’s National Drug Control Strategy supports innovative and proven programs that aim to reduce drug use and its consequences through a combination of public health and public safety interventions.

It boils down to simple arithmetic: The more Americans use drugs, the higher the health, safety, productivity, and criminal justice costs we all have to bear. And if sensible drug laws (in combination with a wide array of prevention, treatment, and other health interventions, of course) help keep those numbers down, then the answer is yes, they are working.

Source: www.whitehouse.gov 2013 ONDCP

Filed under: Alcohol,Global Drug Legalisation Efforts,Nicotine,USA :

Human cells mutated faster than expected after exposure to e-cigarettes

· Previous studies have found e-cigarette smoke causes less cancerous damage than tobacco

· New York University exposed human cells and mice to e-cigarette smoke compared to filtered air

· They found the cells mutated much faster than expected

· The team warns this shows vaping is not as risk-free as we may think By MIA DE GRAAF HEALTH EDITOR FOR DAILYMAIL.COM

PUBLISHED: 16:16, 29 January 2018 | UPDATED: 10:21, 30 January 2018 Vaping causes DNA mutations which lead to cancer, a new study warns.

Researchers subjected cultured human bladder and lung cells to e-cigarette vapor which is designed to avoid the carcinogenic by products of tobacco.

They found the cells mutated and became cancerous at a much higher rate than expected, and mice exposed to the smoke also suffered significant DNA damage.

The New York University team warns their findings, published today, bring into question the popular belief that vaping nicotine is a safe alternative to smoking it in cigarettes.

It comes just days after the Food and Drug Administration rejected Philip Morris’s ‘healthy’ iQOS electronic vaping product, saying it is not healthier than tobacco.

New York University exposed human cells and mice to e-cigarette smoke compared to filtered air, and they found vaping did increase the rate of cancerous DNA mutations

E-cigarette smoke (ECS) delivers nicotine through aerosols without burning tobacco.

While tobacco smoke contains nitrosamines and many carcinogenic chemicals from burning, ECS contains nicotine and some relatively harmless organic solvents.

As a result, ‘vaping’, as it is colloquially called, has been promoted as not carcinogenic; a safer substitute for tobacco.

A recent study even found that e-cigarette smokers had 97 percent less lung carcinogens in their body fluids compared to tobacco smokers.

However, experts warn that does not mean it is safe and void of cancer risk.

The new study by Moon-shong Tang, of the environmental medicine department, was an investigation into the belief that other products in tobacco – not nicotine – are the ones that cause cancer and other health woes.

They subjected mice and human cells to the vapor.

They concluded that although vaping delivers fewer carcinogens than tobacco smoke, e-cigarette smokers might have a higher risk than non-smokers of developing lung and bladder cancers and heart diseases.

Last week the FDA voted unanimously against Philip Morris International’s claims that its e-cigarette could predict lower rates of diseases and death in humans.

The penlike device heats Marlboro-branded sticks of tobacco but stops short of burning them.

It is already sold in more than 30 countries and Philip Morris aims to make it the first ‘reduced risk’ tobacco product ever sanctioned by the US.

FDA clearance would mark a major milestone in efforts by both the industry and government officials to provide alternative tobacco products to US smokers.

The adult smoking rate has fallen to an all-time low of 15 percent, though smoking remains the nation’s leading preventable cause of illness and death.

Source: http://www.dailymail.co.uk/health/article-5325945/Vaping-causes-cancer-new-study-warns.html 29th Jan 2018

Filed under: Health,Nicotine :

Prenatal exposure to smoke and alcohol may increase the risk of children developing conduct problems in adolescence, researchers said.

Conduct disorder (CD) is a mental disorder where children demonstrate aggressive behaviour that causes or threatens harm to other people or animals such as bullying or intimidating others, often initiating physical fights, or being physically cruel to animals.

The findings, led by researchers from the King’s College London, showed that exposure to smoke and alcohol, especially during foetal development, may lead to some epigenetic changes — chemical modifications of DNA that turns our genes on or off — particularly in genes related to addiction and aggression, leading to conduct problems in children.

One of the genes which showed the most significant epigenetic changes is MGLL — known to play a role in reward, addiction and pain perception. Previous research have revealed that conduct problems are often accompanied by substance abuse and there is also evidence indicating that some people who engage in antisocial lifestyles show higher pain tolerance. The researchers also found smaller differences in a number of genes previously associated with aggression and antisocial behaviour.

“There is good evidence that exposure to maternal smoking and alcohol is associated with developmental problems in children, yet we don’t know how increased risk for conduct problems occurs”.

These results suggest that epigenetic changes taking place in the womb are a good place to start,” said Edward Barker from King’s College London. The results highlight the neonatal period as a potentially important window of biological vulnerability, as well as pinpointing novel genes for future investigation.

For the study, published in the journal Development and Psychopathology, the team measured the influence of environmental factors previously linked to an early onset of conduct problems, including maternal diet, smoking, alcohol use and exposure to stressful life events. They found epigenetic changes in seven sites across the DNA of those who went on to develop early-onset of conduct problems. Some of these epigenetic differences were associated with prenatal exposures, such as smoking and alcohol use during pregnancy.

Source: http://www.thehealthsite.com/news/prenatal-exposure-to-smoke-alcohol-may-increase-behaviour-problems-in-kids-ag0617/ Published: June 13, 2017

Filed under: Alcohol,Brain and Behaviour,Drug use-various effects on foetus, babies, children and youth,Nicotine :

(Comment by NDPA: Some shocking figures from the USA in this article)

In 1964 the Surgeon General’s report on smoking and health began a movement to shine the bright light on cigarette smoking and dramatically change individual and societal views. Today, most states ban smoking in public spaces.

Most of us avoid private smoky places and sadly watch as the die-hard huddle 15 feet from the entrance on rainy, snowy or frigid coffee breaks. Employers often charge higher health insurance premiums to employees who smoke, and taxes on cigarettes are nearly triple a gallon of gas. Yet, some heralded progressive states have passed referendums to legalize the recreational use of a different smoked drug.

Now, more than 50 years later, another very profound statement has been made in the introduction to the recent report, “Substance misuse is one of the critical public health problems of our time.”

“Facing Addiction in America: The Surgeon General’s Report on Alcohol, Drugs, and Health,” was released in November 2016 and is considered to hold the same landmark status as that report from 1964. And maybe, just maybe, it will have the same impact.

Many key findings are included that are critical to garnering support in the health care and substance abuse treatment fields. But the facts are just as important for the general public to know:

— In 2015, substance use disorders affected 20.8 million Americans — almost 8 percent of the adolescent and adult population. That number is similar to the number of people who suffer from diabetes, and more than 1.5 times the annual prevalence of all cancers combined (14 million).

— 12.5 million Americans reported misusing prescription pain relievers in the past year.

— 78 people die every day in the United States from an opioid overdose, nearly quadruple the number in 1999.

— We have treatments we know are effective, yet only 1 in 5 people who currently need treatment for opioid use disorders is actually receiving it.

— It is estimated that the yearly economic impact of misuse and substance use disorders is $249 billion for alcohol misuse and alcohol use disorders and $193 billion for illicit drug use and drug use disorders ($442 billion total).

— Many more people now die from alcohol and drug overdoses each year than are killed in automobile accidents.

— The opioid crisis is fuelling this trend with nearly 30,000 people dying due to an overdose on heroin or prescription opioids in 2014. An additional roughly 20,000 people died as a result of an unintentional overdose of alcohol, cocaine or non-opioid prescription drugs.

Our community has witnessed many of these issues first hand, specifically the impact of the heroin epidemic. The recent Winnebago County Coroner’s report indicated that of 96

overdose deaths in 2016, 42 were a result of heroin, and 23 from a combination of heroin and cocaine.

We know that addiction is a complex brain disease, and that treatment is effective. It can manage symptoms of substance use disorders and prevent relapse. More than 25 million individuals are in recovery and living healthy, productive lives. I, myself, know many. Most of us do.

Locally, the disease of addiction hits very close to many of us. I’ve had the privilege of being part of Rosecrance for over four decades, and I have seen the struggle for individuals and families — the triumphs and the tragedies. Seldom does a client come to us voluntarily and without others who are suffering with them. Through research and evidence-based practices at Rosecrance, I have witnessed the miracle of recovery on a daily basis. Treatment works!

If you believe you need help, or know someone who does, seek help. Now. Source: http://www.rrstar.com/opinion/20170304/my-view-addiction-is-public-health-issue-treatment-works. 4th March 2017

Filed under: Addiction,Health,Nicotine,Prevention and Intervention,Treatment and Addiction :

Illegal cigarettes and alcohol seized by police have been turned into electricity at a special recycling plant Almost 150,000 cigarettes and tonnes of illegal alcohol seized during raids in Lincolnshire have been turned into electricity.

The substances were taken to a specialist recycling centre where the cigarettes were broken down and the energy fed into the National Grid.

The counterfeit liquid is mixed with foodstuffs and enzymes to create gas. This gas is then burned to produce electricity, which is then also fed into the National Grid

Emma Milligan, principal trading standards officer at Lincolnshire County Council, said: “Tackling the sale of counterfeit and illegal cigarettes and alcohol is a priority. Some cigarettes are not self-extinguishing and therefore extremely dangerous.

“Illegal brands, such as Pect and Jin Lings, don’t comply with the UK safety standard of Reduced Ignition Propensity, meaning they don’t go out when not actively being smoked.”

She explained that many bottles of alcohol were seized for non-payment of duty, while others were seized as they were counterfeit or fake and potentially very dangerous. They can contain industrial alcohol which is unfit for human consumption.

Emma said: “The cigarettes and alcohol being destroyed today have been seized in several operations involving Lincolnshire Trading Standards and Lincolnshire Police. Tobacco detection dogs are often involved, supported by the Smoke Free Alliance.

“With such potential dangers to the public, it’s vital that these products are taken off the streets. I’m glad we can put the cigarettes and alcohol to use in a productive way.

“If you do suspect anyone of selling cheap, illegal cigarettes or alcohol, you can call Crimestoppers anonymously on 0800 555 111 to avoid tragic cases in the future.”

Source: at http://www.grimsbytelegraph.co.uk/illegal-alcohol-and-cigarettes-seized-by-police-turned-into-electricity/story-30016023-detail/story.html#B9POiDF9gKweB85K.99

Filed under: Nicotine,Social Affairs :

The Smoking Cessation Leadership Center recently had a fascinating, although alarming, web symposium that highlighted the link between cigarette smoking and mental illness. The most important message was that smokers with mental illness are becoming a sizeable percentage of those who continue to smoke in the United States.

Among the highlights from the discussion:

More than 1 in 3 adults (36%) with a mental illness smoke cigarettes, compared with about 1 in 5 adults (21%) with no mental illness.
About 3 of every 10 cigarettes (31%) smoked by adults are smoked by adults with mental illness.
Smoking-related diseases such as cardiovascular disease, lung disease, and cancer are among the most common causes of death among adults with mental health conditions.

What’s more, the prevalence of smoking among those with a serious mental illness is not decreasing. According to the National Health Interview Survey (NHIS), an annual study conducted by the Centers for Disease Control and Prevention (CDC), in 2011 42% of adults with a serious psychological distress status smoked cigarettes, about the same percentage as in 1998. No wonder smoking is the number one cause of death in people with mental illness or addiction.

The panel of experts, which included Dr. Corinne Graffunder, Director of the Office on Smoking and Health at the Centers for Disease Control and Prevention, and Dr. Jill Williams, Director of the Division of Addiction Psychiatry in the Department of Psychiatry at the Rutgers Robert Wood Johnson Medical School, had a number of suggestions for local communities to consider. In the first place, they stressed the importance of challenging the perception that smoking helps with anxiety and depression, which of course it does not, and informing smokers about the mental health benefits associated with quitting.

Just increasing awareness of high smoking rates among those with mental health conditions, and providing factual information about smoking cessation, will help. Currently, only 1 in 4 mental health treatment facilities offers quit smoking services. That has to change. We know that smoking inhibits recovery from illnesses, from being financially stable, from finding and holding a job, and from securing housing. These issues are only exacerbated among the mentally ill.

The Smoking Cessation Leadership Center is encouraging healthcare and mental health professionals, including pharmacists, to include tobacco cessation treatment as part of their overall mental health treatment. Targeted efforts are needed to increase quit attempts and cessation rates. The Center offers outreach materials specifically aimed at this vulnerable population, including print ads, editorial content, digital banners, ad web content, and a downloadable poster; quit guide, and toolkit. Visit http://smokingcessationleadership.ucsf.edu for more information.

Source: http://www.nohealthdisparities.org/ newsletter 13th August 2016

Among the highlights from the discussion:

More than 1 in 3 adults (36%) with a mental illness smoke cigarettes, compared with about 1 in 5 adults (21%) with no mental illness.
About 3 of every 10 cigarettes (31%) smoked by adults are smoked by adults with mental illness.
Smoking-related diseases such as cardiovascular disease, lung disease, and cancer are among the most common causes of death among adults with mental health conditions.

Source: http://www.nohealthdisparities.org/ newsletter 13th August 2016

Filed under: Brain and Behaviour,Nicotine :

Photo:Gage Skidmore/Wikimedia Commons*

“Live long and prosper.” The Vulcan salute is immediately identifiable with the actor Leonard Nimoy and his most famous character, Mr. Spock. The beloved cultural icon was admired for his sterling character on Star Trek and off-screen as well. In recent years and up until his last few months, while suffering the debilitating effects of a respiratory illness, he took steps to ensure that others would indeed “live long and prosper” by speaking clearly about the role that smoking played in the illness that caused his death.

Nimoy started smoking, like many, when he was young. He managed to quit more than 30 years before his death, but not early enough to prevent the respiratory disease that took his life late February. Nimoy took great pains to show us that cigarettes are a deadly addiction – encouraging followers on Twitter to quit or never start. While he was just one of the 480,000 people in the U.S. who will die prematurely from tobacco-related diseases in 2015, he will surely be among the most well-known and widely missed by an admiring public. That makes the steps took to tell his story so vital.

Tobacco is one of the toughest addictions to overcome and by far the most deadly product available. About 14 million major medical conditions in the U.S. can be blamed on smoking. Yet, despite that inescapable fact, more than 42 million Americans still smoke.

And it isn’t just smoking. Smokeless tobacco products, like those used by sports legend,Tony Gwynn, and other professional baseball players, are linked to oral cancer and other illnesses. Like Nimoy, Gwynn was outspoken before his death last year in naming chewing tobacco as the cause of his cancer. His efforts to speak the truth give meaning to the efforts of a coalition working to eliminate tobacco consumption on and around American baseball fields. Knock Tobacco Out of the Park will succeed, in part, because icons like Gwynn and Nimoy shared their stories and demonstrated the painful cost of tobacco-related illness.

The glamour and appeal of smoking and the power of nicotine addiction are forces that we work to counter every day at Legacy. Even that first cigarette does damage to your body and can spur a life-long addiction and struggle. Nimoy could not imagine what would happen to him five decades after he smoked his first cigarette. By sharing his story, he may help other smokers comprehend the illness and death that lie in wait for them.

As fans remember Leonard Nimoy and Tony Gwynn for cherished memories and contributions to our shared culture, we celebrate them as ambassadors of truth and of knowledge in the fight to build a future where illness and death, caused by the use of tobacco, are things of the past.

Source: www.drugfree.org 18^th March 2015

Filed under: Addiction,Drug use-various effects,Health,Nicotine :

Attempts to tackle sales threat by framing criticism of smoking as fundamentalist fanaticism are outlined in cache of documents from 1970s until late 1990s

The tobacco industry attempted to reinterpret Islamic teaching and recruit Islamic scholars in a bid to undermine the prohibition on smoking in many Muslim countries, an investigation has shown.

Evidence from archived industry documents from the 1970s to the late 1990s shows that tobacco companies were seriously concerned about Islamic teaching. In 1996, an internal document from British American Tobacco warned that, because of the spread of “extremist views” from fundamentalists in countries such as Afghanistan, the industry would have to “prepare to fight a hurricane”.

‘We had tobacco industry lawyers actually developing theological arguments’ Prof Mark Petticrew

BAT and other companies, which were losing sales in affluent countries where anti-smoking measures had been introduced, devised strategies to counter this perceived threat to sales in places such as Egypt, Indonesia and Bangladesh, which have large populations of young people who smoke.

The industry was concerned that the World Health Organisation was encouraging the anti-smoking stance of Islamic leaders. A 1985 report from tobacco firm Philip Morris squarely blamed the WHO. “This ideological development has become a threat to our business because of the interference of the WHO … The WHO has not only joined forces with Moslem fundamentalists who view smoking as evil, but has gone yet further by encouraging religious leaders previously not active anti-smokers to take up the cause,” it said.

A No Smoking sign in Syria Photograph: Alamy

“A Moslem who attacks smoking generally speaking would be a threat to existing government as a ‘fundamentalist’ who wishes to return to sharia law,” says one of the archive documents. It adds: “Our invisible defence must be the individualism which Islam allows its believers … smoking and other signs of modern living should encourage governments to a point at which it is possible quietly to suggest their benefits.”

It adds: “With Islam we might ask what other aspects of modern living are similarly open to extremist demands for prohibition under strict interpretation of sharia: motion pictures, television, and art depicting the human being? Use of electronic amplification by muezzin calling from a minaret? The education of women?” the document says.

The earliest fatwa against tobacco was in 1602, but many scholars believed smoking cigarettes or taking tobacco in water pipes or other forms was harmless until evidence of the dangers to health began to emerge in the mid 20th century. Jurists pronounced that tobacco use was makrooh(discouraged). In many Islamic countries, a harder line was taken, with smoking prohibited on the grounds that the Qur’an does not permit self-harm or intoxication.

The WHO negotiated the Framework Convention on Tobacco Control, starting in 1999, in response to what it describes as the “explosive increase in tobacco use”. The convention, which outlines strategies intended to reduce demand, was adopted in 2003.

‘This is an issue to be handled extremely gingerly and sensitively’

BAT internal document

A report in 2000 from the Consumer and Regulatory Affairs (Cora) department at BAT after the first international negotiations said: “It appears that the WHO’s efforts to link religion (specifically Islam) with issues surrounding the use of tobacco are bearing fruit … We will need to discuss separately how we might understand and manage this aspect in line with the Cora strategy.”

The tobacco industry attempted to re-interpret anti-smoking Islamic teachings. A 1996 BAT memo suggests identifying “a scholar/scholars, preferably at the Al Azhar University in Cairo, who we could then brief and enlist as our authoritative advisers/allies and occasionally spokespersons on the issue.

“We agreed that such scholars/authority would need to be paired up with an influential Moslem writer/journalist … such advice would present the most effective and influential opinion able to counter extremist views, which are generally peddled by Islamic fundamentalist preachers largely misinterpreting the Koran … This is an issue to be handled extremely gingerly and sensitively … We have to avoid all possibilities of a backlash.”

Tobacco industry lawyers were also involved in this attempt at revision. A presentation from 2000, prepared by the firm Shook, Hardy and Bacon, gave an overview of the background to Islam and smoking, with slides stating that there is no prohibition on smoking in the Qur’an – and that “making rules beyond what Allah has allowed is a sin in itself”.

Prof Mark Petticrew from the London School of Hygiene and Tropical Medicine, who led the research, said he was amazed by what researchers had found in the archives. “‘You couldn’t make it up’ comes to mind,” he said. “The thing that jumps out at me from all this is the fact that we had tobacco industry lawyers actually developing theological arguments. That was pretty surprising.”

A document suggest Philip Morris wanted to try to recruit Islamic scholars at McGill University in Montreal, Canada. A representative of the Canadian Tobacco Manufacturers’ Council “agreed to make exploratory contact”, it says. Petticrew and his team do not know whether they were successful. “We couldn’t find the papers,” he said.

The tobacco industry is still heavily promoting smoking in countries such as Bangladesh and Egypt, which are predominantly Muslim and have high proportions of smokers.

Its marketing is generally adapted to the “not overly devout”, says the study. The authors call for further research to find out how the industry had approached other faiths.

“The launch of the Faith Against Tobacco national campaign by Tobacco Free Kids and faith leaders in the US, for example, brings together Christianity, Islam, Judaism and other faiths ‘to support proven solutions to reduce smoking’. Understanding efforts by the industry to undermine the efforts of other faith communities brings to light a broader strategy to marginalise tobacco control in diverse communities, and refocuses the problem on tobacco-related health harms,” says the paper.

BAT told the Guardian. “This study, which concerns material written nearly 20 years ago, does not represent the views, policies and position of British American Tobacco. We are a global business that holds itself to strict standards of business conduct and corporate governance, manufacturing and marketing our products in accordance with domestic and international laws and observing the cultural and religious beliefs in the 200 countries in which we operate.”

Philip Morris did not respond to the Guardian’s request for comment.

Source: http://www.theguardian.com/business/2015/apr/20/

Filed under: Nicotine,Social Affairs :

Abstract

INTRODUCTION AND AIMS:

This study aims to evaluate the feasibility and effects of a group cessation program for cannabis and tobacco co-smokers.

DESIGN AND METHODS:

Using a repeated-measures design with pre-, post- and six months follow-up assessments, feasibility (intervention utilisation, safety and acceptability) and changes in substance use behaviour and mental health were evaluated. The intervention consisted of five to six group sessions and was based on current treatment techniques (e.g. motivational interviewing, cognitive-behavioural therapy, and self-control training). In total, 77 adults who used cannabis at least once weekly and cigarettes or similar products at least once daily participated in the study.

RESULTS:

Within nine months, the target sample size was reached. Treatment retention was 62.3%, and only three participants discontinued treatment due to severe problems (concentration problems, sleeping problems, depressive symptoms, and/or distorted perceptions). In total, 41.5% and 23.4% reported abstinence from cigarettes, cannabis or both at the end of treatment and the follow-up, respectively. The individual abstinence rates for cigarettes and cannabis were 32.5% and 23.4% (end of treatment) and 10.4% and 19.5% (follow-up), and 13% (end of treatment) and 5.2% (follow-up) achieved dual abstinence validated for tobacco abstinence. Over the study period, significant decreases in tobacco and cannabis use frequencies and significant improvements in additional outcomes (drinking problems, symptoms of cannabis use disorder, nicotine dependence, depression and anxiety) were achieved.

DISCUSSION AND CONCLUSIONS:

The evaluated intervention for co-smokers is feasible regarding recruitment, intervention retention and safety. The promising results regarding substance use and mental health support a randomised controlled trial to evaluate effectiveness.

Source: Drug Alcohol Rev. 2015 Jul;34(4):418-26. doi: 10.1111/dar.12244. Epub 2015 Feb 11.

Filed under: Cannabis/Marijuana,Drug Specifics,Nicotine :

Abstract

Background

The disease risks from cigarette smoking increased in the United States over most of the 20th century, first among male smokers and later among female smokers. Whether these risks have continued to increase during the past 20 years is unclear.

Methods

We measured temporal trends in mortality across three time periods (1959–1965, 1982–1988, and 2000–2010), comparing absolute and relative risks according to sex and self-reported smoking status in two historical cohort studies and in five pooled contemporary cohort studies, among participants who became 55 years of age or older during follow-up.

Results

For women who were current smokers, as compared with women who had never smoked, the relative risks of death from lung cancer were 2.73, 12.65, and 25.66 in the 1960s, 1980s, and contemporary cohorts, respectively; corresponding relative risks for male current smokers, as compared with men who had never smoked, were 12.22, 23.81, and 24.97.

In the contemporary cohorts, male and female current smokers also had similar relative risks for death from chronic obstructive pulmonary disease (COPD) (25.61 for men and 22.35 for women), ischemic heart disease (2.50 for men and 2.86 for women), any type of stroke (1.92 for men and 2.10 for women), and all causes combined (2.80 for men and 2.76 for women). Mortality from COPD among male smokers continued to increase in the contemporary cohorts in nearly all the age groups represented in the study and within each stratum of duration and intensity of smoking.

Among men 55 to 74 years of age and women 60 to 74 years of age, all-cause mortality was at least three times as high among current smokers as among those who had never smoked. Smoking cessation at any age dramatically reduced death rates.

Conclusions

The risk of death from cigarette smoking continues to increase among women and the increased risks are now nearly identical for men and women, as compared with persons who have never smoked. Among men, the risks associated with smoking have plateaued at the high levels seen in the 1980s, except for a continuing, unexplained increase in mortality from COPD.

Source: N Engl J Med 2013;368:351-64.

Filed under: Nicotine,USA :

The Food and Drug Administration recently announced it intends to require warning labels and child-resistant packaging on liquid nicotine products such as those used in e-cigarettes.

The Centers for Disease Control and Prevention said the popularity of e-cigarettes has resulted in a number of cases of nicotine poisoning in recent years.

Jonathan Foulds, professor of public health sciences at Penn State College of Medicine, says nicotine poisoning is not a new problem. “There is a long history of very young children getting a hold of their parents’ tobacco,” he says. “The most common scenario is that a toddler consumes something, and the parents don’t know how much. Then they call the poison control center or end up in the emergency room.” In the best case that leads to anxiety, and possibly unpleasant investigations for the families, and in the worst case it could lead to loss of consciousness or death for the child, Foulds says.

He adds any substance that could be harmful to children should come in a childproof container. “There are hundreds of cases of poisoning from cigarettes every year, and so all nicotine products, including cigarettes, should be in childproof packages.” Nicotine replacement lozenges and other novelty smokeless tobacco products that resemble candy can also be dangerous.

The liquid used in e-cigarettes is often flavored – anything from strawberry to cookies’n’cream – and may therefore smell appealing to children who come across it.

“All nicotine is a poison as are all tobacco products containing nicotine, so people using any of them should take great care to keep them out of reach of kids,” Foulds says.

A nicotine overdose usually makes a person sweaty, clammy, dizzy and nauseous. It proceeds to vomiting and loss of consciousness. It can also lead to death. Luckily for most children, nicotine doesn’t taste good, so most do not continue to consume it once they have had a taste. But with the highly concentrated liquid nicotine, a child who drinks even a small amount could end up with a lethal dose.

Foulds says the proposed measures alone won’t solve the problem. He adds consumers need to be vigilant about using provided childproofing measures and making sure that any substances that could be harmful to children stay out of reach: “Simply put, nicotine is a poison and consumers need to take responsibility for keeping it away from children, whether it is in a childproof container or not.”

Source: Newsroom: Penn State Milton S. Hershey Medical Center 23-Jul-2015

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine,Parents,Youth :

Cigarette warning labels with images depicting diseases caused by smoking help young adults learn about the dangers of lighting up, new research suggests. A study appearing in the Annals of Behavioral Medicine suggests graphic images accompanying written health warnings on cigarette packs may help people better understand and increase their concern about how smoking can harm their health.

“Our outcomes suggest that focusing on enhancing understanding and knowledge from smoking warning labels that convey true consequences of smoking may not only influence motivation directly – both in terms of quitting and prevention of smoking – but may actually drive the emotional experience of the label, which we know is an important predictor of motivation,” Renee Magnan, an assistant professor of psychology at Washington State University, Vancouver, said in a news release.

Magnan added that this was a preliminary study, but it suggested such labels could contribute to larger anti-smoking education campaigns. Researchers took two groups of people between the ages of 18 and 25, which included both smokers and non-smokers, and asked, via an online survey about how much they learned about the harms of smoking from different warning labels.

Participants were shown labels highlighting the negative impacts of lung cancer, heart disease, stroke, impotence, eye disease, neck, throat and mouth cancers and vascular disease, some of which were accompanied by images of the disease. Some labels included pictures that showed the disease, while others were text only.

Young adults in both groups said the labels paired with images did a better job at giving them better understanding, more knowledge, caused more worry and did a better job at discouraging them from smoking than the text alone.

The only exceptions were images of a cigarette held limply in a hand, which was supposed to represent impotence, and an IV in someone’s hand, which was meant to show a long illness, both of which received similar ratings to the corresponding text-only warning. Magnan said in the news release she wanted to do this study because not much research has been done on whether people learn anything from the labels, although an increasing amount of evidence suggests images on warning labels may help discourage smoking. Magnan’s research was conducted with colleague Linda D. Cameron of the University of California-Merced.

As part of the 2009 Family Smoking Prevention and Tobacco Control Act, the Food and Drug Administration (FDA) published a final rule in 2011 requiring tobacco companies to include color graphics on cigarette packets warning consumers of the negative health implications of smoking. In August 2012, this rule was overturned by the government after it was challenged by several tobacco companies, who claimed such graphic warnings would violate the tobacco industry’s right to free speech. This decision was upturned by the Supreme Court in 2013, giving the FDA permission to enforce graphic warnings on cigarette packets.

Source: CADCA’s online newsletter, April 9, 2015

Filed under: Nicotine,Prevention and Intervention :

December 16, 2014

At the end of a year that has seen further tragic deaths from addiction and new designer drugs that put young people at risk, today’s results from the 2014 Monitoring the Future (MTF) survey of drug use among adolescents provide a dose of welcome optimism. No major drug use indicators increased significantly between last year and this year; use of alcohol, cigarettes, and illicit and prescription drugs either held at the same level or, in many cases, declined among American teens.

Particularly heartening was the fact that students’ marijuana use has not increased in the past two years: This year, 21.2 percent of seniors, 16.6 percent of 10^th graders, and 6.5 percent of 8^th graders used marijuana in the past month—high percentages, but not significantly different from 2013. Cigarette and alcohol use (including binge drinking) continued their steady downward trend that we’ve seen for several years now. Abuse of prescription opioids also declined since 2013 and is down by a third to a half over the last 5 years (depending on the opioid and the grade).

We have also seen diminished abuse of inhalants by the youngest teens, who historically are most likely to abuse these readily available substances, as well as diminished abuse of over-the-counter drugs like cough syrups. And although synthetic cannabinoids like “K2” and “Spice” (also known as “synthetic marijuana”) have only been tracked in the survey for the past two years for all three grades, use of these very dangerous and unpredictable drugs is also down from last year.

Although there are no doubt many possible contributing factors to these trends, I like to think that prevention messages are making an impact. Teens are getting the message from various sources that drugs are not good for their developing brains, and there are much better, healthier, and more enjoyable ways to spend their time.

An exception to the good news may be teens’ perception of the risks associated with marijuana. Although use has not increased since 2012, the numbers of teens who believe marijuana is not harmful continued the steady decline we have seen for a decade; this perception of safety could be linked to the drug’s greater visibility and public debates over its legality and its possible uses as medicine.

The survey also showed that edibles are popular among teen marijuana users, especially in states that have legalized medical marijuana. Forty percent of seniors who had used marijuana in the past year in medical marijuana states reported having consumed it in an edible form, versus 26 percent in non-medical marijuana states. With edible marijuana products there is a great danger (to both adults and kids) of ingesting high doses of THC without intending to, making it very important that these products be properly regulated and labeled.

Scientists and policymakers may endlessly debate the degree of long-term harm marijuana poses, but while there is much we still do not know about the drug’s effects, all available evidence points to significant interference in brain development when marijuana is initiated early and used heavily. In 2014, 5.8 percent of 12^th graders reported daily or near-daily use of marijuana, which may impact this segment of youth for the rest of their lives. (With the collaboration of other NIH institutes, NIDA is planning a major longitudinal study that will examine the effects of teen marijuana and other drug use more closely over the next decade.)

A brand-new area of concern reflected in the MTF survey is the surprisingly high use of e-cigarettes, which were included for the first time in this year’s survey (thus trend data are not available). The survey showed 17.1 percent of seniors, 16.2 percent of 10^th graders, and 8.7 percent of 8^th graders report past-month use of these devices, whose health effects are at this point virtually unknown.

Although e-cigarettes don’t burn tobacco and thus produce no tar, there may be other harmful chemicals in the vapor they produce, and products that deliver nicotine (which depend on the fluid used) can be addictive. Thus it will be very important in coming years to monitor e-cigarette use by young people and learn more about their health effects.

While overall the MTF data this year are encouraging, we of course cannot relax our efforts in educating teens about the dangers of the drugs they encounter now and will continue to encounter as they grow older. The message should be clear and unequivocal: For teens and young adults, whose brains are still not finished maturing and thus can be readily altered in their development by any substance exposure, there are simply no safe drugs.

Filed under: Cannabis/Marijuana,Drug use-various effects on foetus, babies, children and youth,Education Sector,Global Drug Legalisation Efforts,Nicotine,USA :

The largest recent US national survey of drink and drug problems shows that outside the addiction treatment clinic, remission is the norm and recovery common. After 14 years half the people at some time dependent on alcohol were in remission, a milestone reached for cannabis after six years, and for cocaine after just five.

SUMMARY Among the US general adult population, and for each of nicotine, alcohol, cannabis and cocaine (including crack), this study sought to estimate the time from onset of dependence to remission, the cumulative probability of remission in different racial/ethnic groups, and to identify factors related to the probability of remission.

It drew its data from the National Epidemiological Survey of Alcohol and Related Conditions (NESARC) conducted in 2000–2001, which focused on drinking disorders but also asked about other forms of drug use and psychological problems. The aim was to interview a representative sample of civilian, non-institutionalised adults aged 18 and over living in households and group residences such as college halls, boarding houses and non-transient hotels. About 8 in 10 of the sample responded to the survey yielding 43,093 respondents. The featured report investigated the subgroups who had some time in their lives been dependent on nicotine (of which there were 6937), alcohol (4781), cannabis (530) or cocaine (408).

Dependence was defined as meeting the dependence criteria of the applicable version of the American Psychiatric Association’s DSM manual, DSM-IV. ‘Lifetime’ dependence was diagnosed if the respondent reported having experienced at least three specific signs of this syndrome within the same 12-month period at some point in their life. The age this first happened for any particular substance was the onset year, while the remission year was based on the age when the respondent’s answers indicatedthey had last stopped meeting dependence criteria for the drug, and had continued to do so for at least a year until interviewed for the survey – essentially, the most recent (at least so far) lastinglysuccessful remission. It was on this basis that the study calculated remission rates for individual substances and related them to the time between the onset of dependence and remission.

Main findings

Proportion of dependent users in remission

Within a year of first becoming dependent, 3% each of smokers and drinkers were in remission and remained so until they were surveyed. For cannabis the figure was nearly 5% and for cocaine, nearly 9%. After ten years the proportions in remission had risen to 18% for nicotine, 37% for alcohol, 66% for cannabis and 76% for cocaine chart. It could be estimated that by the end of their lives 84% of formerly dependent smokers would be in remission, 91% for alcohol, 97% for cannabis and 99% for cocaine. About 26 years after first becoming dependent, half the people at some time dependent on nicotine were in remission, a milestone reached for alcohol after 14 years, for cannabis six years, and for cocaine five years.

Once other factors had been taken in to account, for each of the substances, men who had been dependent at some time were significantly less likely than women to be in remission, especially in respect of the two illegal drugs, cannabis and cocaine; for every 10 women only about six men were in remission from dependence on these drugs. Black Americans once dependent on nicotine or cocaine were less likely to be in remission than white Americans – for cocaine, half as likely. After four years, about 50% of whites had sustained remission from dependence on cocaine; African Americans took nine years to reach the same milestone.

About 80% of people at some time dependent on nicotine or alcohol and almost all those once dependent on cannabis or cocaine had also at some time met diagnostic criteria for another psychiatric disorder, including conduct (antisocial behaviour in early life) and personality disorders. Once other factors had been taken in to account, people who had met criteria for conduct disorder were much more likely than others to have overcome their dependence on cannabis. In contrast, a diagnosis of a personality disorder was associated with a lower probability of remission from cannabis (and also alcohol) dependence. Having once experienced mood and anxiety disorders was unrelated to remission from dependence on any of the four substances.

The authors’ conclusions

The general picture is that the vast majority of people in the USA once dependent on nicotine, alcohol, cannabis or cocaine stop being dependent at some point in their lives, and this happens after fewer years for cannabis or cocaine than for nicotine or alcohol. Black Americans stay dependent longer on nicotine and cocaine than white Americans, and probabilities of remission are associated with social and psychological characteristics and dependence on other substances. However, the fact that that many people once dependent were no longer at the time of the survey should be interpreted with caution given the irregular course of addictions punctuated by remissions and relapses; their remission may have been temporary. Possible explanations for these findings are considered below.

More than two thirds of remissions from cannabis and cocaine dependence occurred within the first decade after onset of dependence, but only a fifth for nicotine and a third for alcohol. These differences may be explained in part by how quickly adverse physical, psychological and social consequences become apparent. For instance, the risk of early cardiovascular problems is much higher among individuals dependent on cocaine than among those dependent on nicotine or alcohol. Behavioural disturbances resulting from cannabis or cocaine dependence and their illegal status impose stronger social pressures to remit. The pervasive availability of alcohol and nicotine also means pervasive environmental prompts to using the drugs. Particularly for nicotine, perceived immediate benefits including anxiety and stress reduction, improved cognitive performance, and weight control, may initially outweigh perceived potential harms from long-term use.

Consistent with previous studies, black Americans once dependent on cocaine were less likely to remit than their white counterparts. Psychosocial factors that commonly affect black populations, including discrimination and lower levels of social capital, have been recognised as barriers to remission and triggers to use or relapse; genetic factors may also contribute.

Men were less likely than women to remit from dependence, perhaps because substance use is more damaging (physically, mentally and socially) for women, heightening motivation to stop using. Feelings of guilt and concerns about substance use during pregnancy and child-rearing may also play a particular part in prompting remission among women.

Individuals who met criteria for a personality disorder were less likely to remit from alcohol or cannabis dependence. This may be because characteristics of these disorders such as being impulsive, intolerant to stress, anxious, and craving new experiences, also predispose to substance use, and these characteristics tend to persist.

Among the limitations of the study were that it omitted institutionalised individuals including prisoners. People whose substance use led to their early death would also have been missed, as may some with severe but non-fatal consequences. These omissions may have caused an overestimation of the probability of remission across the entire population. The study also had no information on the number and duration of remission episodes over an individual’s lifetime; it could only relate other factors to the latest of these remissions.

COMMENTARY The good news from this analysis is that, in the US context, rather than continued dependence, remission is the norm. Most people overcome or grow out of their dependence on the drugs analysed by the study – for cocaine and cannabis, after just five or six years, and for alcohol, after 14, and over their lives people continue to remit until nearly all are no longer dependent. But at least in respect of drinking, there are a set of multiply problematic drinkers who despite treatment, take many more years to stop being dependent. The findings on black versus white Americans suggest that remission rates depend on socioeconomic factors; sampled at another period in the USA’s economic cycles or in respect of drugs used predominantly by more or less advantaged sections of the population, remission rates too might differ, and look more or less like the chronic disease model.

The data presented in the featured article did not show whether the user ‘in remission’ had simply become dependent on another drug. Within the set of illegal drugs and medicines, this seemed uncommon, because the total remission rate was so high. But it seems more than possible that some who matured out of illegal drug use instead took up heavy drinking, in social and legal terms, a dependence easier to live with as an adult.

Remission rates looking forward

An acknowledged weakness of the featured report is that it asked respondents to recall changes which may have happened many years ago. However, the survey was repeated about three years later when 87% of the people who still qualified for the survey were re-interviewed. The follow-up offered an opportunity to see how many dependent at the time of the first survey had recovered three years later. These analyses seem only to have been done for drinking, for which they confirm that most people cease to be dependent though most too continue to experience drink-related problems and to sometimes drink heavily, and remain vulnerable to relapse. This average impression results from the pooling of dramatically different trajectories, from older multiply problematic alcoholics who usually do not remit despite treatment, to youngsters who generally quickly remit without formal help. Details below.

Among the re-interviewed sample were 1172 of the 1484 people who had been dependent on alcohol in the year before the first interview three years before. Nearly two thirds were longer dependent in the year before the follow-up interview. So complete was their recovery that a fifth of those previously dependent had in the past year experienced no indications of abuse or dependence; of these, three quarters were still drinking. About 11% not only had no symptoms, but were exclusively drinking within low-risk guidelines, evenly split between those drinking moderately and those not drinking at all.

But this broad-brush picture hid substantial variation in the fates of different types of dependent drinkers. At one extreme were the most severely affected drinkers with multiple psychological problems and on average about nine years of dependence behind them, two thirds of whom were still dependent at the second interview. At the other were young adults and older drinkers with few complicating psychological disorders and few years of dependent drinking. For most of these the dip in to dependence was a phase which (at least for time being) was over by the the second interview, when just under 30% were still dependent.

At least for the three years between the surveys, remission was very stable. Among the re-interviewed sample were 1772 of the 2109 who three years before had been in “full remission” from past dependence on alcohol, meaning that even though they may sometimes have drunk above low-risk guidelines, for the past 12 months they had reported no symptoms of alcohol abuse or dependence. Of these just 5% had slipped back to being dependent in the year before the second interview, though a third who had been drinking above low-risk guidelines had re-experienced some symptoms of alcohol abuse or dependence. Most stable in their recovery were the abstainers, of whom just 1 in 50 experienced such symptoms. The much greater stability of recovery in abstainers and low-risk drinkers was confirmed when other factors had been taken in to account, but was not apparent among the younger adults in the sample.

Treatment’s impact

Few dependent drug users recover through treatment and fewer still dependent on alcohol – in theNESARC survey on which the featured analysis was based, of those no longer dependent on alcohol,just 24% had at any time been in any kind of treatment for their drinking problems. Over two thirds of those who achieved more complete forms of recovery also did so without treatment.

While this shows that in the USA, treatment is generally not needed to recover from substance dependence, treatment may still make recovery more likely. In respect of dependence on alcohol, one analysis of data from the NESARC survey was consistent with formal treatment promoting recovery characterised by abstinence or low-risk drinking and no symptoms of abuse or dependence, but another and perhaps more reliable analysis found no such association.

Both however found that when treatment had been accompanied by attendance at 12-step mutual aid groups, recovery was more likely – especially abstinent recovery. These analyses could not however disentangle the possible effects of the motivation and conditions which drive someone to seek help, from the effect of actually receiving that help. Complicating the picture is the fact in this survey, the most severely affected and multiply comorbid drinkers with many years of dependence behind them were far more likely to seek treatment than less severely affected types of dependent drinkers. Despite seeking help, they were by a large margin the ones most likely to still be dependent when the survey was repeated three years later.

What about heroin and other opiates?

A notable omission from the illicit drugs included in the featured report was heroin and other opiates. Fortunately these were the subject of the greatest number of relevant studies in another review of follow-up studies of remission from dependence on amphetamine, cannabis, cocaine or opiate-type drugs. It included only studies of general populations or people who entered treatment in the normal way rather than enrolling in treatment trials.

Across the ten studies relevant to opiate-type drugs, every year on average between 22% and 9% of people were either abstinent or no longer dependent; the higher figure is the average of the proportions remitted among people who could be followed up, while the lower estimate includes cases who could not be followed and assumes they are still dependent. Generally the subjects were patients in treatment. Based mainly on patients in treatment, corresponding figures for cocaine were between 14% and 5%. The single study (from the USA) of a general population sample of cocaine-dependent people found that 39% had remitted four years after initially surveyed. For cannabis, the estimate was 17% per annum based on general population surveys and assuming people not followed up were still dependent.

In accordance with the featured article, such figures imply that within 10 years most dependent users of these drugs will no longer be dependent and may have entirely ceased use.

Racial differences reflect socioeconomic status

An analysis of data from the NESARC survey showed that taking alcohol and other drugs together, the longer dependence careers of black versus white Americans was associated with their having less social and socioeconomic resources, signified by fewer being married and fewer having completed their schooling. Once these were taken in to account, racial differences were no longer significant. The implication is that it is not race as such which makes the difference, but the position black people tend to occupy in US society. Given the same disadvantages, white Americans has dependence careers just as extended as black Americans.

Diagnostic system affects remission rate

Much in this analysis depends on the definitions used in the survey. Specifically, the probability of remission equates to the probability that someone will for at least the past 12 months have dropped below experiencing three or more dependence symptoms together in respect of the same drug. From the same survey, it is known for alcohol that many will still be consuming heavily, experiencing symptoms of dependence such as withdrawal and compulsive use, and suffering poor physical and mental health (1 2). They may be remitted from their dependence, but not according to most understandings, ‘recovered’.

Had the line been drawn elsewhere, the chances of remission might have been substantially lower – for example, as commonly in NESARC reports on drinking (1 2 3 4), if remission had been defined as non-problem moderate use or abstinence.

The latest version of the DSM manual (DSM-5) softens this binary system by diagnosing a substance use disorder when at least two symptoms are present in the same 12 months, and rating this as moderate if there were two or three, severe if four or more. ‘Abuse’ and ‘dependence’ are now subsumed within this continuum. The change seems likely to bring many more less severely affected people under the same substance use disorder umbrella as the three-symptom population investigated by the featured analysis. Their remission rates too may differ.

It is also theoretically possible that ‘remission’ may partly reflect the lack of noticeable change or struggle as with the years dependence becomes more deeply embedded and dominant in one’s life, and the change processes probed by some diagnostic questions cease to be live issues – not a sign of recovery, but of the lack such a prospect and the narrowing of life to substance use. For example, having plateaued in their use levels, long-term dependent users may no longer (or not for the past 12 months) have found themselves needing to take more of the drug to feel the desired effects, or taking more than they intended. Perhaps too in the past they had tried unsuccessfully to stop using, or had at least persistently wanted to, but now no longer tried or even wanted to. Ensuring a steady supply of drink or drugs they made no attempt to interrupt would minimise experience of withdrawal. They may also have no important interests and activities left to sacrifice to their dependence – all among the symptoms used to diagnose dependence.

Some findings from NESARC are consistent with this possibility. In the three years between the first interview and the re-interview, the alcohol dependence symptoms which fell away most often and most consistently across different types of drinkers were “taking alcohol often in larger amounts or over a longer period than was intended”, “a persistent desire or unsuccessful efforts to cut down or control use”, and withdrawal.

Similarly, young adult dependent drinkers tend not to endorse the dependence symptom relating to inability to stop drinking or cut back, presumably because they have yet to try.

Related analyses

This data from the featured report has been reanalysed to show that for each of these drugs, the probability that someone would have ceased being dependent remained the same no matter how long ago they had first become dependent. For the author this falsified theories which assume that the longer it lasts, the deeper dependence becomes embedded in neural circuits or lifestyles.

The survey on which the featured article was based and other US national surveys were among those included in a synthesisof hundreds of studies of remission and recovery from substance use problems. This too concluded that “Recovery is not an aberration achieved by a small and morally enlightened minority of addicted people. If there is a natural developmental momentum within the course of [these] problems, it is toward remission and recovery”.

Last revised 24 October 2013. First uploaded 19 October 2013

Source: Probability and predictors of remission from life-time nicotine, alcohol, cannabis or cocaine dependence: results from the National Epidemiologic Survey on Alcohol and Related Conditions.

Lopez-Quintero C., Hasin D.S., Pérez de los Cobos J. et al.
Addiction: 2011, 106(3), p. 657–669.

Filed under: Alcohol,Cannabis/Marijuana,Cocaine,Effects of Drugs,Nicotine,Treatment and Addiction,USA :

AS the e-cigarette industry booms, poison control workers say the number of children exposed to the liquid nicotine that gives hand-held vaporizing gadgets their kick also has spiked.

More than 2,700 people have called the US’ poison control so far in 2014 to report an exposure to liquid nicotine, more than half of those cases in children younger than six, according to national statistics. The number shows a sharp rise from only a few hundred cases just three years ago.

The battery-powered electronic vaporizers often resemble traditional cigarettes and work by heating liquid nicotine into an inhalable mist. The drug comes in brightly coloured refill packages and an array of candy flavours that can make it attractive to young children, heightening the exposure risk and highlighting the need for users to keep it away from youngsters.

“With kids, the exposure we’re seeing is usually parents or family members leave out refill bottles that they try and open,” said Ashley Webb, director of the Kentucky Regional Poison Control Center.

Poison control workers often see a spike in calls with new and growing products, Webb said. The number of e-cigarette users has climbed to several million worldwide, and the devices have become the centre of an industry that has grown in the last four years from about $US82 million to $US2.5 billion ($A88.72 million to $A2.70 billion) in annual sales, at least $US500 million of which comes from liquid nicotine.

Despite the recent increase, liquid nicotine exposures are still less than half of traditional cigarettes, but e-juice is potentially more toxic, said Robert Bassett, a medical toxicologist in Philadelphia. “It would be really hard for a child to eat a whole pack of cigarettes, but now we’re dealing with these very, very concentrated forms you get more than a pack of cigarettes in a small, ingestible amount,” Bassett said.

Bassett consulted on the case of a 10-month-old boy who drank from a refill bottle while his mother’s back was turned. The toddler recovered within hours, but he had vomited, and his heart was pounding when he was brought to the emergency room. “Unfortunately, with little kids it’s hard,” Bassett said. “They simply can’t tell you what they’re feeling.”

Liquid nicotine also stands out because it doesn’t have to be swallowed to be harmful. Skin exposure can be toxic. Officials are calling for child-resistant caps, which many manufacturers have already begun using, but there is no uniform protocol.

The e-cigarette industry doesn’t face the strict government regulations on traditional smokes that aim to keep them away from children, including prohibitions on lolly or fruit flavours. The US Food and Drug Administration has proposed issuing regulations, but no rules have been drafted.

Source: www.news.com.au 23rd October 2014

Filed under: Nicotine :

Smoking and the breast cancer risk gene BRCA2 combine to “enormously” increase the chance of developing lung cancer, a study of 27,000 people has suggested. The research, published in the journal Nature, found the gene could double the likelihood of getting lung cancer.

And some men and women faced a far greater risk, a team at the Institute of Cancer Research in London said. Cancer Research UK suggested drugs targeted at breast cancer may work in some lung cancers.

The links between variants of the BRCA genes and breast cancer are well established – a diagnosis led Hollywood actress Angelina Jolie to have a preventative double mastectomy – but it has also been linked with an increased risk of other cancers affecting women such as ovarian cancer and prostate cancer in men.

The study compared the genetic codes of people with and without lung cancer. Smokers have 40 times the chance of developing lung cancer, but those with a BRCA2 mutation were nearly 80 times more likely, the analysis showed. A quarter of those carrying the mutation, and who also smoke, will go on to develop lung cancer, the research team said.

“It is a massive increase in the risk of developing lung cancer,” said Prof Richard Houlston from the team. “There is a subset of the population who are at very significant risk. “The most important thing is reducing smoking; it is so bad for other diseases, as well as [increasing] the risk of lung cancer.”

Mutations to the BRCA genes stop DNA from repairing itself effectively.

“In the context of smoking there is such an enormous amount of DNA damage that any loss of DNA repair is going to be an issue,” Prof Houlston added.

The discovery could mean treatments that are being developed for breast cancer may also work in some cases of lung cancer. “We’ve known for two decades that inherited mutations in BRCA2 made people more likely to develop breast and ovarian cancer, but these new findings show a greater risk of lung cancer too, especially for people who smoke,” said Prof Peter Johnson, Cancer Research UK’s chief clinician.

“Importantly this research suggests that treatments designed for breast and ovarian cancer may also be effective in lung cancer, where we urgently need new drugs. “But, with or without one of these genetic flaws, the single most effective way to reduce the risk of lung cancer is to be a non-smoker.”

Source: bbc.co.uk/news/health 1st June 2014

Filed under: Drug use-various effects,Health,Nicotine :

Find out what exactly is in a cigarette. SmokeFreeForsythe.org

Over 3,200 Americans under the age of 18 smoke their first cigarette every day, and most of them are unaware of what they are getting into. Many new smokers may not realize how quickly their new habit can lead to heart disease, stroke, diabetes, lung diseases, and certain types of cancer. If you’re looking for an explanation as to why cigarette smoke results in more than 480,000 deaths each year in the United States, look no further than its ingredients. The average cigarette contains upward of 600 different ingredients on top of over 7,000 chemicals produced by cigarette smoke. Where these ingredients and chemicals also show up may shock some smokers into quitting once and for all.

“One of the issues with cigarettes is that they have hundreds of added ingredients, not just what is naturally in the tobacco plant,” environmental health scientist with Mount Sinai School of Medicine, Dr. Luz Claudio told Medical Daily in an email. “What complicates this even more is that when these chemicals burn, they form other chemicals that may have additional effects on health.” While tobacco companies like R.J. Reynolds insist that a lot of the ingredients found in cigarettes are also found in Food and Drug Administration-approved foods and beverages, a few of these ingredients are also found in products that you would never think to put in your body otherwise. Take for example arsenic, an inorganic substance found in wood preservatives and rat poison. On the FDA’s Established List of Harmful and Potentially Harmful Constituents in Tobacco Products and Tobacco Smoke, arsenic’s dangers include: carcinogen, cardiovascular toxicant, and reproductive or developmental toxicant.

Some of cigarettes’ harmful ingredients and chemicals are more familiar, such as carbon monoxide, which can be found in car exhaust fumes, and nicotine, also found in insecticides. There’s also formaldehyde, a cancer-causing ingredient of embalming fluid. Others may not seem so dangerous by name alone like cadmium, an active ingredient in batteries, or hexamine, sometimes found in barbecue lighters. Approximately 70 of the chemicals and ingredients found in a cigarette are considered carcinogenic, meaning they have the potential to cause cancer. Almost all of these ingredients can lead to death in some way or another.

“Cigarette smoke can affect the flow of oxygen within our bodies in two ways,” pulmonologist specializing in pulmonary rehab with City of Hope, Dr. Brian Tiep told Medical Daily. “First, carbon monoxide grabs on to the hemoglobin molecule, which prevents the transport of oxygen through red blood cells. Secondly, cyanide hinders tissue’s ability to take up and utilize oxygen. Tissue cannot function without this steady flow of oxygen.” According to the American Cancer Society, cigarette smoke accounts for at least 30 percent of all cancer-related deaths in the U.S. This includes 87 percent of lung cancer deaths among men and 70 percent of among women. Cigarette smoke can also lead to certain lung diseases including emphysema, bronchitis, and chronic airway obstruction. There are currently more than 16 million Americans suffering from a disease that was caused by smoking. If appropriate prevention strategies are not put in place to curb the number of young Americans who pick up smoking, an estimated 5.4 million people under the age of 18 will die prematurely due to a smoking-related illness.

Source: www.medicaldaily.com 30th April 2014

Filed under: Drug use-various effects,Health,Nicotine :

Addiction makes it difficult for people to look beyond immediate gratification to the longer term consequences of their actions. Accordingly, patients in drug abuse treatment are often coached to make and rehearse mental associations between situations that trigger drug cravings and the problems that are likely to ensue from succumbing to them. The cognitive behavioral programs that incorporate this strategy generally are effective, but researchers have shed little light on the neurological basis for their efficacy—until now.

In a study led by Dr. Kevin N. Ochsner of the Social Cognitive Neuroscience Laboratory at Columbia University, smokers reported milder cigarette cravings when they thought about smoking’s harmful effects while viewing smoking cues than when they focused on its pleasures. Brain imaging correlated the reductions in craving with altered activity levels in regions associated with emotional regulation and reward.

Mental Adjustment Alters Brain Activity

Dr. Ochsner and colleagues recruited smokers as study subjects because smoking accounts for more illness and death than any other addiction. To gain insight on the smokers’ ability to regulate cravings in general, the team also investigated their responses to cues for high-fat food.

The participants were 21 men and women who had smoked for 10 years, on average, and were not trying to quit. In preparation for the study, the participants practiced turning their thoughts to rewarding effects of cigarettes or high-fat food consumption when given the instruction “NOW” and to negative effects when given the instruction “LATER.” In the study itself, the researchers gave each participant 100 such instructions, in random order, each followed by a 6-second exposure to a screen image of either cigarettes or food. Then, after a 3-second delay with the screen blank, the participant reported how much he or she desired to smoke or eat, on a scale of 1 (not at all) to 5 (very much).

The power of thinking about negative effects proved to be considerable. The participants reported 34 percent less intense urges to smoke and 30 percent less intense food cravings after the LATER instruction compared with the NOW instruction.

Brain scans taken during the experiment showed how concentrating on long-term negative consequences alters brain activity to reduce craving. Functional magnetic resonance imaging (fMRI) of the participants’ whole brain revealed increased activity levels in areas—the dorsomedial, dorsolateral, and ventrolateral regions of the prefrontal cortex (PFC)—that support cognitive control functions, such as focusing, shifting attention, and controlling emotions. Activity decreased in regions that previous studies have linked with craving; these areas include the ventral striatum and ventral tegmental area, which are parts of the reward circuit; the amygdala; and the subgenual cingulate. Individual participants who reported larger reductions in craving exhibited these changes to a more marked degree. A specialized mediation analysis of the images found that the increase in PFC activity drove the decrease in ventral striatum activity, which, in turn, fully accounted for the reduction in craving.

“These results show that a craving-control technique from behavioral treatment influences a particular brain circuit, just as medications affect other pathways,” says Dr. Steven Grant of NIDA’s Division of Clinical Neuroscience and Behavioral Research.

The researchers noted that the study participants reduced their smoking and food cravings to the same extent, even though smoking cravings were initially more intense. This finding suggests that calling undesirable consequences to mind has potential to help people overcome a variety of unhealthy urges.

Scans Show Effects of Craving Regulation in the Brain When study participants thought of the long-term negative consequences of cigarette consumption (after receiving the instruction “LATER”), rather than short-term pleasures (“NOW”), they reduced their craving. Brain scans showed increased activity in the dorsolateral prefrontal cortex—a region critical to setting goals, planning, and controlling behavior—which, in turn, inhibited the ventral striatum, part of the reward pathway that generates craving. Text Description of Scans Show Effects of Craving Regulation in the Brain Graphic

Healing Perspectives

“Cognitive reappraisal—mentally changing the meaning of an event or object to lessen its emotional impact and therefore alter the behaviors it triggers—is a strategy that helps a variety of problems,” says Dr. Ochsner. Cognitive-behavioral therapists train patients to use this approach, among others, to cope with negative emotions, stress, and substance cravings. Dr. Ochsner says, “People may not realize that they can control cravings or emotions using cognitive strategies—for example, thinking of negative consequences and distracting and distancing oneself—but patients can learn these techniques and then must continue to apply them over time.”

Dr. Ochsner says there is broad scientific interest in the neurobiological mechanisms underlying cognitive control over thoughts and emotions that promote unhealthy behaviors. Such studies generally find that although there is some overlap in the regions of the PFC engaged when people exert cognitive control, different areas seem to support different strategies for the regulation of emotional responses.

“The mediation analysis that Dr. Ochsner and colleagues conducted is unique among imaging studies and is a particular strength of this research,” says Dr. Grant. “Because the researchers examined the interaction of brain regions, the results provide a perspective on the neural circuits involved in cognitive control of craving.”

Dr. Grant suggests two important next steps in this area of research: identifying why some people have more problems than others in controlling the desire for cigarettes and determining whether brain activity predicts the ability to quit smoking.

Sources

Kober, H., et al. Prefrontal-striatal pathway underlies cognitive regulation of craving. Proceedings of the National Academy of Sciences 107(33):14811–14816, 2010. Kober, H., et al. Regulation of craving by cognitive strategies in cigarette smokers. Drug and Alcohol Dependence 106(1):52–55, 2010. NIDA Notes April 19, 2012

Filed under: Addiction,Brain and Behaviour,Nicotine :

Each day almost 600 children are taking up the habit, putting themselves at a much greater risk of lung cancer and other diseases.

More children are starting to smoke in London than anywhere else

Almost 600 children aged under 16 take up smoking every day in the UK, research has suggested. A survey of secondary school pupils in years 7 to 11 (children mostly aged 11-15) estimated there were 207,000 new child smokers between 2010 and 2011. The Health and Social Care Information Centre said the figures, published in the journal Thorax, were particularly high in London.

“Each day, 67 children, more than two classrooms full, start smoking in London,” said the experts, who included specialists from Cancer Research UK and Imperial College London.

An estimated 463 children start smoking every day in England, with 50 in Scotland, 30 in Wales and 19 in Northern Ireland.

The experts said: “Smoking is among the largest causes of preventable deaths worldwide. The present data should help to raise awareness of childhood smoking and to focus attention on the need to address this important child protection issue.”

People who start smoking before the age of 15 have a higher risk of lung cancer than those who start later, they said. The team also pointed to “compelling evidence” that young people are susceptible to branding and advertising and are influenced by the depiction of smoking in films. The experts said: “Legislation is needed to counter the efforts of the tobacco industry, but this requires political will by legislators at both national and local levels.” Dr Penny Woods, chief executive of the British Lung Foundation, said: “Although the thought of nearly 20 classrooms full of children taking up smoking every day should be shocking, the sad thing is that it comes as no surprise.

“It is even sadder to think that, at current rates, half of these children are likely to eventually die as a result of their habit if they continue smoking.”

Source: news.sky.com Thursday 05 December 2013

Filed under: Nicotine,Youth :

Abstract

Background

Exposure to tobacco and alcohol imagery in films is strongly associated with uptake and consumption of both tobacco and alcohol in young people. In an analysis of popular UK films over the 20 years from 1989 to 2008, we have previously documented substantial tobacco and alcohol content in films marketed to children and young people. In view of increasing awareness of the potential harm of this exposure, this study was undertaken to assess whether these exposures continue to be prevalent in more recent films, by analysing the most popular films in the years 2009—11.

Methods

Occurrence of tobacco (tobacco use, implied use, tobacco paraphernalia, and tobacco brand appearances) and alcohol (alcohol use, inferred alcohol use, other alcohol reference, and alcohol brand appearances) imagery was measured by 5-min interval coding in the 15 most commercially successful films in the UK in each year from 2009 to 2011. Each 5-min period of film was coded as positive for each category of tobacco or alcohol imagery, or both, if at least one such incident occurred during the 5-min period.

Findings

All of the 45 most popular films for 2009—11 were rated by UK film classifiers as suitable for youth audiences (those aged younger than 18 years). Any tobacco was present in a third of all films (15 of 45), whereas any alcohol was present in more than four-fifths (37 of 45 [82%]). Tobacco use occurred in 11 films, and alcohol use occurred in 26. Tobacco branding was infrequent, but two brands, Marlboro and K & J, were clearly identifiable. Alcohol branding was far more frequent, occurring in 22% (ten of 45) of films, with the most frequently occurring brands being Jagermeister, Singha, and Budweiser. When combined with earlier findings using the same methods in films from 1989 to 2008, tobacco was present in 65% (225 of 345) of films, and alcohol in 86% (295 of 345) of films. Tobacco content in each of the coded categories decreased between 1989 and 2010, but increased again in 2011, largely as a result of two films: The King’s Speech and Sherlock Homes: a Game of Shadows. Alcohol content fluctuated over the 23 years, without any significant decline overall (p>0·05). Overall, the most commonly represented tobacco brands were Marlboro, Silk Cut, and Embassy, and the most common alcohol brands were Budweiser, Miller, and Coors.

Interpretation

Although conventional tobacco promotion is heavily restricted in the UK, tobacco imagery continues to be evident in films classified for and popular with youth audiences. The amount of tobacco content in films has decreased over the years but increased again in 2011. Alcohol advertising and promotion remains largely self-regulated in the UK, and there has been no appreciable reduction in any alcohol depictions in youth classified films. UK film regulators are aware of the effects of film content on youth audiences, but in practice do not seem to consider either tobacco or alcohol imagery in the age classification process of films suitable for young people.

Funding

This research was done as part of the research undertaken by AL as part of a research fellowship funded by the UK Centre for Tobacco Control Studies, which is a UKCRC Centre of Public Health Research Excellence. Funding was from the British Heart Foundation, Cancer Research UK, the Economic and Social Research Council, the Medical Research Council, and the Department of Health.

Source: The Lancet, Volume 382, Issue , Page S66, 29 November 2013

Filed under: Alcohol,Nicotine,Prevention and Intervention :

National figures on smoking prevalence are available, but the researchers wanted to estimate smoking uptake among children, to provide some baseline data to inform efforts for preventive measures, and focus attention and resources on what is “essentially a child protection issue.”

This is because taking up smoking at a young age is an even greater risk to health than starting later in life, they say. Smoking at a young age affects lung development and boosts the risk of progressive lung disease (COPD).

And people who start smoking before the age of 15 run a higher risk of developing lung cancer than those who take up the habit later on, even if the cumulative number of cigarettes smoked is smaller, they add.

The researchers based their analysis on data taken from the 2011 ‘Smoking, drinking and drug use among young people in England’ survey, which targets schoolchildren in England between the ages of 11 and 15 every year.

Questionnaires were completed by 6519 children in 219 schools. And by comparing the numbers of current smokers — regular and occasional — with smoking rates among the same age band surveyed the previous year, the researchers were able to estimate the numbers of new 11 to 15 year olds starting to smoke in 2010-11 in the UK.

To calculate the number of new child smokers for each locality, this estimate of 207,000 was then split across geographical areas according to population size and smoking prevalence among adults, on the assumption that there would be more child smokers where the proportion of adult smokers was high. Parental smoking is one of the strongest predictors of smoking among children.

The researchers then used population and adult smoking prevalence data for each of the four UK countries to calculate the number of new child smokers for each locality.

The analysis indicated that among the 3.7 million children aged between 11 and 15 in the UK, an estimated 463 start smoking every day in England, with the equivalent figures for Scotland, Wales and Northern Ireland, 55, 30, and 19, respectively.

Of 74,000 children in this age group in Birmingham, nine take up smoking every day, while the daily tally in London is 67 out of 458,000 children in this age group.

The authors acknowledge that as their figures are calculated from survey data, they can only be approximate, but the fact that they are regional might be more helpful to healthcare professionals and regulators, they say.

Smoking rates among both adults and children are falling in the UK, but the figures are still high, so the pressure needs to be kept up to reduce smoking further, say the authors.

This means increasing taxation, curbing smuggling, and running well-funded anti-smoking media campaigns, as a well as banning smoking in cars and introducing plain packaging to reduce children’s exposure to branding, they say.

“Smoking is among the largest causes of preventable deaths worldwide,” they write. “The present data should help to raise awareness of childhood smoking and to focus attention on the need to address this important child protection issue,” they conclude.

Source: www.sciencedaily.com 4th Dec. 2013

Filed under: Health,Nicotine,Youth :

Schizophrenia affects approximately 1% of the general population. It is characterized by positive symptoms, such as delusions, hallucinations, and disorganized speech, and negative symptoms, including blunted affect, reduced motivation, and poor social relationships.1 In addition, studies have consistently identified neurocognitive deficits as clinically relevant core features that affect 75% to 85% of schizophrenia patients and that may serve as critical indices of social functioning, treatment strategies, and functional outcomes.2 Neurocognitive dysfunction is observed across several domains, including working memory, attention, executive function, response inhibition, and processing speed.3

Approximately 50% of patients with schizophrenia will have a comorbid lifetime substance use disorder.4 Tobacco and cannabis are the most commonly used substances among these patients.5 The presence of a substance use disorder has been associated with alterations in neurocognitive performance.5,6 While previous studies have found positive effects of nicotine and tobacco smoking on neurocognition in schizophrenia, the effects of cannabis on neurocognitive function in schizophrenia are inconsistent and inconclusive.7,8

The aim of this article is to evaluate the effects of nicotine and cannabis on neurocognitive function in individuals with schizophrenia and to review potential pharmacological treatment strategies.

Nicotine and tobacco

Persons with schizophrenia are more likely to smoke cigarettes and to be-gin smoking at a younger age, extract more nicotine from each cigarette, have a preference for higher-tar cigarettes, and have reduced smoking cessation rates.9 Hypotheses have been proposed to explain comorbid smoking behaviors in these patients. The self-medication hypothesis suggests that schizophrenia patients smoke, in part, to alleviate negative symptoms, dysphoric mood, and neurocognitive impairments by ameliorating a dysfunctional dopamine system.10 The addiction vulnerability hypothesis suggests that genetic and neurobiological factors associated with schizophrenia (ie, alterations in nicotinic acetylcholine receptors [nAChRs] and central dopamine systems) may predispose schizophrenia patients to nicotine addiction.11

Examining the effects of tobacco smoking on neurocognition in schizophrenia is crucial because it may help clarify the rationale for high consumption of tobacco products and inform treatment interventions. Table 1 summarizes the significant findings on the effects of nicotine on neurocognition in persons with schizophrenia. A recent cross-sectional study by Wing and colleagues6 found smoking history and current smoking status to be associated with neurocognition in schizophrenia. Patients without any history of tobacco smoking performed worse than former and current smokers with schizophrenia on neurocognitive tasks that assess processing speed, attention, and response inhibition.

A study of the effects of prolonged (up to 10 weeks) smoking abstinence on visuospatial working memory in patients with schizophrenia and controls found that the patients had impaired visuospatial working memory.12 Subsequently, a study by Sacco and colleagues7 examined visuospatial working memory under conditions of overnight smoking abstinence. They found that smoking abstinence specifically impaired visuospatial working memory in schizophrenia patients but not in controls. Abstinence-induced neurocognitive deficits were restored following restart of smoking. The effects of restarting smoking were blocked by treatment with the nAChR antagonist mecamylamine, which suggests that these pro-neurocognitive effects were dependent on nAChR stimulation.

On the basis of these studies, there is consensus that cigarette smoking may transiently enhance visuospatial working memory and attention in schizophrenia. Whether these pro-neurocognitive effects extend to other domains has not been studied extensively in the literature. While a few studies of cigarette smoking in patients with schizophrenia have found positive effects on tasks that involve sensory gating, motor speed, processing speed, working memory, and executive function, other studies have demonstrated no significant differences in neurocognitive performance apart from modest improvements on attentional and spatial processing tasks.6,13-15 Interestingly, the studies that reported modest effects used brief, general neurocognitive batteries, which are not as sensitive as more comprehensive batteries.14,15

Comparative analyses across studies may be difficult to interpret because of methodological differences. For instance, while some studies have participants abstain from smoking for 2 hours, other studies have participants refrain from smoking overnight or for up to 7 days.15 This may create discrepancies among samples because individuals with schizophrenia who can maintain abstinence for 7 days may represent a less neurocognitively vulnerable subgroup of patients, even more so than patients who are able to refrain from smoking for shorter periods, also hypothesized to be inherently less susceptible to neurocognitive deficits.6 Furthermore, several studies do not provide comprehensive information concerning confounders and use small samples, lack control groups, and employ cross-sectional designs without consideration of longitudinal outcomes. These limitations should be addressed in future studies to provide a more uniform picture about the effects of tobacco use and neurocognitive function in schizophrenia.

Cannabis (marijuana)

Epidemiological studies indicate high rates of cannabis use disorders among individuals with schizophrenia, with lifetime prevalence of 13% to 64%.16 Evidence from longitudinal studies shows an increased risk of schizophrenia and psychotic symptoms following heavy cannabis use.17 Previous studies have proposed self-medication with cannabis to remedy symptoms of schizophrenia.18 In contrast to these studies, recent data show that cannabis misuse often occurs before the onset of psychosis and that psychotic and affective symptoms worsen after cannabis use.19

Two recent meta-analyses have addressed the relationship between cannabis use and neurocognition in schizophrenia. Yücel and colleagues25 published a meta-analysis that focused on the effects of cannabis on neurocognition in patients with established schizophrenia. Our group recently examined the same relationship while controlling for the confounding influence of other substance use disorders. Findings from both meta-analyses show superior neurocognitive performance among cannabis-using patients versus non-using patients.

Schnell and colleagues20 investigated the impact of cannabis use disorders and patterns of consumption on neurocognition in a large sample of schizophrenia patients. The cannabis-using group performed better on tests of verbal and working memory, visuomotor speed (Digit Symbol Test), and executive function. More frequent cannabis use was associated with better performance in attention and working memory tasks. Jockers-Scherübl and colleagues26 evaluated the effects of long-term cannabis consumption on neurocognition in schizophrenia patients and controls. Schizophrenia patients performed significantly better than controls on a test of psychomotor speed, while control cannabis users showed impaired performance. Results were even more pronounced when patients began regular cannabis consumption before the age of 17.

Indeed, patients with comorbid cannabis use disorders may belong to a subgroup of schizophrenia patients with better premorbid adjustment and socialization.27 Drug-seeking individuals may possess essential skills required in communicating with drug dealers and negotiating the subculture required to procure illicit drugs; such traits have been associated with higher neurocognitive capacities among those with schizophrenia.28

Findings from other studies show no significant difference in neurocognitive performance between schizophrenic cannabis users and non-users across various cognitive domains, including decision making, while others report worse performance on tasks assessing verbal learning and memory, executive function, working memory, and semantic fluency among cannabis-using patients.29,30

While positive effects of cannabis may be unexpected, they should also be interpreted with caution. The majority of studies assessing this relationship employed cross-sectional designs. Longitudinal studies that examine the effects of cannabis on neurocognition in schizophrenia are needed to determine the true effects of cannabis on core symptoms associated with the illness.

Future studies should control for potential confounding variables, such as premorbid IQ and other substance use, especially tobacco, given its modulating role on neurocognitive processes. How investigators define cannabis-using status should also be uniform across studies. Furthermore, the amount of cannabis used should be taken into account, by using indices that capture cumulative consumption, such as joint-years. Thus, both confounding factors and methodological differences between previous studies may be responsible for the discrepant findings across studies.

Treatment strategies

Pharmacotherapies that target the nAChRs, which mediate the reinforcing properties and neurocognitive effects of nicotine in smokers, may have therapeutic effects on neurocogni-tive dysfunction in schizophrenia.7,12 Several promising nAChR agents, including galantamine (an allosteric modulator of central nAChRs), DMXB-A (α7-selective agonist), TC-5619 (a selective α4β2 nAChR agonist), and varenicline (α4β2 partial agonist), have been studied in patients with schizophrenia.31-34 A recent study by Hong and colleagues35 found that varenicline treatment in stable, medication-compliant schizophrenia patients for 8 weeks (1 mg/d) improved sensory gating, startle reactivity, and executive function. However, there were no significant effects on other neurocognitive domains, such as spatial working memory, sustained attention, and processing speed.

Cannabinoid antagonists or partial agonists have also been suggested to improve neurocognition in patients with schizophrenia given that cannabinoids increase prefrontal norepinephrine, acetylcholine, dopamine, and glutamate levels. Verrico and colleagues36 established that acute administration of a synthetic CB1 receptor agonist selectively decreased medial prefrontal cortical dopamine turnover in rodents. Thus, caution needs to be used because cannabinoid agonism may increase neurocognitive deficits in patients with schizophrenia by exacerbating frontal cortical dopamine, a critical neurotransmitter involved in neurocognitive processes.

Although there are reports of improved attention, processing speed, and executive function with cannabis use in schizophrenia, negative effects on other domains of neurocognition, such as immediate memory, have also been reported.37 Are these probable benefits worth the trade-off for impairments across certain aspects of memory? Coulston and colleagues37 argue that indeed the trade-off may be beneficial because high-order prefrontal brain processes could, in turn, help patients compensate for other neurocognitive shortfalls (eg, memory). Future investigations are required to determine whether specific neurocognitive components are more beneficial to functioning in schizophrenia than other components.

The second most abundant cannabinoid, cannabidiol (CBD) constitutes up to 40% of cannabis extracts.38 Recently, CBD has been deemed as a safe and efficacious treatment option for schizophrenia.38 Comparable to typical neuroleptics and unlike tetrahydrocannabinol (THC), CBD has been found to induce proneurocognitive, anxiolytic, and antipsychotic effects.38 A recent functional MRI study showed that THC and CBD exerted opposite effects on activation in the striatum, hippocampus, amygdala, superior temporal cortex, and occipital cortex.39 The researchers also found that pretreatment with CBD averted the induction of psychotogenic effects typically produced by THC.

Understanding the mechanisms by which nicotine and cannabis influence neurocognition in schizophrenia may help guide future rehabilitation strategies. The best approach may be an integrative one that combines pharmacotherapy with psychosocial interventions (eg, neurocognitive enhancement therapies). The development of novel agents that target neurocognitive dysfunction in substance-dependent schizophrenia patients is an important endeavor, given the clinical importance of tobacco and cannabis use in schizophrenia.

Conclusions

Future research should consider comorbid substance dependence among persons with schizophrenia in order to eliminate confounding variables that distort the association between smoking (eg, nicotine or cannabis) and neurocognitive performance. It is also important to consider whether neurocognition is altered in a general manner or whether specific neuropsychological parameters are affected differently by nicotine and cannabis.

The general consensus on the effects of nicotine on neurocognition in schizophrenia seems to be that nicotine transiently improves spatial working memory and sustained attention. On the other hand, the effects of cannabis on other domains of neurocognition remain unclear. Future studies are required to evaluate the true nature of this relationship.

Clinicians who treat patients with schizophrenia need to be aware of several caveats. While the research suggests opposite effects of nicotine and cannabis on neurocognitive function in patients with schizophrenia, treating comorbid tobacco and cannabis dependence should be a priority, given their negative health effects. In addition, when neurocognitive assessments of patients with schizophrenia are conducted, knowledge of tobacco and cannabis use status is important in interpreting the test results. The findings that constituents of tobacco (nicotine) and cannabis (CBD) may have therapeutic effects on neurocognition in schizophrenia hold promise for the development of novel treatments for cognitive dysfunction in persons with schizophrenia.

Source: www.psychiatrictimes.com 14th Oct. 2013

Filed under: Brain and Behaviour,Cannabis/Marijuana,Drug use-various effects,Health,Nicotine :

American middle and high school students seem increasingly taken with electronic cigarettes — and that alarms health officials who worry the devices will turn teenagers to regular cigarettes, according to a recent Centers for Disease Control and Prevention report.

The battery-powered electronic devices are marketed as safer and more socially acceptable than regular cigarettes and come with “flavor cartridges” — cherry, chocolate and lime and coconut, to name a few — that could appeal to youngsters.

Teenagers’ use of the electronic devices — sometimes call e-cigs — in 2012 was about double what they reported in 2011.

About 10 percent of high school students reported they’d used the e-cigarettes in 2012 along with 3 percent of middle-schoolers.

The devices do not contain tobacco, so they are not regulated like traditional cigarettes and can be purchased by minors.

But health officials said they still deliver nicotine and other chemicals and can serve as the proverbial gateway to regular cigarettes and all of their known health hazards. They also say the devices have not been well studied, so there may be other health risks that are yet unknown.

“The increased use of e-cigarettes by teens is deeply troubling,” said Dr. Tom Frieden, director of the CDC, in a statement. “Nicotine is a highly addictive drug. Many teens who start with e-cigarettes may be condemned to struggling with a lifelong addiction to nicotine and conventional cigarettes.”

Source: Erie Times-News, October 3,2013

Filed under: Nicotine,Youth :

Teenagers’ use of the electronic devices — sometimes call e-cigs — in 2012 was about double what they reported in 2011.

About 10 percent of high school students reported they’d used the e-cigarettes in 2012 along with 3 percent of middle-schoolers.

The devices do not contain tobacco, so they are not regulated like traditional cigarettes and can be purchased by minors.

Source: Erie Times-News, October 3,2013

Filed under: Drug use-various effects on foetus, babies, children and youth,Education Sector,Nicotine,USA :

Anyone who has ever walked into a “non-smoking” hotel room and caught the distinct odor of cigarette smoke will not be surprised by the findings of a new study: When a hotel allows smoking in any of its rooms, the smoke gets into all of its rooms, the study suggests.

Nicotine residues and other chemical traces “don’t stay in the smoking rooms,” says Georg Matt, a psychologist from San Diego State University who led the study, published Monday in the journal Tobacco Control. “They end up in the hallways and in other rooms, including non-smoking rooms.”

The study found smoke residue on surfaces and in the air of both smoking and non-smoking rooms in 30 California hotels where smoking was allowed. Levels were highest in the smoking rooms, but levels in non-smoking rooms were much higher than those found at 10 smoke-free hotels.

Volunteers who stayed overnight in the smoking hotels also ended up with sticky nicotine residues on their fingers, whether they stayed in smoking rooms or not. Urine tests found additional evidence of nicotine exposure in those who stayed in smoking rooms, but not those who stayed in the non-smoking rooms.

The research comes as smoke-free hotels are becoming more common, though not as common as smoke-free bars and restaurants. Many large chains, including Marriott, Westin and Comfort Inn, have gone smoke-free and hotels must be smoke-free by law in four states and 71 cities and counties, according to the Americans for Nonsmokers’ Rights Foundation. Nearly two-thirds of hotels responding to a recent survey by the American Hotel & Lodging Association said they were smoke-free, though just 39% of economy hotels said so.

The reason many hotels still offer smoking rooms is that some domestic and international travelers still want them, says Kathryn Potter, senior vice president of marketing and communications for the hotel association, based in Washington, D.C. “I have family members (and) friends who book hotels based on where they can smoke,” Potter says.

About one in five U.S. adults still smoke, according to the federal Centers for Disease Control and Prevention (CDC). Matt says his study suggests non-smokers should choose only hotels with no smoking. He says it’s likely that non-smoking guests are routinely exposed to second-hand smoke seeping under doorways and moving through ventilation systems as people smoke elsewhere in hotels. Yet the study also shows widespread contamination with what researchers call “third-hand smoke,” the pollutants left behind on furniture, drapes, carpets and in the air, long after cigarettes are extinguished.

Matt says it is possible people are sneaking cigarettes in some of the smoke-free rooms, but other research shows second- and third-hand smoke can travel through homes and apartment buildings.

Second-hand smoke is linked with health effects, including asthma attacks, heart disease and lung cancer, according to the CDC. The effects of third-hand smoke are not as clear.

“We do know third-hand smoke contains many of the same toxins we find in second-hand smoke,” Matt says. “When the smoke disappears, the danger does not end.”

Source: USA TODAY May 13, 2013

Filed under: Health,Nicotine,USA :

Cigarette smoking and cannabis use overlap—over 90 percent of people who have used cannabis are cigarette smokers or have smoked at least once in their lives. A new large study from Australia reveals that cigarette smoking is linked to how early a person is exposed to cannabis or begins using it and also to a person’s initial experiences with the drug. The study, of nearly 4,000 Australian twins and siblings between ages 21 and 46, found that regular cigarette smokers were more likely to report both an earlier opportunity to use cannabis and trying the drug at an earlier age. Regular cigarette smokers also reported more positive initial experiences with cannabis (e.g., enjoying the taste and experiencing pleasant reactions like relaxation) and were more likely to smoke cannabis a second time within a week of their first try. This study points to the importance of viewing cannabis use within the context of tobacco use. It also suggests the possibility that the ongoing decline in cigarette smoking among youth could potentially bring corresponding reductions in cannabis use, although such a trend is not yet apparent in national data.

Source: www.drugabuse.gov Jan.2013

Filed under: Cannabis/Marijuana,Drug use-various effects on foetus, babies, children and youth,Nicotine :

Smoking prevention in schools reduces the number of young people who will later become smokers, according to a new review published in The Cochrane Library. World-wide, smoking causes five million preventable deaths every year, a number predicted to rise to eight million by 2030. The researchers analyzed data from 134 studies, in 25 different countries, which involved a total of 428,293 young people aged 5-18. Of these, 49 studies reported smoking behavior in those who had never previously smoked. The researchers focused on this group because it offered the clearest indication of whether smoking interventions prevent smoking. Although there were no significant effects within the first year, in studies with longer follow up the number of smokers was significantly lower in the groups targeted by smoking interventions than in the control group. In 15 studies which reported on changes in smoking behavior in a mixed group of never smokers, previous experimenters and quitters, there was no overall long term effect, but within the first year the number smoking was slightly lower in the control group. The analysis revealed two key points: • School programs designed to discourage young people from smoking appear to be effective at least one year after their use. • Programs that included social skills training were more effective than those that just provided information or training on resisting peer pressure. “This review is important because there are no other comprehensive reviews of world literature on school-based smoking prevention programs,” Julie McLellan, one of the authors of the review based at the Department of Primary Care Health Sciences at the University of Oxford in the United Kingdom, wrote in the journal. “The main strength of the review is that it includes a large number of trials and participants. However, over half were from the United States, so we need to see studies across all areas of the world, as well as further studies analyzing the effects of interventions by gender.”

Source: ‘Smoking’ reported in www.cadca.org 2nd May 2013

Filed under: Drug use-various effects on foetus, babies, children and youth,Education,Nicotine :

Abstract

Objectives To determine the prevalence of recent alcohol, nicotine or cannabis use in young persons presenting for mental healthcare.

Design A cross-sectional study of young people seeking mental healthcare completed self-report questionnaires regarding their use of alcohol, nicotine or cannabis.

Setting Data were collected from two sites as part of the national headspace services programme.

Participants 2122 young people aged 12–30 years provided information as part of a patient register; a subset of N=522 participants also provided more detailed information about their patterns of alcohol use.

Outcome measures Prevalence levels of recent alcohol, nicotine or cannabis use within relevant age bands (12–17, 18–19 and 20–30) or primary diagnostic categories.

Results The rates for use at least weekly of alcohol for the three age bands were 12%, 39% and 45%, and for cannabis 7%, 14% and 18%, respectively. The rates of daily nicotine use for the three age bands were 23%, 36% and 41%. The pattern of alcohol use was characterised by few abstainers as well as many risky drinkers. Age of onset across all three substances was approximately 15 years. Individuals who used any of the three substances more frequently were likely to be older, male or have psychotic or bipolar disorders.

Conclusions Frequent use of alcohol, nicotine or cannabis in young people seeking mental healthcare is common. Given the restricted legal access, the patterns of use in those aged 12–17 years are particularly notable. Reductions in substance use needs to be prioritised within services for at-risk young people.

Source: BMJ Open 2013;3:e002229 doi:10.1136/bmjopen-2012-002229

Filed under: Alcohol,Brain and Behaviour,Cannabis/Marijuana,Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

Cigarettes and alcohol serve as gateway drugs, which people use before progressing to the use of marijuana and then to cocaine and other illicit substances; this progression is called the “gateway sequence” of drug use. An article in Science Translational Medicine by study author Denise Kandel, PhD, of the Mailman School of Public Health; and Amir Levine, MD; Eric Kandel, MD; and colleagues at Columbia University Medical Center provides the first molecular explanation for the gateway sequence. They show that nicotine causes specific changes in the brain that make it more vulnerable to cocaine addiction — a discovery made by using a novel mouse model.

Alternate orders of exposure to nicotine and cocaine were examined. The authors found that pre-treatment with nicotine greatly alters the response to cocaine in terms of addiction-related behavior and synaptic plasticity (changes in synaptic strength) in the striatum, a brain region critical for addiction-related rewards. On a molecular level, nicotine also primes the response to cocaine by inhibiting the activity of an enzyme?histone deacetylase?in the striatum. This inhibition enhances cocaine’s ability to activate a gene called FosB gene, which promotes addiction.

The relationship between nicotine and cocaine was found to be unidirectional: nicotine dramatically enhances the response to cocaine, but there is no effect of cocaine on the response to nicotine. Nicotine’s ability to inhibit histone deacetylase thus provides a molecular mechanism for the gateway sequence of drug use.

Nicotine enhances the effects of cocaine only when it is administered for several days prior to cocaine treatment and is given concurrently with cocaine. These findings stimulated a new analysis of human epidemiological data, which shows that the majority of cocaine users start using cocaine only after they have begun to smoke and while they are still active smokers. People who begin using cocaine after they’ve started smoking have an increased risk of cocaine dependency, compared with people who use cocaine first and then take up smoking.

“These studies raise interesting questions that can now be further explored further in animal models,” said Dr. Kandel, a professor of Sociomedical Sciences at the Mailman School. “Do alcohol and marijuana — the two other gateway drugs — prime the brain by the same mechanism as nicotine? Is there a single mechanism for all gateway sequences, or does each sequence utilize a distinct mechanism?”

The results also emphasize the need for developing effective public health prevention programs encompassing all nicotine products, especially those targeted toward young people. Effective interventions not only would prevent smoking and its negative health consequences but could also decrease the risk of progression to chronic use of illicit drugs.

Source: ScienceDaily (Nov. 2, 2011)

Filed under: Alcohol,Brain and Behaviour,Nicotine :

Say goodbye to the drug-fuelled raver and hello to the clean-living ecowarrior. Teenagers are changing and, for perhaps the first time in history, their parents approve.

Rates of drug- taking, drinking and smoking among children have plummeted in the past decade. Girls, it seems, are more likely to emulate the polite, studious Hermione Granger, played by Emma Watson in the Harry Potter films than wild-child party girls like Peaches Geldof in her heyday.

Among 11 to 15 year olds, the proportion who admitted to having taken drugs fell from 29 per cent in 2001 to 17 per cent in 2011. Regular smokers of at least one cigarette a week halved from one in 10 to one in 20. The number who said they had drunk alcohol in the past week was down from 26 per cent to 12 per cent.

Experts said a “profound shift” had taken place in the new generation’s attitude to drink and drugs. The findings were based on a survey of 6,500 children aged 11 to 15 at secondary schools in England, conducted between September and December 2011.

Tim Straughan, the chief executive of the NHS Health and Social Care Information Centre, said: “The report shows pupils appear to be leading an increasingly clean-living lifestyle and are less likely to take drugs as well as cigarettes and alcohol. All of this material will be of immense interest to those who work with young people and aim to steer them towards a healthier way of life.”

Siobhan McCann, of the charity Drinkaware, said: “While the decline in the number of children trying alcohol is good news, the report still shows there are 360,000 young people who reported drinking alcohol in the past week alone. Parents are the biggest suppliers of alcohol to young people aged 10 to 17 and also the biggest influence on their child’s relationship with drink.”

Drug-taking, drinking and smoking increases with age, the study found. Among 11-year-olds, fewer than one in 30 said they had taken drugs in the past year, compared with almost one in four 15-year-olds.

Cannabis was the most popular drug but its use fell during the decade. In 2011, one in 13 young people said they had smoked it, compared with one in seven in 2001.

Drug use was found to be highest in southern England and lower in the Midlands and the North. The proportion of children saying they had smoked cigarettes at least once was the lowest since the survey was first carried out in 1982 – reflecting the pressure created by anti-smoking laws. Even so, one in five said they had tried cigarettes and one in 20 did so regularly.

In 2001, one in five teenagers said they drank alcohol at least once a week. By 2011, that proportion was down to one in 14. Miles Beale, of the Wine and Spirit Trade Association, said: “The increase in the number of young people who have never drunk alcohol, and the fact those who do drink appear to be drinking less, suggests that the messages about the risks of underage consumption are being heard.”

‘Most of us think of our future, and drink won’t help’
Rosie Brighton, 13, Watford

“I know a few people my age that drink but not many. When you look at people that turn up for school hung-over, not caring and not getting the grades, it is off-putting. Most of us are working hard to get good exam results because we look at the high unemployment rates and think we’ll need all the help we can get. We’re thinking about our future, and drink is not going to help that.

“I don’t know anyone who smokes or takes drugs. A lot of people are afraid of how mad their parents would be if they were caught. I think health authorities and schools have to educate children about drugs early. I had my first lesson in school about drugs in Year 6, but have been made aware of the dangers by my mum.”

Source: The Independent July 2012

Filed under: Alcohol,Cannabis/Marijuana,Nicotine,Parents :

New research from BioMed Central’s journal Substance Abuse Treatment, Prevention, and Policy, and reported in Medical News Today, found a link between traumatic childhood experience, especially for women, and adult smoking patterns. Researchers suggest that treatment and strategies to stop smoking need to take into account the psychological effects of childhood trauma.

Traumatic childhood experiences can range from emotional, physical, and sexual abuse to neglect and household dysfunction and affect a large range of people. In one of the largest studies of adverse childhood experiences (ACE), more than 60 percent of adults reported a history of at least one event. ACEs are thought to have a long term effect on the development of children and can lead to unhealthy coping behavior later in life.

Since psychiatric disorders, including depression and anxiety, are known to increase the risk of smoking, researchers across the U.S. collaborated to investigate the effects of psychological distress on the relationship between ACE and current adult smoking. The ACE
questionnaire was completed by over 7000 people, about half of whom were women.

Even after adjusting the data for factors known to affect a person’s propensity for smoking, such as their parents smoking during the subject’s childhood, and whether or not they had drunk alcohol in the previous month), women who had been physically or emotionally abused were 1.4 times more likely to smoke. Having had a parent in prison during childhood doubled chances of women smoking.

“Since ACEs increase the risk of psychological distress for both men and women, it seemed intuitive that an individual experiencing an ACE will be more likely to be a tobacco cigarette smoker. However, in our study, ACEs only increased the risk of smoking among women. Given this, men who have experienced childhood trauma may have different coping mechanisms than their female counterparts,” notes Dr Tara Strine, who led this study.

Source: http://www.medicalnewstoday.com/releases/247797.php. July 2012

Filed under: Nicotine,Youth :

Nicotine appears to be a “gateway” drug that primes the brain to be susceptible to cocaine, according to a new study in mice. The researchers say if further studies show the findings apply to humans, a decrease in smoking rates in young people would be expected to lead to a decrease in cocaine addiction, the Los Angeles Times reports.

The study found mice exposed to nicotine in drinking water for at least seven days showed an increased response to cocaine. The researchers also looked at data on cocaine use among a group of high school students, and found 81 percent of those who started using cocaine did so in a month when they were smoking tobacco.

The findings appear in the journal Science Translational Medicine.
Previous studies have shown that most illegal drug users report using tobacco products or alcohol before they started illicit drug use, according to a news release by the National Institute on Drug Abuse, which funded the study. Until now, studies have not shown a biological mechanism through which exposure to nicotine increases vulnerability to illegal drug use, the release notes.

“Now that we have a mouse model of the actions of nicotine as a gateway drug this will allow us to explore the molecular mechanisms by which alcohol and marijuana might act as gateway drugs,” lead author Eric Kandel, MD, of Columbia University Medical Center, said in the release. “In particular, we would be interested in knowing if there is a single, common mechanism for all gateway drugs or if each drug utilizes a distinct mechanism.”

Source: www.drugfree.org. 4th Nov.

Filed under: Cocaine,Nicotine,Youth :

Removing branding and wrapping cigarettes in plain packaging helps remove the appeal of smoking according to new a Cancer Research UK-funded study published in Tobacco Control.
The researchers found that more women than men smoked less and found smoking less enjoyable when using the plain packs.

Some smokers also claimed that they would be more likely to attempt quitting if all cigarettes came in the dark brown unbranded packs used in this study.
In the first study of its kind nearly 50 young adult smokers used non branded cigarette packets in normal everyday situations for two weeks. The researchers then compared the reaction to this packaging to the reactions of using regular packs for two weeks.
The plain brown packs were given a fictional name with standard branding and the health warning “Smoking Kills”. Twice weekly questionnaires were followed up with face to face interviews for more in depth analysis of reaction.
Plainly wrapped cigarettes were rated negatively against the original packs. Taking out the cigarettes less often, handing out cigarettes less frequently and hiding the pack more were all reported as a result of the plain packaging.
Dr Crawford Moodie, the study’s lead author based at the University of Stirling, said: “Despite the small size of this study it adds an important real world dimension to the research on the way smokers respond to plain packaging. The study confirms the lack of appeal of plain packs, with the enjoyment and consumption of cigarettes being reduced. We’re now looking to build on this research to understand more about the impact of packaging on smokers.”
The UK government is expected to begin a public consultation on the future of tobacco packaging later this year.
Australia should be the first country in the world to wrap cigarettes in plain packaging. The Australian government has announced that all tobacco must be sold in plain packaging from July 1, 2012. Picture health warnings will also cover 75 per cent of the front and 90 per cent of the back of packs.
Jean King, Cancer Research UK’s director of tobacco control, said: “While a small study, this research provides important insights into the power of cigarette packaging. Colourful and slickly designed packs are one of the last remaining avenues for tobacco companies to market their deadly product, so it’s interesting to see what might happen if and when this is removed. It’s important to remember that smoking remains the single biggest preventable cause of death in the UK, so preventing more people from starting and helping smokers to quit is vital. We look forward to the possibility of removing the silent salesman of cigarette packets.”

Source: http://www.cancerresearchuk.org/ 8th Sept. 2011

Filed under: Nicotine,Prevention and Intervention :

Smoking is an important risk factor in brain shrinkage and a decline in brain function in later years, a new study suggests. The study found smoking, along with high blood pressure, diabetes and excess weight, all contributed to potentially dangerous changes in the brain that could lead to a decline in mental functioning as soon as 10 years later. The study appears in the journal Neurology.
HealthDay reports the study included 1,352 people without dementia whose average age was 54. Each person was weighed, measured, given blood pressure, cholesterol and diabetes tests and underwent brain MRI scans over 10 years. The researchers found smokers lost brain volume overall and in the hippocampus—the part of the brain which converts short-term memory into long-term memory—at a faster rate than nonsmokers. They were also more likely to have a rapid increase in small areas of damage to the brain’s blood vessels.
Study author Charles DeCarli, M.D., of the University of California at Davis Alzheimer’s Disease Center, said in a journal news release, “Our findings provide evidence that identifying these risk factors early in people of middle age could be useful in screening people for at-risk dementia and encouraging people to make changes to their lifestyle before it’s too late.”

Source: ThePartnership @drugfree.org. Aug.2011

Filed under: Brain and Behaviour,Drug use-various effects,Health,Nicotine :

Electronic cigarettes, or “e-cigarettes,” are crude drug delivery systems for refined nicotine that pose unknown risks, two experts write in this week’s New England Journal of Medicine. Researchers from the American Legacy Foundation’s Steven A. Schroeder National Institute for Tobacco Research and Policy Studies write that e-cigarettes have more in common with asthma inhalers than with cigarettes, according to Science Daily.
E-cigarettes are designed to deliver nicotine in the form of a vapor, which is inhaled by the user. They usually have a rechargeable, battery-operated heating element, a replaceable cartridge with nicotine or other chemicals and a device called an atomizer that converts the contents of the cartridge into a vapor when heated. E-cigarettes often are made to look like regular cigarettes.
The Food and Drug Administration (FDA) announced in April that it would regulate e-cigarettes as tobacco products, not as drug-delivery devices.
Last year, the FDA lost a court case after it tried to treat e-cigarettes as drug-delivery devices, which must satisfy stricter requirements than tobacco products, including clinical trials to prove they are safe and effective. FDA tests found that the liquid in some e-cigarettes contained toxins besides nicotine, as well as cancer-causing substances found in tobacco. Some public health experts say the level of the cancer-causing agents is similar to those found in nicotine replacement therapy, which contains nicotine extracted from tobacco.
The authors list several safety concerns about e-cigarettes. They note that the devices do not reliably deliver nicotine, and have not been sufficiently studied in the same way the FDA requires other smoking-cessation drugs and devices to be evaluated. Therefore, smokers who try to use e-cigarettes to help them quit smoking are likely to find them ineffective because of their variable nicotine content and unreliable delivery, they say.
They also note that smokers may use e-cigarettes in places where traditional tobacco smoking is not allowed, thus encouraging them to keep smoking instead of quitting. E-cigarettes also may become a smoking “starter” product for young people. E-cigarette cartridges can be bought over the Internet with flavors such as chocolate and grape, they write.

Source: DrugFreee.org 21st July 2011

Filed under: Drug use-various effects,Health,Nicotine :

Women who smoke while pregnant should be aware that they are increasing the chance their baby will be born malformed, say experts.
The risk for having a baby with missing or deformed limbs or a cleft lip is over 25% higher for smokers, data show. Along with higher risks of miscarriage and low birth weight, it is another good reason to encourage women to quit, say University College London doctors.
In England and Wales 17% of women smoke during pregnancy. And among under 20s the figure is 45%. Although most will go on to have a healthy baby, smoking can cause considerable damage to the unborn child.
Missing limbs
Researchers now estimate that each year in England and Wales several hundred babies are born with a physical defect directly caused by their mother’s smoking. Every year in England and Wales around 3,700 babies in total are born with such a condition. The experts base their calculations on 172 research papers published over the last 50 years, which looked at maternal smoking and birth defects.
The findings, from 174,000 cases of malformation and 11.7 million healthy births, revealed that smoking increased the risk of many abnormalities. The chance of a baby being born with missing or deformed limbs is 26% higher, and cleft lip or palate is 28% more likely.
Similarly, the risk of clubfoot 28% greater, and gastrointestinal defects 27% more. Skull defects are 33% more likely, and eye defects 25% more common. The greatest increase in risk – of 50% – was for a condition called gastroschisis, where parts of the stomach or intestines protrude through the skin. Professor Allan Hackshaw, who led the research, suspects many women who smoke while pregnant do not know about these risks.
“There’s still this idea among some women that if you smoke the baby will be small and that will make it easier when it comes to the delivery. “But what is not appreciated is that smoking during pregnancy increases the risk of defects in the child that are life-long.”
Women should quit smoking before becoming pregnant, or very early on, to reduce the risks
He said very few public health educational policies mention birth defects when referring to smoking and those that do are not very specific – this is largely because of past uncertainty over which ones are directly linked. “Now we have this evidence, advice should be more explicit about the kinds of serious defects such as deformed limbs, and facial and gastrointestinal malformations that babies of mothers who smoke during pregnancy could suffer from,” he said.
Of the 700,000 babies born each year in England and Wales, around 120,000 babies are born to mums who smoke. Amanda Sandford of Action on Smoking and Health said: “This study shows some of the worst outcomes of smoking during pregnancy. Pregnant smokers will be shocked to learn that their nicotine habit could cause eye or limb deformities in their baby.
“There is clearly a need to raise awareness of these risks among girls and to ensure pregnant women are given all the support they need to help them quit smoking and to stay stopped after the birth.” Basky Thilaganathan of the Royal College of Obstetricians and Gynaecologists said women who struggled to quit should at least cut down on how much they smoke.
Professor Hackshaw said the risk was likely dose-related – meaning the more a woman smokes, the bigger the risk to her unborn child.

Source: www.bbc.co.uk 12th July 2011

Filed under: Drug use-various effects on foetus, babies, children and youth,Nicotine,Youth :

This study sets out to broaden the evidence base by running a trial, based in UK general practice, where only brief support was available for participants while they compared nicotine nasal spray to placebo. It was based in 27 general practices and there was a total of 761 heavy smokers (at least 15 cigs/day for at least 3 years) who received brief support and 12 weeks of treatment with either nicotine nasal spray or placebo. The primary outcome was biochemically-verified complete abstinence from smoking throughout weeks 3-12.

The results showed that nicotine nasal spray more than doubled the number who successfully stopped smoking (15.4% vs 6.7%) from weeks 3-12 giving an odds ratio of 2.6 (95% CI 1.5-4.4). Although many reported minor irritant adverse effects it was noted to be particularly effective amongst those who were highly dependent on nicotine.

SMMGP comment: Tobacco harm reduction strategies is a neglected area although we know
that replacing smoking with a smokeless delivery system for the primary drug, nicotine, can reduce risks by about 99%, about the same as abstinence. Because smoking is so popular, the total health benefits from tobacco harm reduction dwarf those from any other area of HR.
There is an increasing array of nicotine replacement therapy options and this study shows one effective way of delivery. One interesting facet was the tiny number (0.2%) that went on to achieve abstinence if they were still smoking at one week. This infers that it may be worth prescribing a single week of nicotine nasal spray and reassessing abstinence. It?s a relatively small, inexpensive punt and it can double the chance of abstinence for that individual – even without the more comprehensive smoking cessation services which some prescribing is based around.

Source: Stapleton JA, Sutherland G. Addiction 2011;106:824-832

Filed under: Nicotine,Treatment and Addiction :

A single 15-minute exposure to nicotine caused a long-term increase in the excitability of neurons involved in reward, according to a study published in The Journal of Neuroscience. The results suggest that nicotine and cocaine hijack similar mechanisms of memory on first contact to create long-lasting changes in a person’s brain.
“Of course, for smoking it’s a very long-term behavioral change, but everything starts from the first exposure,” said Danyan Mao, PhD, postdoctoral researcher at the University of Chicago Medical Center. “That’s what we’re trying to tackle here: when a person first is exposed to a cigarette, what happens in the brain that might lead to a second cigarette?”
Learning and memory are thought to be encoded in the brain via synaptic plasticity, the long-term strengthening and weakening of connections between neurons. When two neurons are repeatedly activated together, a stronger bond forms between them, increasing the ability of one to excite the other.
Previous research in the laboratory of Daniel McGehee, PhD, neuroscientist and associate professor in the Department of Anesthesia & Critical Care at the Medical Center, discovered that nicotine could promote plasticity in a region of the brain called the ventral tegmental area (VTA). Neurons that originate in the VTA release the neurotransmitter dopamine, known to play a central role in the effects of addictive drugs and natural rewards such as food and sex.
“We know that a single exposure to physiologically relevant concentrations of nicotine can lead to changes in the synaptic drive in the circuitry that lasts for several days,” said McGehee, senior author of this study. “That idea is very important in how addiction forms in humans and animals.”
In the new experiments, Mao monitored the electrical activity of VTA dopamine neurons in slices of brain dissected from adult rats. Each slice was bathed for 15 minutes in a concentration of nicotine similar to the amount that would reach the brain after smoking a single cigarette. After 3-5 hours, Mao conducted electrophysiology experiments to detect the presence of synaptic plasticity and determine which neurotransmitter receptors were involved in its development.
Mao discovered that nicotine-induced synaptic plasticity in the VTA is dependent upon one of the drug’s usual targets, a receptor for the neurotransmitter acetylcholine located on the dopamine neurons. But another element found necessary for nicotine’s synaptic effects was a surprise: the D5 dopamine receptor, a component previously implicated in the action of cocaine. Blocking either of these receptors during nicotine exposure eliminated the drug’s ability to cause persistent changes in excitability.
“We found that nicotine and cocaine employ similar mechanisms to induce synaptic plasticity in dopamine neurons in VTA,” Mao said.
While the subjective effects of nicotine and cocaine are very different in humans, the overlapping effects of the two drugs on the reward system of the brain may explain why both are highly addictive substances, the researchers said.
“We know without question that there are big differences in the way these drugs affect people,” McGehee said. “But the idea that nicotine is working on the same circuitry as cocaine does point to why so many people have a hard time quitting tobacco, and why so many who experiment with the drug end up becoming addicted.”
The overlap between nicotine and cocaine effects at the D5 receptor may also offer a novel strategy for preventing or treating addiction. However, currently-known blockers of the receptor also block another dopamine receptor, D1, that is important for normal, healthy motivation and movement.
“This dopamine receptor is attractive as a potential target,” McGehee said. “The real challenge is to tweak the addictive effect of drugs like nicotine or other psychostimulants without totally crushing the person’s desire to pursue healthy behavior.”
Future research will also focus on whether repeated exposure to nicotine, as would occur in a regular smoker, changes the drug’s effects on synaptic plasticity in the VTA. In the meantime, the current study builds evidence that addictive drugs appropriate the neurobiological tools of learning and memory to create long-term changes in brain reward pathways.
“It’s all fitting with the overriding idea that changes in synaptic strength are part of the way these drugs motivate behavior in a persistent way,” McGehee said.
The study, “Nicotine Potentiation of Excitatory Inputs to Ventral Tegmental Dopamine Neurons,” will be published May 4, 2011 by The Journal of Neuroscience. In addition to Mao and McGehee, Keith Gallagher of the University of Chicago is a co-author.
The research was supported by grants from the Women’s Council of the Brain Research Foundation and the National Institutes of Health.

Source: University of Chicago Medical Center (2011, May 4). Nicotine and cocaine leave similar mark on brain after first contact. ScienceDaily. Retrieved May 8, 2011, from http://www.sciencedaily.com¬ /releases/2011/05/110503171745.htm

Filed under: Brain and Behaviour,Cocaine,Nicotine :

Exposure to second hand smoke has a direct, measurable impact on the brain—and the effect is similar to what happens in the brain of the person doing the smoking. In fact, exposure to this secondhand smoke evokes cravings among smokers, according to a study funded by the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health.

The study, published in Archives of General Psychiatry, used positron emission tomography to demonstrate that one hour of secondhand smoke in an enclosed space results in enough nicotine reaching the brain to bind receptors that are normally targeted by direct exposure to tobacco smoke. This happens in the brain of both smokers and non-smokers.

Previous research has shown that exposure to secondhand smoke increases the likelihood that children will become teenage smokers and makes it more difficult for adult smokers to quit. Such associations suggest that secondhand smoke acts on the brain to promote smoking behavior.

“This study gives concrete evidence to support policies that ban smoking in public places, particularly enclosed spaces and around children,” said Arthur Brody, M.D., of the University of California at Los Angeles Department of Psychiatry and Biobehavioral Sciences and corresponding author for the article

Source: www.cadca.org 5th May 2011

Filed under: Drug use-various effects,Drug use-various effects on foetus, babies, children and youth,Nicotine :

A public-smoking ban in Australia has led more parents to smoke at home, raising health risks for kids, researchers say.
The research from the Australian National University’s Research School of Social Sciences concluded that “bans in recreational public places can perversely increase tobacco exposure of nonsmokers … Children seem to be particularly affected. The level of cotinine (a nicotine by product measurable in saliva) in children considerably increases as a result of bans in public places.”
Public smoking bans tend to “displace smokers to private places where they contaminate nonsmokers,” said authors Jerome Adda, Ph.D., and Francesca Cornaglia, Ph.D., visiting scholars from University College London.

Source: Medical Post April 4 2006

Filed under: Drug use-various effects on foetus, babies, children and youth,Nicotine :

Abstract

Objective To examine the association between smoking and risk of invasive breast cancer using quantitative measures of lifetime passive and active smoking exposure among postmenopausal women.

Design Prospective cohort study. Setting 40 clinical centres in the United States. Participants 79?990 women aged 50–79 enrolled in the Women’s Health Initiative Observational Study during 1993–8. Main outcome measures Self reported active and passive smoking, pathologically confirmed invasive breast cancer.

Results In total, 3520 incident cases of invasive breast cancer were identified during an average of 10.3 years of follow-up. Compared with women who had never smoked, breast cancer risk was elevated by 9% among former smokers (hazard ratio 1.09 (95% CI 1.02 to 1.17)) and by 16% among current smokers (hazard ratio 1.16 (1.00 to 1.34)). Significantly higher breast cancer risk was observed in active smokers with high intensity and duration of smoking, as well as with initiation of smoking in the teenage years. The highest breast cancer risk was found among women who had smoked for =50 years or more (hazard ratio 1.35 (1.03 to1.77) compared with all lifetime non-smokers, hazard ratio 1.45 (1.06 to 1.98) compared with lifetime non-smokers with no exposure to passive smoking). An increased risk of breast cancer persisted for up to 20 years after smoking cessation. Among women who had never smoked, after adjustment for potential confounders, those with the most extensive exposure to passive smoking (=10 years’ exposure in childhood, =20 years’ exposure as an adult at home, and =10 years’ exposure as an adult at work) had a 32% excess risk of breast cancer compared with those who had never been exposed to passive smoking (hazard ratio 1.32 (1.04 to 1.67)). However, there was no significant association in the other groups with lower exposure and no clear dose response to cumulative passive smoking exposure.

Conclusions Active smoking was associated with an increase in breast cancer risk among postmenopausal women. There was also a suggestion of an association between passive smoking and increased risk of breast cancer.

Source: BMJ 2011; 342:d1016

Filed under: Drug use-various effects,Health,Nicotine :

Admiral Regina M. Benjamin, released a new report that shows that tobacco smoke, even occasional smoking or secondhand smoke, damages the human body and leads to disease and death.

The 700-page report, “A Report of the Surgeon General: How Tobacco Smoke Causes Disease-The Biology and Behavioral Basis for Smoking,” finds that cellular damage and tissue inflammation from tobacco smoke are immediate, and that repeated exposure weakens the body’s ability to heal the damage.

Even brief exposure to secondhand smoke can cause cardiovascular disease and could trigger acute cardiac events, such as heart attack. The report describes how chemicals from tobacco smoke quickly damage blood vessels and make blood more likely to clot. The evidence in this report shows how smoking causes cardiovascular disease and increases risks for heart attack, stroke, and aortic aneurysm.

The report also explains why it is so difficult to quit smoking. According to the research, cigarettes are designed for addiction. The design and contents of current tobacco products make them more attractive and addictive than ever before. Today’s cigarettes deliver nicotine more quickly and efficiently than cigarettes of many years ago.

You can read the full report at www.surgeongeneral.gov. Last week, CADCA hosted a webinar on tobacco cessation and smoking prevention. A recording of this session, as well as the PowerPoint presentations used during the session, can be accessed online.

Source: www.cadca.org Dec. 2010

Filed under: Drug use-various effects,Health,Nicotine :

Teens may smoke to “self-medicate” against depression, but researchers in Canada say smoking may increase depressive symptoms in some adolescents.

Lead author Michael Chaiton of the Ontario Tobacco Research Unit of the University of Toronto and co-author Jennifer O’Loughlin of the University of Montreal Hospital Research Centre say the study involved 662 high-school teenagers who completed as many as 20 questionnaires from grades 7-11 about their use of cigarettes to affect mood.

Study participants were divided into groups of: teens who never smoked; smokers who did not use cigarettes to self-medicate, improve mood or physical state; and smokers who used cigarettes to self-medicate. Study participants were asked to rate on a rating scale depressive symptoms such as: felt too tired to do things; had trouble going to sleep or staying asleep; felt unhappy, sad, or depressed; felt hopeless about the future; felt nervous or tense; and worried too much about things.

Smokers who used cigarettes as mood enhancers had higher risks of elevated depressive symptoms than teens who had never smoked, researchers concluded.

Source: Journal of Addictive Behaviors.Sept 2010

Filed under: Addiction,Brain and Behaviour,Nicotine,Youth :

A new study from the David Geffen School of Medicine at UCLA suggests that increasing cigarette taxes could be an effective way to reduce smoking among individuals with alcohol, drug or mental disorders.

The study, published online in the American Journal of Public Health, found that a 10 percent increase in cigarette pricing resulted in an 18.2 percent decline in smoking among people in these groups.

The findings demonstrate that increasing cigarette taxes could be a way to curb smoking, which is still the leading preventable cause of death in the United States, according to the study’s lead author, Dr. Michael Ong, an assistant professor of medicine in the division of general internal medicine and health services research at the Geffen School of Medicine.
“Whatever we can do to reduce smoking is critical to the health of the U.S.,” said Ong, who is also a researcher at UCLA’s Jonsson Cancer Center. “Cigarette taxes are used as a key policy instrument to get people to quit smoking, so understanding whether people will really quit is important.

Individuals with alcohol, drug or mental disorders comprise 40 percent of remaining smokers, and there is little literature on how to help these people quit smoking.”

Prior research on the effect of cigarette pricing on smoking, which had been conducted using information from 1991, suggested that individuals with mental illness were less likely than other individuals to quit due to price increases. Unlike that research, however, the current study expanded the research to include people with alcohol and drug disorders.

The researchers based their work on data from 7,530 individuals from the 2000-01 Healthcare for Communities Household Survey. Of those, 2,106 people, or 23 percent, had alcohol, drug or mental disorders during the previous year. Of that group, 43.8 percent were smokers — a much higher proportion than among rest of the population.

Though the researchers found that people with alcohol dependence did not cut down on cigarettes when prices rose, people with binge-drinking problems, substance-use disorders and mental disorders were significantly more likely to quit smoking if prices rose, as would occur with a cigarette tax increase.

While the study does suggest that increasing cigarette prices through taxation could reduce smoking among individuals with alcohol, drug or mental disorders, the authors note that further study is needed to determine if recent cigarette price increases have reduced smoking among individuals with such disorders, and whether the identified association is causal.

Source: http://www.sciencedaily.com/releases June 3, 2010

Filed under: Alcohol,Brain and Behaviour,Drug use-various effects,Health,Nicotine :

It is well-known that maternal smoking during pregnancy can have long-term effects on the physical health of the child, including increased risk for respiratory disease, ear infections and asthma. New research shows that prenatal smoking also can lead to psychiatric problems and increase the need for psychotropic medications in childhood and young adulthood.

Finnish researchers found that adolescents who had been exposed to prenatal smoking were at increased risk for use of all psychiatric drugs especially those uses to treat depression, attention-deficit/hyperactivity disorder (ADHD) and addiction compared to non-exposed youths. The study was presented Tuesday, May 4 at the Pediatric Academic Societies (PAS) annual meeting in Vancouver, British Columbia, Canada.

“Recent studies show that maternal smoking during pregnancy may interfere with brain development of the growing fetus,” said Mikael Ekblad, lead author of the study and a pediatric researcher at Turku University Hospital in Finland. “By avoiding smoking during pregnancy, all the later psychiatric problems caused by smoking exposure could be prevented.”

Ekblad and his colleagues collected information from the Finnish Medical Birth Register on maternal smoking, gestational age, birthweight and 5-minute Apgar scores for all children born in Finland from 1987 through 1989. They also analyzed records on mothers’ psychiatric inpatient care from 1969-1989 and children’s use of psychiatric drugs.

Results showed that 12.3 percent of the young adults had used psychiatric drugs, and of these, 19.2 percent had been exposed to prenatal smoking.

The rate of psychotropic medication use was highest in young adults whose mothers smoked more than 10 cigarettes a day while pregnant (16.9 percent), followed by youths whose mothers smoked fewer than 10 cigarettes a day (14.7 percent) and unexposed youths (11.7 percent).

The risk for medication use was similar in males and females, and remained after adjusting for risk factors at birth, such as Apgar scores and birthweight, and the mother’s previous inpatient care for mental disorders.

Smoking exposure increased the risk for use of all psychotropic drugs, especially stimulants used to treat ADHD (unexposed: 0.2 percent; less than 10 cigarettes/day: 0.4 percent; and more than 10 cigarettes/day: 0.6 percent) and drugs for addiction. An increased risk for use of drugs to treat depression also was seen (unexposed: 6 percent; less than 10 cigarettes/day: 8.6 percent; and more than 10 cigarettes/day: 10.3 percent).

“Smoking during pregnancy is still quite common even though the knowledge of its harmful effects has risen in recent years,” Ekblad concluded. “Recent studies have shown that smoking during pregnancy has negative long-term effects on the health of the child. Therefore, women should avoid smoking during their pregnancy.”

Source: MediLexicon International Ltd 6th May 2010
American Academy of Pediatrics

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

The brain’s nucleus accumbens (NAC) is a core region of the mesocorticolimbic dopaminergic system and is interconnected with the ventral tegmental area (VTA) and the prefrontal cortex. The mesocorticolimbic system is thought to be central to the reinforcing effects of many drugs and plays an important role in addiction. A new study has found that alcohol abuse elevated the expression of a distinct set of genes in the NAC and VTA, while nicotine blunted this effect in the VTA.

Results will be published in the July 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

“In spite of their differences in pharmacology, alcohol and tobacco consumption are often intimately linked,” said Traute Flatscher-Bader, a postdoctoral research fellow at The University of Queensland and corresponding author for the study. “Nonetheless, the molecular mechanisms that underlie alcohol and nicotine abuse, and particularly their co-abuse, are still incompletely understood.”

“One thing that researchers have encountered is that it is often difficult to find ‘pure’ alcoholics, that is, alcoholics that only abuse alcohol and nothing else,” agreed Simon Worrall, director of postgraduate coursework programs in molecular biology at The University of Queensland. “Many alcoholics are poly-drug abusers, with the most common other drug being nicotine. Thus, many studies which have studied the effects of alcohol on the brain and other organs have been compromised because they have not taken account of the effects of nicotine addiction which is often superimposed on the effects of alcohol addiction.”

In the first part of the current study, Flatscher-Bader and her colleagues used DNA microarray technique to study the expression of many thousands of genes in the brains of non-smoking and smoking alcoholics and non-drinking smokers.

“We examined the impact of alcoholism and smoking on gene expression in the NAC in 20 chronic alcohol abusers and controls with and without recent smoking history,” said Flatscher-Bader. “The results revealed that in this brain region, the abuse of alcohol and nicotine had distinct effects on the expression of genes. In addition, altered expression of a number of genes was associated with both alcohol and nicotine abuse. Within the latter group was a set of genes which play a crucial role in a molecular pathway regulating cell structure.”

The researchers then went on to investigate in more detail the altered expression of six selected genes within the pathway regulating cell structure in two brain regions, using 30 cases comprised again of smoking and non-smoking controls and alcohol abusers. For this part of the study they used the method called “real time polymerase chain reaction.”

“This expanded investigation revealed that one of the genes, called RHOA, was elevated by alcohol abuse and its highest expression was evident in the smoking alcoholics in both brain regions,” said Flatscher-Bader. “The RHOA gene had previously been implicated in the initiation of tobacco smoking. In the NAC, the expression of a further four of the six selected genes was increased by alcohol abuse. Interestingly, the highest expression for each of the genes in the NAC was in the smoking alcoholics. In the other brain region called the VTA, alcohol abuse had a similar effect and elevated the expression of all six selected genes. In contrast to the NAC, however, concurrent smoking dampened the induction of five of these alcohol-sensitive genes in the VTA.”

“Many studies have analyzed the changes in gene expression in this brain system to try to untangle the molecular pathology of alcohol addiction,” said Worrall, “but this is amongst the first to take into account the effect of co-administration of nicotine with alcohol.

Flatscher-Bader stressed that there are several cell types in the brain and there are several steps between gene expression and impact on cell structure and function. “It has to be emphasized that our study is important as a first step in identifying molecular pathways underlying the effects of alcohol abuse and smoking and their co-joint abuse on the human NAC and VTA, “she said. “It now needs to be tested if our findings are, indeed, associated with changes to neuronal structure and function.”

“A better understanding of the molecular basis of withdrawal may help in the development of new treatments to ameliorate the symptoms,” added Dr Worrall. “Not many previous studies took into account the potential effects of nicotine addiction that may be superimposed on top of those from alcohol, so these results may help clinicians better use present therapy/drugs to treat patients abusing both alcohol and/or nicotine and may also lead to the development of new drugs.”

Source: www.medicalnewstoday.com 5.5.2010

Filed under: Alcohol,Brain and Behaviour,Drug use-various effects,Health,Nicotine :

Results will be published in the July 2010 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

Source: www.medicalnewstoday.com 5.5.2010

Filed under: Addiction,Alcohol,Brain and Behaviour,Health,Nicotine :

A Canadian-led international study finds that the causes of a heart attack are the same for people throughout the world, with cigarette smoking one of the main risk factors, the “There hasn’t been a study like this ever in the world,” said lead investigator Dr. Salim Yusuf, head of the Population Health Research Institute at McMaster University in Hamilton. “The risk factors that we’ve been able to measure account for 90 percent or more of heart disease. The impact of these risk factors in developing heart disease is global. It’s there in every ethnic group, in men, in women, in every region of the world, in young and old. It means we should be able to prevent the majority of premature heart attacks in the world.”

The research concluded that cigarette smoking and a poor ratio of bad to good cholesterol contribute to two-thirds of all heart attacks worldwide.

The five-year study involved 30,000 people in 52 countries. About half of the participants had suffered a heart attack. They were compared to an equal number of people with no heart disease, matched for age, sex, and city of residence.

“So now we’ll say: What causes the risk factor, not what causes the disease. And from a public-health point of view, there should be no more wallowing about that we need more information. We’ve got it,” said Dr. Sonia Anand, a specialist in vascular medicine and a member of the McMaster research team.

The latest figures show that 15 million people died from heart attacks worldwide in 1998. “The important issue is that the risk factors outlined in this study, the vast majority of them are modifiable,” said Toronto cardiologist Anthony Graham, a spokesman for the Heart and Stroke Foundation of Canada. “And what it suggests is that tobacco control is going to be as important in the developing world as it is in the western world.”

The study’s findings are published in issue of the British medical journal
Source: The Lancet. Sept. 11 2004

Filed under: Health,Nicotine :

New research suggests that people who smoke and drink heavily are more at risk for oral cancer, the Researchers from King’s College in London, England, found an increase in oral cancer among men and women in their 20s and 30s who smoke and binge drink.

The researchers said that when tobacco smoke combines with alcohol, it produces dangerous levels of cancer-causing chemicals that attack the lining of the mouth.

“Our data show that smoking, drinking and poor diet are major risk factors, and that the younger people start smoking and drinking, the higher the risk,” said Newell Johnson, a professor of oral pathology at King’s College

Source: Daily Telegraph, London reported Nov. 9.2004

Filed under: Addiction,Alcohol,Health,Nicotine :

SMOKERS who suffer damage to a particular part of their brains appear to be able to quit their nicotine habit easily – a discovery that might open new avenues of addiction research.
A study of smokers who had suffered brain damage of various kinds after a stroke showed that those with injuries to a part of the brain called the insula were in many cases able to quit smoking quickly and easily – saying they had lost the urge to smoke altogether.
The insula receives information from the body and translates it into subjective feelings such as hunger, pain and craving, including craving for drugs.
However, the insula has not attracted much attention in studies on drug addiction, according to the research in the latest edition of the journal Science.
Deliberately damaging people’s insulas is not considered a realistic treatment option, because the risks are too great and the insula also has a role in many essential functions, such as the desire to eat.
But in the long term, the authors said, drugs might be developed to target the insula.
Other techniques for affecting the insula might in future also include electrical stimulation, already used in patients with depression. However, current techniques cannot penetrate the brain deeply enough to reach the insula.
The study was inspired by the experience of a man who had smoked 40 cigarettes a day before his insula was damaged in a stroke. He quit smoking immediately after, telling researchers his body “forgot the urge to smoke”.
Additional reporting: The Times

Source: news.com.au January 27th 2007

Filed under: Brain and Behaviour,Nicotine :

Fact sheet September 2006

Overall Mortality
• Tobacco use is the leading preventable cause of death in the United States.1 Cigarette smoking causes an estimated 438,000 deaths, or about 1 of every 5 deaths, each year.2,3 This estimate includes approximately 38,000 deaths from secondhand smoke exposure.2

• Cigarette smoking kills an estimated 259,500 men and 178,000 women in the United States each year.2

• More deaths are caused each year by tobacco use than by all deaths from human immunodeficiency virus (HIV), illegal drug use, alcohol use, motor vehicle injuries, suicides, and murders combined.2,4

• On average, adults who smoke cigarettes die 14 years earlier than nonsmokers.5

• Based on current cigarette smoking patterns, an estimated 25 million Americans who are alive today will die prematurely from smoking-related illnesses, including 5 million people younger than 18.6
Mortality from Specific Diseases
• Lung cancer (124,000), heart disease (108,000), and the chronic lung diseases of emphysema, bronchitis, and chronic airways obstruction (90,000) are responsible for the largest number of smoking-related deaths.2

• The risk of dying from lung cancer is more than 22 times higher among men who smoke cigarettes and about 12 times higher among women who smoke cigarettes compared with never smokers.7

• Since 1950, lung cancer deaths among women have increased by more than 600%.1 Since 1987, lung cancer has been the leading cause of cancer-related deaths in women.1

• Cigarette smoking results in a two- to three-fold increased risk of dying from coronary heart disease.7

• Cigarette smoking is associated with a ten-fold increased risk of dying from chronic obstructive lung disease.6 About 90% of all deaths from chronic obstructive lung diseases are attributable to cigarette smoking.1,7

• Pipe smoking and cigar smoking increase the risk of dying from cancers of the lung, esophagus, larynx, and oral cavity.8 Smokeless tobacco use increases the risk for developing oral cancer.8,9
References
1. U.S. Department of Health and Human Services. Women and Smoking: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, CDC, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health; 2001. Available at: http://http://www.cdc.gov/tobacco/sgr/sgr_forwomen/index.htm. Accessed December 2006.

2. CDC. Annual Smoking–Attributable Mortality, Years of Potential Life Lost, and Productivity Losses — United States, 1997–2001. MMWR 2005: 54(25) 625-628. Available at http://0-www.cdc.gov.mill1.sjlibrary.org:80/mmwr/preview/mmwrhtml/mm5425a1.htm. Accessed: September 2006.

3. CDC. Health United States, 2005 With Chartbook on Trends in the Health of Americans. ( PDF–119KB) Hyattsville, MD: U.S. Department of Health and Human Services, CDC, National Center for Health Statistics; 2006. Accessed September 2006.

4. McGinnis J, Foege WH. Actual causes of death in United States. Journal of American Medical Association 1993;270:2207–2212.

5. CDC. Annual smoking-attributable mortality, years of potential life lost, and economic costs—United States, 1995–1999. MMWR 2002; 51(14):300–303. Accessed September 2006.

6. CDC. Perspectives in disease prevention and health promotion, smoking-attributable mortality and years of potential life lost—United States, 1984. MMWR 1997;46:444–451. Available at: http://0-www.cdc.gov.mill1.sjlibrary.org:80/mmwr/preview/mmwrhtml/00047690.htm. Accessed February 2004.

7. Novotny TE, Giovino GA. Tobacco use. In: Brownson RC, Remington PL, Davis JR (eds). Chronic Disease Epidemiology and Control. Washington, DC: American Public Health Association; 1998;117–148.

8. U.S. Department of Health and Human Services. Reducing the Health Consequences of Smoking—25 Years of Progress: A Report of the Surgeon General. Atlanta, GA: U.S. Department of Health and Human Services, CDC; 1989. DHHS Pub. No. (CDC) 89–8411. Available at: http://profiles.nlm.nih.gov/NN/B/B/X/S/. Accessed September 2006.

9. U.S. Department of Health and Human Services. The Health Consequences of Using Smokeless Tobacco: A Report of the Advisory Committee to the Surgeon General, 1986. Bethesda, MD: U.S. Department of Health and Human Services, Public Health Service. NIH Pub. No. 86–2874. Accessed September 2006.
Note: More recent information may be available at the CDC’S Office on Smoking and Health Web site: http://0-www.cdc.gov.mill1.sjlibrary.org:80/tobacco.

Source: Centers for Disease Control and Prevention
National Center for Chronic Disease Prevention and Health Promotion
Office on Smoking and Health. tobaccoinfo@cdc.gov Sept.2006

Filed under: Health,Nicotine :

Summary

DURHAM, N.C. — Within the mind of every smoker trying to quit rages a battle between the higher-order functions of the brain wanting to break the habit and the lower-order functions screaming for another cigarette, say researchers at Duke University Medical Center. More often than not, that cigarette gets lit.
Brain scans of smokers studied by the researchers revealed three specific regions deep within the brain that appear to control dependence on nicotine and craving for cigarettes. These regions play important roles in some of the key motivations for smoking: to calm down when stressed, to achieve pleasure and to help concentration.
“If you can’t calm down, can’t derive pleasure and can’t control yourself or concentrate, then it will be extremely difficult for you to break the habit,” said lead study investigator Jed E. Rose, Ph.D., director of the Duke Center for Nicotine and Smoking Cessation Research. “These brain regions may explain why most people try to quit several times before they are successful.”
Understanding how the brain responds to cigarette cravings can help doctors change nicotine cessation treatments to address all three of these components of withdrawal, Rose said. Drugs or therapies that target these regions may help smokers stave off the cravings that often spoil their attempts to quit.
The team’s findings are now online in the journal Neuropsychopharmacology. The research was funded by Phillip Morris USA.
Approximately one in five Americans smokes. Even though 70 percent of smokers report that they would like to quit, only 5 percent do so successfully.
In this study, the researchers manipulated the levels of nicotine dependence and cigarette craving among 15 smokers and then scanned their brains using positron emission tomography, or PET scans, to see which areas of the brain were most active.
Three specific regions of the brain demonstrated changes in activity when the smokers craved cigarettes versus when they did not.
One region that lights up, called the thalamus, is considered to be the key relay point for sensory information flowing into the brain. Some of the symptoms of withdrawal among people trying to quit stem from the inability to focus thoughts and the feeling of being overwhelmed, and could thus be explained by changes in this region, according to the researchers. The researchers found that changes in this region were most dramatic among those who said they smoked to calm down when under stress.
Another region that lights up is a part of the pleasure system of the brain. Changes in this region, called the striatum, were most notable in people who smoked to satisfy craving and for pleasurable relaxation, the researchers said.
A third region that lights up, called the anterior cingulate cortex, is vital to cognitive functions such as conflict, self regulation, decision making and emotion. People whose brain scans showed the most differences in this region also reported that they smoked to manage their weight.
“This knowledge gives us new clues about brain mechanisms underlying addiction to cigarettes and could allow us design better methods to help smokers quit,” Rose said.
Rose and his colleagues are now planning to perform brain scans on smokers undergoing nicotine replacement therapy, such as the nicotine patch, to determine how these treatments affect the same regions of the brain.
Other researchers participating in the study were Frederique M. Behm, Alfred N. Salley, James E. Bates, R. Edward Coleman, Thomas C. Hawk and Timothy G. Turkington.

Source: www.dukemednews March 2007

Filed under: Addiction,Brain and Behaviour,Nicotine :

* Popular and clinical lore support the strong connection between smoking and alcohol consumption.

* Adolescent smokers appear to have a greater vulnerability to developing alcohol-use disorders.

* Results indicate that smoking “primes” the brain for subsequent addiction to alcohol and possibly other drugs.

Both academic studies and casual observation support the view that smokers tend to drink, and drinkers tend to smoke. New research using nationally representative data from the U.S. finds that smokers – particularly adolescent smokers – clearly have a greater vulnerability to alcohol-use disorders (AUDs) than do non-smokers.

Results are published in the December issue of Alcoholism: Clinical & Experimental Research.

“Smoking and alcohol – separately, or together – account for more than 20 percent of deaths in the United States,” said Richard A. Grucza, an epidemiologist at Washington University School of Medicine and corresponding author for the study. “Cigarettes and alcohol are also known to be ‘gateway’ drugs, that is, the overwhelming majority of illegal drug users begin their use with one or both of these legal drugs.”

“We have known about the link between cigarette smoking and alcohol use for a while, but we have not really asked the question, as the authors here asked, whether use of one could increase the vulnerability of becoming addicted to the other,” said Kevin W Chen, associate professor at the University of Maryland School of Medicine.

“Ours was the first,” added Grucza, “to examine quantity of drinking in relationship to smoking and AUDs. Our central questions were: Can this association be explained by the fact that smokers are heavier drinkers, or is there something else going on? In other words, do smokers appear to be more sensitive to the effects of alcohol?” The short answer appears to be yes.

Researchers examined data from an aggregate of 2002 through 2004 U.S. National Surveys on Drug Use and Health. Randomly selected, household-dwelling adolescents and young adults (n=74,836) were selected from the non-institutionalized and civilian American population and queried about their drinking and smoking practices.

Results indicate that smokers – particularly adolescent smokers -have a greater vulnerability to AUDs than do non-smokers.

“In general, smokers were at more than a 50 percent higher risk, although the differences were larger in younger adolescents and among light drinkers,” said Grucza. “For example, among 15- to 17-year-olds who drank fewer than eight drinks in the month before the survey, more than 20 percent reported an AUD, compared with about five percent among the non-smoking group with the same level of drinking. We conclude that, although smokers do drink higher rates of alcohol, this alone does not explain their higher vulnerability to AUDs.”

Grucza said that these findings go beyond the popular view that bad behaviors like smoking and drinking to excess simply tend to “go together,” especially during adolescence. “It seems that smoking makes the adolescent brain more vulnerable to other addictions,” he said. “Addictive drugs all act on a part of the brain that is described as the ‘central reward circuitry.'” Once this system is exposed to one drug, the brain may become more sensitive to the effects of other drugs, as demonstrated by a number of rodent studies.

“Studies like this will set up an alert – for those who consider adolescent smoking tolerable – to rethink the issue, or perceive the problem differently,” noted Chen. “Although we do not know the exact causal relation between the two, the damage to our health is so severe that we need to create a more objective image to reject both smoking and drinking among adolescents.”

“Ours is the first study to – establish a correlation between adolescent smoking and AUDs that cannot be explained by heavier drinking,” said Grucza. “Now we, and hopefully others, need to investigate whether or not smoking actually causes adolescents to be more susceptible to AUDs. Our results are in line with an emerging literature that shows adolescence may be a unique window of vulnerability for addictions development. If it is proven that nicotine directly impacts vulnerability to alcoholism and other addictions, then that is a new, strong message to add to the health-education arsenal. However, even if this correlation is completely non-causal, these results can help to identify kids who are at risk for AUDs.”

Source:Alcoholism: Clinical & Experimental Research. (ACER) Article Date: 30 Nov 2006 – 13:00 PDT

Filed under: Addiction,Alcohol,Nicotine :

Research in Archives of Dermatology observed the effect by looking at the upper part of the inner arm in smokers and non-smokers.

Previous studies have focused on the face, where skin can also be damaged by exposure to the sun.

But the University of Michigan, Ann Arbour, team say this study shows smoking alone makes the skin age, which may help persuade some to quit.

The researchers photographed 82 people’s upper inner right arms.

Participants were aged 22 to 91. Such a wide age range was used in order to record the natural state of old and young skin.
There is strong evidence suggesting cigarette smoke has a negative effect on the appearance of skin
Indy Rihal, British Skin Foundation

Half of those studied had a history of smoking and had smoked, on average, for 24 years.

The number of packs of cigarettes they smoked ranged from a quarter of a packet to four packs per day.

The team created a nine-point scale to measure damage to skin which is not exposed to the light.

In those aged over 65, there was almost a two-point difference between smokers and non-smokers.

In the over-45s, the difference was around a point.

Writing in Archives of Dermatology, the researchers led by Dr Yolanda Helfrich, said: “We found that the number of packs of cigarettes smoked per day, total years of smoking and pack-years of smoking [an average of packs per day over the number of years of smoking] were correlated with the degree of skin aging.

“After controlling for age and other variables, we found that only packs of cigarettes smoked per day was a major predictor of the degree of photo-protected skin ageing.”

Evidence ‘mounting up’

Dr Helfrich said: “Previous studies have shown that smokers have a greater degree of skin ageing, but those have looked at facial skin.

“There are some sceptics who said the sun was having some of the effect.

“We have demonstrated that there was a significant degree of damage just from smoking.”

She added: “The evidence is certainly mounting up that smoking is not good for you. This just adds to all of that.”

She said more research was needed to show exactly how smoking damaged the skin.

Indy Rihal, of the British Skin Foundation, said: “In addition to UV light from the sun and sun beds, cigarette smoke is a main environmental factor that causes changes in the skin often associated with ‘looking old’ such as coarse wrinkling and a sallow, leathery texture.

“There is strong evidence suggesting cigarette smoke has a negative effect on the appearance of skin.

“Smoking enhances an enzyme in the skin, matrix metalloproteinase-1, resulting in increased collagen breakdown and diminished collagen production. The overall effect causes wrinkling and inelasticity.

“In addition the constriction of tiny blood vessels in the skin caused by smoking reduces the oxygen supply to the skin negatively affecting skin health and appearance in general.”

Amanda Sandford, of Action on Smoking and Health (ASH) said: “This study provides further evidence of the detrimental effects that smoking can have on the skin.

“No amount of anti-ageing cream will remove the wrinkles caused by cigarettes so the best way for smokers to avoid the wrinkled prune look is to stop smoking.”

Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/1/hi/health/6466041.stm

Published: 2007/03/21 00:03:21 GMT

Filed under: Drug use-various effects,Health,Nicotine :

Research Summary
A pair of new studies find that smokers take many more sick days annually than nonsmokers and perform worse when they are on the job, Bloomberg News reported March 29.
A Swedish study by Petter Lundborg and colleagues from Free University of Amsterdam found that smokers took an average of 34 sick days per year, compared to 20 per year for people who never smoked and 25 per year among former smokers.
Sweden has one of the highest rates of sickness absence in the industrialized world; in the U.S., the average worker takes off nine days annually for illness. “The results suggest that policies that reduce and/or prevent smoking may also reduce the number of days of sick leave,” wrote Lundborg.
In a study of women in the U.S. Navy, San Diego State University researcher Terry Conway and colleagues found that smokers were more likely to be discharged for medical reasons, bad behavior, misconduct, drug misuse and personality disorders. Smokers also were more apt to resign from the Navy before serving their full terms, and were paid less.
However, noted Conway, “Cigarette smoking might simply be a marker for other underlying factors such as nonconformity and high risk-taking, that contribute to poorer performance.”
The research was published in the journal Tobacco Control.

Source: Bloomberg News March 29 2007

Filed under: Brain and Behaviour,Nicotine :

Research Summary

Smoking among young adults has plummeted since California implemented a groundbreaking tobacco-control plan 12 years ago, according to new research from the University of California at San Diego.

The California Tobacco Control Program, established in 1989, has been credited with reducing smoking among all adult smokers, but the decline among young adults has been especially striking, researchers said. Notably, cessation rates among young Californians were higher than among young adults in New York and New Jersey, which have similarly high tobacco prices but lack comprehensive stop-smoking campaigns, as well as compared to young adults in tobacco-growing states (TGS).

“We were surprised to find that, since the advent of the California campaign, young people have increased their rate of quitting by 50 percent, far more than their older counterparts,” said study author Karen Messer, Ph.D. “It used to be that smokers over age 50 were the ones quitting because they understood the health consequences of smoking …
“These young adults have grown up in a tobacco-controlled climate, where smoking isn’t the norm and isn’t socially supported. We may be seeing the first generation who believe it’s not cool to smoke, which could pay huge dividends in their future health.”

Another UCLA study focused on tobacco consumption trends. “We found that there is a national trend of declining cigarette consumption for all age groups, but the most significant by far was observed in California smokers over age 35,” noted researcher Wael K. Al-Delaimy, M.D., Ph.D.
“The data suggest that — compared with states with no tobacco control initiatives (TGS) or states with an increased cigarette price as the principal tobacco control measure (NY/NJ) – California’s comprehensive tobacco control program is more effective in decreasing cigarette consumption for those over age 35.”

Source: journal Tobacco Control April 2007

Filed under: Addiction,Nicotine,Treatment and Addiction,Youth :

A prescription-only pill with a high success rate in helping people to quit smoking is to become available on the NHS after a decision yesterday by the government’s drugs watchdog.
The National Institute for Clinical Excellence gave draft approval for the health service to provide varenicline, which is manufactured by Pfizer under the brand name Champix. Trials showed the twice-daily pill provided relief from cravings and withdrawal symptoms experienced by smokers in the weeks after quitting.

The manufacturers said it also reduced the satisfaction smokers would get from cigarettes in the event of a relapse.
During the trials, 44% of smokers had quit by the end of a 12-week course. This compared with a 30% success rate for the anti-smoking drug Zyban and 18% for smokers who were given a placebo.
The recommended 12-week course of treatment costs about £163.80.
Giving draft approval allows NHS trusts or professional bodies to register objections before a decision in July. NHS trusts would then have three months to make funding available. A spokeswoman for Nice said: “Having looked at all the evidence, our independent committee has concluded that varenicline appears to be a good way to help people who want to quit smoking.”
Robert West, professor of health psychology at University College London, said: “This guidance gives smokers who are serious about stopping another choice from a good range of clinically proven treatments. Smokers who combine treatments with the right support…could significantly increase their odds of successfully quitting for life.”

Source Thursday May 31, 2007 The Guardian

Filed under: Nicotine,Treatment and Addiction :

Nicotine reaches the brain as quickly as 10 seconds after inhalation, triggering feelings of pleasure, increasing heart rate and raising blood pressure.
But alongside the nicotine, smokers breathe in a deadly cocktail of chemicals including arsenic, formaldehyde and polonium.
“Cigarette smoke contains at least 69 different cancer-causing chemicals and thousands of other poisons which can increase the risk of several different types of cancer,” said Ed Yong of Cancer Research.
“Nicotine itself doesn’t cause cancer, it just keeps the smokers hooked,” he added.
Tobacco is so addictive that doctors writing in the Lancet medical journal this year said it should be classified as an illegal drug, on a par with amphetamines and barbiturates.
The government says 70 per cent of smokers want to give up but are held back by the power nicotine has over them.
Only one in five who try quitting manage to abstain for a year, while just three per cent succeed in breaking the habit by willpower alone, according to statistics compiled by health charity Action on Smoking and Health (ASH).
One in six smokers say they light up within five minutes of waking up, with half having their first cigarette inside the first 30 minutes of the day.
The government says 106,000 people die a year in Britain from smoking-related illnesses.
From July 1 smoking is banned in enclosed public spaces across all of the United Kingdom when England introduces its own prohibition to match those already in place in Scotland, Wales and Northern Ireland.
But while this may help many adults give up, there are some groups who will need much greater assistance, says ASH.
Around a quarter of all adults smoke but among the most disadvantaged, such as single parents on benefit, the rates are as high as 70 per cent.
“It’s a response to stress,” said ASH director Deborah Arnott. “If your life is very stressful then smoking seems to help in some way.”
She said such disadvantaged groups should be prescribed nicotine patches for longer periods than the usual maximum of 12 weeks to help them quit.
“It’s the nicotine they are addicted to, but it’s the smoke that’s killing them,” she said.
Prime Minister Gordon Brown cut the value added tax on nicotine replacement products to five per cent in his last budget as chancellor of the exchequer.
The tax break will last for a year but ASH says the price reduction should be made permanent to help the most addicted and disadvantaged.

Source: www.smh.com.au June 30, 2007

Filed under: Addiction,Nicotine :

November 9, 2006

Men diagnosed with cancer are less likely to survive the disease if they were smokers or heavy drinkers. Smoking and drinking are well-known risk factors for cancer, but researchers have begun looking into how these addictions affect survivability, as well. Researcher Young Ho Yun and colleagues at the National Cancer Center in Goyang, South Korea tracked 14,578 cancer patients for about nine years and compared mortality data to patients’ history of smoking and alcohol use.
The researchers found that former smokers were more likely to die from any kind of cancer than nonsmoking cancer patients, possibly because smoking causes tumors to grow more aggressively. Smokers also may be less likely to get cancer screening tests, the authors noted, so their disease is often further advanced when treatment begins.
Among patients with head, neck, or liver cancer, heavy drinkers were more likely to die than nondrinkers, with risk increasing with consumption levels.
“Our findings suggest that groups at high risk of cancer need to be educated continually to improve their health behaviors — not only to prevent cancer, but also to improve prognosis,” the study authors noted.

Source: Journal of Clinical Oncology Nov. 1, 2006.

Reference:
Park, S.M., Lim, M.K., Shin, S.A., Yun, Y.H. (2006) Impact of Prediagnosis Smoking, Alcohol, Obesity, and Insulin Resistance on Survival in Male Cancer Patients: National Health Insurance Corporation Study. Journal of Clinical Oncology, 24(31): 5017-5024.

Filed under: Alcohol,Drug use-various effects,Health,Nicotine :

The truth youth anti-smoking campaign has the power to save hundreds of thousands of lives and billions of dollars in smoking related health care costs and productivity losses, according to the Citizens’ Commission to Protect the Truth, a group composed of every former U.S. Secretary of Health, Education and Welfare and Health and Human Services with the exception of Michael Leavitt; every former U.S. Surgeon General; and every former Director of the Centers for Disease Control and Prevention.
A recent study published in the American Journal of Preventive Medicine indicated that the medical care costs averted by the truth® campaign – due to prevention of smoking – were far greater than the costs of the campaign itself and found that for every dollar invested in truth®, it is estimated that society saved over $6.80. The study focused on the period of 2000–2002. During this period of time, the truth® campaign has been credited with reducing the number of children and teen smokers by 300,000.
We believe that if the truth® campaign continues for another five years (2009-2014) with similar effectiveness, there will be up to 500,000 fewer youth smokers with savings of up to $9.0 billion in future medical costs.
The Commission based its analysis on the findings of the study presented in the May 2009 issue of the American Journal of Preventive Medicine, which found that the decrease in the number of youth who initiated smoking as a result of truth® during the period of 2000–2002 may result in averting up to $5.4 billion in future medical costs.
According to the U.S. Centers for Disease Control and Prevention, one-third of young smokers will die prematurely from smoking-related diseases. Since 80% of adult smokers began using tobacco products before the age of 18, the hundreds of thousands of children who opt not to smoke because of their exposure to truth® will almost certainly not become adult smokers.
“Ending smoking by American children and teens is crucial to the health and cost of healthcare to our nation. The truth® campaign provides a return on investment that would make the greediest corporate CEOs salivate. The truth® campaign is one of the most effective investments in the history of public health,” said Joseph A. Califano, Jr., Commission Chairman and former U.S. Secretary of Health, Education, and Welfare who started the national anti-smoking campaign in 1978. “truth® is the only national smoking prevention campaign not directed by the tobacco industry which exposes the tactics of the tobacco industry, the truth about addiction, and the health effects and social consequences of smoking.”
The American Legacy Foundation’s life-saving truth® campaign is the largest national youth smoking prevention campaign and an extraordinary public health story. The campaign is a national peer-to-peer intervention that works. In its first two years, truth® was responsible for 22% of the overall decline in youth smoking—a decrease which represents approximately 300,000 fewer smokers. Peer reviewed studies, both old and new, underscore that truth® can inoculate teens against tobacco addiction. The truth® campaign’s successes are unassailable.
Source : Citizens Commission to Protect the Truth April 19, 2009

Filed under: Nicotine,Prevention and Intervention,Youth :

Nicotine addiction relies on brain receptors that have been difficult to fully study and characterize. Scientists at the University of Colorado in Boulder have demonstrated that an immunolabeling technique can effectively analyze receptor subunits.

Background: Nicotine’s effects on the brain are triggered upon its binding to nicotinic acetylcholine receptors, each of which consists of five subunits: two alphas, one beta, one delta and one gamma. Different combinations of these subunits produce different receptor subtypes, which may vary in their pharmacology, biophysical properties, and distribution. To more fully understand how to interfere with nicotine’s effects in the brain, scientists must first understand where these different receptors are and how they work. Two of the most important subunits, a4 and b2, have been hard to study because current study methods can only locate the fully assembled receptor unit. Researchers wanted to know if an alternative strategy of immunolabeling (i.e., using antibodies to tag individual proteins), which has been fraught with technical challenges, would be able to identify, map, and quantify separate subunits.

Study Design: Scientists at the University of Colorado worked with brain sections of mice genetically engineered to express particular a4 and b2 subunit combinations. Using a sensitive immunolabeling technique, they explored the expression of the a4 and b2 subunits at both the gene and protein levels. Additional mice strains, missing the subunits under study, were used as controls.

What They Found: The two predominant nicotinic receptor subtypes (a4 and b2) were reliably detected using immunolabeling. Expression of the a4 subunit protein was almost universally dependent on b2, whereas most, but not all, b2 subunit protein expression was a4-dependent.

Comments from the Authors: Immunolabeling using specific antibodies offers a powerful approach for mapping the distribution of nicotine receptor subunits and can produce reliable quantitative results.

What’s Next: Similar studies can be designed to locate other nicotine receptor subtypes. In many cases, the antibody recognition sites are inside the cell membrane. It will likely take alternative biochemical approaches to uncover these less accessible sites. A better understanding of receptor composition and function may eventually have important implications for developing interventions at the receptor level.

Source: The study, led by Dr. Paul Whiteaker of the Institute for Behavioral Genetics at the University of Colorado, Boulder, with Dr. Jon Lindstrom of the University of Pennsylvania, was published in volume 499, number 6, pages 1016-1038 (2006) of the Journal of Comparative Neurology.

Filed under: Addiction,Brain and Behaviour,Nicotine :

Research Summary
There is compelling evidence that second hand smoke can trigger heart attacks, according to a new report from the Institute of Medicine (IOM), and people with heart conditions are urged to avoid exposure to tobacco smoke, the Associated Press reported Oct. 15.
The report, requested by the U.S. Centers for Disease Control and Prevention (CDC), said there is no safe level of exposure to second hand smoke, and that people with cardiovascular disease could risk heart attack with less than an hour’s exposure to environmental tobacco smoke, which restricts blood vessels and increases clotting.
“If you have heart disease, you really need to stay away from second hand smoke. It’s an immediate threat to your life,” said researcher Neal Benowitz of the University of California at San Francisco.
Benowitz added that everyone, in fact, should avoid second hand smoke, since many people who have heart disease are not aware of the problem if they have never had a heart attack. “Even if you think you’re perfectly healthy, second hand smoke could be a potential threat to you,” he said.
“The evidence is clear,” said CDC head Thomas Frieden. “Smoke-free laws don’t hurt business … but they prevent heart attacks in non-smokers.”
Researchers found “clear and consistent” evidence that smoking bans cut the rate of heart attacks, according to statistician Stephen Feinberg of Carnegie Mellon University, a member of the IOM committee that compiled the report.
Source: Associated Press Oct.15th 2009

Filed under: Health,Nicotine :

Research Summary
A recent University of California at Riverside study found that second hand smoke from tobacco can lead to nonalcoholic fatty liver disease (NAFLD), which can cause fat to accumulate in the liver of people even if they drink moderately or don’t drink alcohol at all.
Researchers studied mice exposed to second hand smoke for a year and found that fat accumulated in their liver cells, a sign of NAFLD.
The researchers focused their attention on two main fat metabolism regulators that are also found in human cells: the protein that stimulates synthesis of fatty acids in the liver and AMPK (adenosine monophosphate kinase), which regulates that protein. They found that AMPK activity is inhibited when exposed to second hand smoke, leading the other protein to synthesize more fatty acids. The result is NAFLD, according to the report.
“Our study provides compelling experimental evidence in support of tobacco smoke exposure playing a major role in NAFLD development,” said Manuela Martins-Green, who led the study.
Source: Journal of Hepatology September 2009.

Filed under: Health,Nicotine :

The heart attack rate fell 10 percent in England and 14 percent in Scotland after the U.K. countries imposed bans on public smoking, the Similar results are expected from a study in Wales.
“We always knew a public smoking ban would bring rapid health benefits, but we have been amazed by just how big and how rapid they are,” said John Britton, director of the U.K. Center for Tobacco Control Studies at Nottingham University. The research is expected to boost calls for further curbs on secondhand smoke, such as banning smoking in cars with children.
“Exposure to cigarette smoke induces rapid changes in blood chemistry, making it much more prone to clotting,” explained Ellen Mason, a senior cardiac nurse at the British Heart Foundation. “In someone who has narrowed or damaged coronary arteries, smoke exposure can tip the balance and cause a heart attack.”
The findings echo those in other nations where public smoking has been banned, such as France, Ireland and Italy.

Source: Sunday Times reported Sept. 13th.2009

Filed under: Health,Nicotine :

Research Summary
A genetic study has found that children who were exposed to secondhand smoke are more likely to develop lung cancer as adults, according to researchers from the National Cancer Institute and the Mayo Clinic.
Childhood exposure to secondhand smoke raised lung-cancer risk even among study subjects who never smoked themselves. Researchers drew their conclusions in part from analysis of a gene called MBL2, known to increase susceptibility to respiratory diseases.
Source: Cancer Epidemiology, Biomarkers and Prevention. December 2009

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

Research Summary
Continuing to use nicotine patches or gums after cancer surgery — to say nothing of smoking — makes chemotherapy less effective, according to researchers at the University of South Florida.
The Associated Press reported April 2 that a study of lung-cancer patients found that nicotine appears to protect cancer cells from chemotherapy drugs like gemcitabine, cisplatin, and taxol. Srikumar Chellappan of the University of South Florida and colleagues studied the impact of nicotine on non-small cell lung cancer, the most common form of the disease.
“Our findings are in agreement with clinical studies showing that patients who continue to smoke have worse survival profiles than those who quit before treatment,” the study noted. “They also raise the possibility that nicotine supplementation for smoking cessation might reduce the response to chemotheraputic agents.”
Source: The research appears in the online edition of Proceedings of the National Academy of Sciences. Reported in Join Together April 2006

Filed under: Health,Nicotine :

Babies born to women who smoke during pregnancy are more likely to have heart defects that are not related to genetics, Reuters reported April 9.
Researcher Sadia Malik of the University of Arkansas for Medical Sciences and colleagues compared more than 3,000 infants born with heart defects to a similar group of infants without heart problems. They found that heart defects were more common among children of women who smoked during the month before they became pregnant or during the first trimester of their pregnancy. Moreover, the risk of babies being born with heart problems was higher when mothers smoked more.
“If even a fraction of congenital heart defects and other birth defects could be prevented by decreasing maternal tobacco use, it would result in improved reproductive outcomes and a saving of millions of health care dollars,” the researchers said.
Source: April 2008 issue of the journal Pediatrics.

Filed under: Drug use-various effects on foetus, babies, children and youth,Nicotine :

A new study found a link between secondhand smoke and sudden infant death syndrome (SIDS), the Toronto Globe and Mail reported Feb. 21.
The study was conducted by researchers at Toronto’s Hospital for Sick Children and the University of Maryland.
In analyzing 44 SIDS deaths, researchers found twice the amount of nicotine levels in the lung tissue of babies whose parents acknowledged that they were smokers than in babies who died of other causes.
“It’s biochemical proof that smoke is associated with SIDS,” said Gideon Koren, lead investigator and senior scientist at the hospital’s research institute. “Some parents may feel guilty, and probably we underestimate the contribution of smoking to the risk of SIDS.”
Koren said additional research is needed to determine which of the toxic substances in tobacco smoke increases the risk for SIDS.
The study’s findings also are raising questions as to whether parents should be held responsible for exposing their babies to tobacco-filled air at home.
“In light of this new research, we and other agencies will be looking at it and rethinking our position to see if a stronger position is more feasible,” said Gail Vandermeulen of the Ontario Association of Children’s Aid Societies.
Source: Journal of Pediatrics February. 2002

Filed under: Drug use-various effects on foetus, babies, children and youth,Nicotine :

The children of women who smoke during pregnancy are at increased risk of suffering strokes or heart attacks later in life, a new study concludes.
Reuters reported March 2 that children of smokers — studied as young adults — were found to have thicker walls around the carotid arteries in their necks, making them more vulnerable to stroke and heart attacks. Children of women who smoked the most during pregnancy had the thickest arterial walls, researchers found.
“There is the possibility that the compounds in tobacco smoke go through the placenta and directly damage the cardiovascular system of the fetus,” said researcher Cuno Uiterwaal at the University Medical Center Utrecht in the Netherlands. “The damage appears to be permanent and stays with the children.”
Source: Findings presented at a recent American Heart Association conference in Orlando. March 5, 2007

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

A study from the United Kingdom finds that children of mothers who smoke have smaller lung volumes and are more at risk for serious lung disease later in life, Reuters reported Feb. 26.
The study by researchers at the University of Bristol and the University of Glasgow involved 2,000 men and women in their 30s, 40s, and 50s whose parents smoked and took part in a study in the 1970s.
After conducting respiratory tests, the researchers found that children of mothers who smoked had smaller lungs, regardless of whether they also smoked. In addition, these children were more at risk for chronic obstructive pulmonary disease (COPD). If they themselves smoked, the risk was as high as 70 percent.
“Our results suggest that the effects of maternal smoking on lung size are permanent,” said Dr. Mark Upton, lead author of the study.
Children from households where the father smoked, but not the mother, showed poorer lung function, but not as great as those whose mothers smoked.
Source: American Journal of Respiratory and Critical Care Medicine. Feb. 15, 2004

Filed under: Drug use-various effects on foetus, babies, children and youth,Nicotine :

Children exposed to secondhand smoke at home are more likely to carry the streptococcus pneumonia bacteria in their nose and throat, according to Israeli researchers.
A study involving more than 200 children and their mothers found that 76 percent of children exposed to secondhand smoke carried the bacteria in their noses and throats, compared to 60 percent of those not exposed to smoking. The bacteria can cause minor illnesses like ear infections or more dangerous conditions like sinusitis, pneumonia, and meningitis.
Among the mothers, 32 percent of smokers carried the bacteria, compared to 15 percent of nonsmokers exposed to tobacco smoke and 12 percent of nonsmokers not exposed to secondhand smoke.
“Since carriage in the nose is the first step in causing disease, the increased rate of carriage suggests more frequent occurrence of the disease. Indeed, active and passive smoking are associated with increased rate of respiratory infectious diseases,” said lead study author David Greenberg, M.D. “This should definitely encourage the parents not to smoke in the presence of their child, especially if this child has predisposing factors such as asthma.”
Source: Clinical Infectious Diseases. April 1, 2006

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

Researchers have found that infants as young as three months old accumulate nicotine and carcinogens in their bodies when they are exposed to tobacco smoke, the Guardian reported May 12.
Authors of the study — the first to test smoking exposure on children so young — said that parents who smoking around infants could raise children’s’ risk of addiction, cancer, and other health problems later in life. “The take-home message is that parents should not smoke around their children, because they will suffer from the exposure,” said Stephen Hecht of the University of Minnesota cancer center.
The study of 144 children (ages three months to one year) who lived with family members who smoked found that 98 percent had nicotine in their urine, and 93 percent had cotinine, a marker for nicotine metabolism. Further, 47 percent of the infants had detectable levels of NNAL, a carcinogenic metabolite of cigarette smoke.
“Persistent exposure to environmental tobacco smoke in childhood could be related to cancer later in life,” said Hecht
Source: Cancer Epidemiology Biomarkers and Prevention. May 2006

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

Infants with at least one parent who smokes have higher levels of a nicotine metabolite in their bodies than the children of nonsmokers, the Guardian reported June 19.
Researchers from the University of Leicester and Warwick Medical School said the study showed that smoking parents are turning their infants into passive smokers, putting them in danger of breathing problems and crib death. “Babies and children are routinely exposed to cigarette smoke by their [caregivers] in the home without the legislative protection available to adults in public places,” the authors stated.
Babies whose mothers smoked had cotinine levels four times higher than children whose parents were both nonsmokers, while babies with fathers who smoked had cotinine levels twice as high.
Cotinine levels were higher among babies who shared a bed with their parents, and during the winter. “Higher cotinine levels in colder times of year may be a reflection of the other key factors which influence exposure to passive smoking, such as poorer ventilation or a greater tendency for parents to smoke indoors in winter,” the authors said.
Source: Archives of Diseases in Childhood. June 2007

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

Research Summary
Within five years of quitting former female smokers have no greater risk of dying from coronary heart disease than nonsmokers, according to a new study.
HealthDay News reported May 6 that while risk for other smoking-related health problems lingers longer, heart health seems to bounce back more quickly.
Lung-cancer risk persisted 30 years after quitting, however, and former smokers face higher odds of dying from chronic obstructive pulmonary disease for more than 20 years after quitting, the study found.
The study was conducted by researcher Stacey Kenfield of the Harvard School of Public Health and colleagues. “It’s never too early to stop, and it’s never too late to stop,” said Kenfield.
“This shows the power of quitting smoking,” said Jay Brooks, study co-author and chairman of hematology/oncology at Ochsner Health System in Baton Rouge, La. “We’ve known this for a number of years, but the beauty of this study is it is a very large and well-studied group of people. When I tell people to quit smoking, I say the effect of the heart precedes that of the lungs. If you’ve smoked, you need to be cognizant that you’re still at an increased risk of lung cancer.”
Source: May 7, 2008 issue of the Journal of the American Medical Association.

Filed under: Health,Nicotine :

• Compared to 12- and 13-year olds who have frequent family dinners, those who have infrequent family dinners are six times likelier to use marijuana, four times likelier to use tobacco, and three times likelier to use alcohol.
• Compared to teens who attend religious services at least weekly, those who never attend services are more than twice as likely to try cigarettes, and twice as likely to try marijuana and alcohol.
• Compared to teens who have frequent family dinners, those who have infrequent family dinners are one and a half times likelier to report getting grades of C or lower in school.

Source: www.casacolumbia.org Sept.2009

Filed under: Alcohol,Cannabis/Marijuana,Drug use-various effects on foetus, babies, children and youth,Health,Nicotine,Parents,Prevention and Intervention :

A recent study published in the Journal of Epidemiology and Community Health has revealed that women who continue to smoke during pregnancy are more likely to have children with behavioral problems. Disturbances caused can show signs as early as when the child is three years old.
For the sake of the study, over 14,000 mothers and child pairs were observed. The pairs were picked from the millennium cohort study. All the children observed had been born between 2000 and 2001. Professor Kate Pickett from the Hull York medical school, University of York, carried out the research.
Mothers, who were categorized as light or heavy smokers with regards to the number of cigarettes they smoked each day during pregnancy, were given a questionnaire which required them to score their children’s behavior. While 12.5% women said they smoked lightly and 12.4% said they had stopped smoking altogether when pregnant, 10% admitted to smoking heavily all throughout the term.
Based on the data collected, the study confirmed that children whose mothers smoked heavily were two times more prone to behavioral problems, a thing which kept going down as the number of cigarettes smoked during pregnancy went down. According to the study, smoking when pregnant, damages the developing structure and functioning of the fetus’s brain. Boy fetuses are more prone to damage.
Source:www.topnews.net.nz 3/11/2009

Filed under: Drug use-various effects on foetus, babies, children and youth,Nicotine,Parents :

Men diagnosed with cancer are less likely to survive the disease if they were smokers or heavy drinkers, Reuters reported Nov. 7.
Smoking and drinking are well-known risk factors for cancer, but researchers have begun looking into how these addictions affect survivability, as well. Researcher Young Ho Yun and colleagues at the National Cancer Center in Goyang, South Korea tracked 14,578 cancer patients for about nine years and compared mortality data to patients’ history of smoking and alcohol use.
The researchers found that former smokers were more likely to die from any kind of cancer than non-smoking cancer patients, possibly because smoking causes tumors to grow more aggressively. Smokers also may be less likely to get cancer screening tests, the authors noted, so their disease is often further advanced when treatment begins.
Among patients with head, neck, or liver cancer, heavy drinkers were more likely to die than non-drinkers, with risk increasing with consumption levels.
“Our findings suggest that groups at high risk of cancer need to be educated continually to improve their health behaviors — not only to prevent cancer, but also to improve prognosis,” the study authors noted.
The research appears in the Nov. 1, 2006 issue of the Journal of Clinical Oncology.

Filed under: Drug use-various effects,Nicotine,Others (International News) :

A tiny genetic mutation is the key to understanding why nicotine–which binds to brain receptors with such addictive potency–is virtually powerless in muscle cells that are studded with the same type of receptorBy all rights, nicotine ought to paralyze or even kill us, explains Dennis Dougherty, the George Grant Hoag Professor of Chemistry at Caltech and one of the leaders of the research team. After all, the receptor it binds to in the brain’s neurons–a type of acetylcholine receptor, which also binds the neurotransmitter acetylcholine–is found in large numbers in muscle cells. Were nicotine to bind with those cells, it would cause muscles to contract with such force that the response would likely prove lethal. Obviously, considering the data on smoking, that is not what happens. The question has long been: Why not?

“It’s a chemical mystery,” Dougherty admits. “We knew something subtle had to be going on here, but we didn’t know exactly what.” That subtlety, it turns out, lies in the slight tweaking of the structure of the acetylcholine receptor in muscle cells versus its structure in brain cells.
The shape of the acetylcholine receptor, and the way the chemicals that bind with it contort themselves to fit into that receptor, is determined by a number of different weak chemical interactions. Perhaps most important is an interaction that Dougherty calls “underappreciated”–the cation-π interaction, in which a positively charged ion and an electron-rich π system come together.

Back in the late 1990s, Dougherty and colleagues had shown that the cation-π interaction is indeed a key part of acetylcholine’s ability to bind to the acetylcholine receptors in muscles. “We assumed that nicotine’s charge would cause it to do the same thing, to have the same sort of strong interaction that acetylcholine has,” says Dougherty. “But we found that it didn’t.”
This would explain why smoking doesn’t paralyze us; if the nicotine can’t get into the muscle’s acetylcholine receptors, it can’t cause the muscles to contract.

But how, then, does nicotine work its addictive magic on the brain? It took another decade for the scientists to be able to peek at what happens in brain cells’ acetylcholine receptors when nicotine arrives on the scene. Turns out that in brain cells, unlike in muscle cells, nicotine makes the exact same kind of strong cation-π interaction that acetylcholine makes in both brain and muscle cells. “In addition,” Dougherty notes, “we found that nicotine makes a strong hydrogen bond in the brain’s acetylcholine receptors. This same hydrogen bond, in the receptors in muscle cells, is weak.”

The cause of this difference in binding potency, says Dougherty, is a single point mutation that occurs in the receptor near the key tryptophan amino acid that makes the cation-π interaction. “This one mutation means that, in the brain, nicotine can cozy up to this one particular tryptophan much more closely than it can in muscle cells,” he explains. “And that is what allows the nicotine to make the strong cation-π interaction.”

Dougherty says the best way to visualize this change is to think of the receptor as a box with one open side. “In muscle cells, this box is slightly distorted, so that the nicotine can’t get to the tryptophan,” he says. “But in the brain, the box is subtly reshaped. That’s the thing: It’s the shape, not the composition, of the box that changes. This allows the nicotine to make strong interactions, to become very potent. In other words, it’s what allows nicotine to be addictive in the brain.”

“Several projects in our labs are converging on the molecular and cellular mechanisms of the changes that occur when the brain is repeatedly exposed to nicotine,” adds study coauthor Henry Lester, the Bren Professor of Biology at Caltech. “We think that the important events begin with the rather tight and selective interaction between nicotine and certain receptors in the brain. This Nature paper teaches us how this interaction occurs, at an unprecedented level of resolution.”
Dougherty notes that these findings might one day lead to better drugs to combat nicotine addiction and other neurological disorders. “The receptor we describe in this paper is an important drug target,” he says. “It might help pharmaceutical companies develop a better drug than nicotine to do the good things nicotine does–enhance cognition, increase attention–without being addictive and toxic.”

Source: Xiu et al. Nicotine binding to brain receptors requires a strong cation–π interaction. Nature, March 26, 2009; DOI: 10.1038/nature07768 Science Daily 29.03.09

Filed under: Addiction,Brain and Behaviour,Nicotine :

The National Cancer Institute (NCI) released a report today, co-edited by University of Minnesota professor Barbara Loken, that reaches the government’s strongest conclusion to date that tobacco marketing and depictions of smoking in movies promote youth smoking. “There is now incontrovertible evidence that marketing of tobacco, and the depiction of smoking in the movies, promote youth smoking and can cause young people to begin smoking,” said Loken, professor of marketing at the Carlson School of Management and one of the report’s five scientific editors.
The 684-page monograph, “The Role of the Media in Promoting and Reducing Tobacco Use,” presents definitive conclusions that a) tobacco advertising and promotion are causally related to increased tobacco use, and b) exposure to depictions of smoking in movies causes youth smoking initiation. The report also concludes that while mass media campaigns can reduce tobacco use, youth smoking prevention campaigns sponsored by the tobacco industry are generally ineffective and may even increase youth smoking.
“The role of marketing in the success of the tobacco companies is conclusive,” according to Loken. “The report’s recommendations offer the best approach to employ marketing techniques and the media to help prevent a further increase in youth smoking.”
The NCI report reaches six major conclusions:
1. Cigarettes are one of the most heavily marketed products in the United States.
2. Tobacco advertising targets psychological needs of adolescents, such as popularity and peer acceptance. Advertising creates the perception that smoking satisfies these needs.
3. Even brief exposure to tobacco advertising influences adolescents’ perceptions about smoking, smokers, and adolescents’ intentions to smoke.
4. The depiction of cigarette smoking is pervasive in movies, occurring in 75 percent or more of contemporary box-office hits, with identifiable brands in about one-third of movies.
5. A comprehensive ban on tobacco advertising and promotion is an effective policy intervention that prevents tobacco companies from shifting marketing expenditures to permitted media.
6. The tobacco industry works hard to impede tobacco control media campaigns, including attempts to prevent or reduce their funding.
“This direct link between marketing and tobacco use is very powerful.” Loken said, “Anti-tobacco ads before films and a comprehensive ban on tobacco advertising are two effective strategies found to curb effects of tobacco images on youth. Now we need to use marketing to steer youth and others away from tobacco.”
The report provides the most current and comprehensive analysis of more than 1,000 scientific studies on the role of the media in encouraging and discouraging tobacco use. The report is Monograph 19 in the NCI’s Tobacco Control Monograph series examining critical issues in tobacco prevention and control. Research included in the review comes from the disciplines of marketing, psychology, communications, statistics, epidemiology and public health.Source: National Cancer Institute Report. National Press Club Release 21 August

Filed under: Nicotine,Youth :

New research suggests that it takes less exposure to tobacco to increase the risk of colorectal cancer among women than men.
Researchers Joseph C. Anderson, M.D., of the University of Connecticut and Zvi A. Alpern, M.D. of Stony Brook University conducted a large cross-sectional study, analyzing data on patients who underwent colonoscopies. Utilizing a measurement called “pack years” — determined by multiplying the number of cigarettes smoked per day by the number of years smoked — researchers compared the amount of tobacco exposure in men and women to increased colorectal cancer risk.
The analysis, controlling for age, body mass index and family history, showed that women who smoked up to 30 pack-years had an 82 percent greater risk for significant colorectal neoplasia than nonsmoking women, while men who smoked up to 30 pack-years showed 21 percent greater risk than nonsmoking men. Female smokers faced double the risk or more of colorectal cancer if they smoked less than 30 pack years, while men achieved the same level of risk only when they smoked more than 30 pack years.
The study was presented at the American College of Gastroenterology’s annual scientific meeting.

Source: Reported in Join Together Oct. 7 2008

Filed under: Drug use-various effects,Health,Nicotine :

Research SummaryJust as smoking causes hardening of the arteries, quitting smoking can improve arterial health, although recovery from arterial stiffness may take up to a decade, Reuters reported March 19.
Researcher Noor Ahmed Jatoi and colleagues compared current smokers, ex-smokers and people who never had smoked. “We categorized ex-smokers according to how long they were off cigarettes — under one year, more than one but less than 10 years and more than 10 years,” said Jatoi.
The researchers found that arterial health improved over with time once smokers quit, but only reached normal levels after more than a decade of abstinence.
The study was published in the journal Hypertension.

Source: Reported in Join Together March 23 2007

Filed under: Nicotine :

Research Summary

Continuing to use nicotine patches or gums after cancer surgery — to say nothing of smoking — makes chemotherapy less effective, according to researchers at the University of South Florida.
The Associated Press reported April 2 that a study of lung-cancer patients found that nicotine appears to protect cancer cells from chemotherapy drugs like gemcitabine, cisplatin, and taxol. Srikumar Chellappan of the University of South Florida and colleagues studied the impact of nicotine on non-small cell lung cancer, the most common form of the disease.
“Our findings are in agreement with clinical studies showing that patients who continue to smoke have worse survival profiles than those who quit before treatment,” the study noted. “They also raise the possibility that nicotine supplementation for smoking cessation might reduce the response to chemotheraputic agents.”
The research appears in the online edition of Proceedings of the National Academy of Sciences.

Source:Reported in Join Together April 2006

Filed under: Nicotine,Treatment and Addiction :

PURPOSE: To determine the risk for malignant primary adult-onset glioma (MPAG) associated with cigarette smoking and other lifestyle behaviors in a large, multiethnic, managed-care cohort. METHODS: The study population included a cohort of 133,811 subscribers to the Kaiser Permanente Medical Care Program of Northern California who had received a multiphasic health checkup and questionnaire between 1977 and 1985, were at least 25 years old at their start of follow-up, and had no prior history of benign or malignant brain tumors. In this cohort, patients were followed for up to 21 years for the development of MPAG. RESULTS: Risk for MPAG among women increased with increasing packs of cigarettes smoked per day (p-for-trend = 0.04), adjusting for cigar and pipe smoking, patient age, sex, race, education, alcohol use and coffee consumption. A similar pattern was not observed for men. Individuals who smoked marijuana at least once a month, adjusting for cigarette smoking (packs smoked per day) and for the factors noted above, had a 2.8-fold (CI = 1.3-6.2) increased risk for MPAG. Relative risk for MPAG increased with increasing consumption of coffee (p-for-trend = 0.05). CONCLUSIONS: Cigarette smoking was associated with an increased risk for MPAG among women but not among men. Individuals who smoked marijuana at least once a month had an increased risk for MPAG, although no dose-response relation was observed. Drinkers of >7 cups of coffee per day had a 70% increased risk for MPAG and smaller risk elevation for lower consumption. Alcohol usage was not associated with an increased risk for MPAG.
Source: J Neurooncol. 2004 May;68(1):57-69

Filed under: Health,Nicotine :

In a new study, researchers have determined that prenatal exposure to cigarette smoking, when combined with a specific genetic variant, places children at increased risk for aggressive behavior and other behavioral problems.
The study, led by scientists at the Institute for Juvenile Research at the University of Illinois at Chicago, identified a long-lasting influence on a child’s behavior precipitated by the monoamine oxidase A (MAOA) gene variant in conjunction with prenatal exposure to tobacco. MAOA is an enzyme which regulates key neurotransmitters in the brain.
The genetic variant responsible for increased risk of behavioral problems differs between boys and girls, researchers said. In boys exposed to tobacco smoke prenatally, the low-activity MAOA (MAOA-L) gene variant was associated with increased disruptive social interactions, aggressive behavior, and serious rule-violating.
Among girls, the high-activity MAOA (MAOA-H) gene variant was associated with increased disruptive behavior. In addition, girls with both the MAOA-H variant and prenatal exposure to cigarette smoke had an increased “hostile attribution bias” — a tendency to perceive anger in a range of facial expressions — that was not seen among boys.
There was a higher risk of disruptive behavior for both boys and girls the more their mother smoked during pregnancy, according to the study.
“The tendency to over-perceive anger suggests the possibility that the combination of prenatal tobacco exposure and the MAOA risk variant affects the brain’s processing of emotional cues,” said Lauren Wakschlag, the study’s principal investigator. “Clearly, close attention to sex differences in these patterns will be critical for future studies,” she said.

Source:Join Together. March 16th 2009

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine,Parents :

Cigarette smoking is more strongly associated with head and neck cancers than drinking alcohol, according to a new study. The study found that smoking is responsible for a quarter of head and neck cancers among individuals who do not drink alcohol.

At least 75 percent of head and neck cancers are caused by a combination of cigarette smoking and drinking alcohol, but researchers have not known the individual contributions of these risk factors because people who smoke are more likely to drink than the general population and vice versa. In a new study, researchers sought to tease out the independent effect of each risk factor on head and neck cancer development.
Mia Hashibe, Ph.D., of the International Agency for Cancer Research in Lyon, France, and colleagues examined head and neck cancer risk among smokers who never drank alcohol and people who drink but never used tobacco products. They pooled data from 15 case–control studies, which included 10,244 head and neck cancer patients and 15,227 controls. About 16 percent of the patients and 27 percent of the controls never drank, and about 11 percent of the patients and 38 percent of the controls never smoked.
Cigarette smoking was associated with an increased risk of head and neck cancer–especially cancer of the larynx–among patients who never drank alcohol. About 24 percent of head and neck cancers were due to smoking among patients who never drank.
Drinking alcohol was also associated with greater risk of head and neck cancers among never smokers, but mainly for patients who drank three or more drinks per day. They had twice the risk of head and neck cancers as people who never drink. Only seven percent of head and neck cancers were due to drinking among never smokers.
“The major strength of our pooled analyses was assembly of a very large series of never users of tobacco and never drinkers among head and neck cancer patients and control subjects, which allowed us to examine head and neck cancer risks in detail and to explore differences in risks by cancer subsite, geographic region, and sex,” the authors write.

Source: Journal of the National Cancer Institute 2007, May 16. 99: 777-789

Filed under: Alcohol,Health,Nicotine :

Research Summary
Teenagers expect and want adults to discourage them from using tobacco, according to new research from the
Researcher Maria Nilsson evaluated the impact of an anti-smoking program, Tobacco-Free Duo, which started in 1993. The program targets children between the ages of 13-15 and includes adults supporting the teenagers in staying tobacco-free.
Nilsson found that smoking rates declined among adolescents in the program over a seven-year period, while no corresponding change was observed at the national level. In addition, one in four tobacco-using adults participating in the program stopped smoking in order to take part.
“Children expect adults to work against tobacco. They say this is important and that grown-ups can make a difference by showing a clear and positive commitment,” said Nilsson.
Survey results on 15-year-old smokers showed that close relationships with caring adults played an important role in getting teenagers to smoke less or stop smoking all together.
Source: Promoting Health in Adolescents: Preventing the Use of Tobacco. Umea University in Sweden, Science Daily reported May 5.

Filed under: Nicotine,Youth :

Smoking appears to be associated with an increased risk of acute and chronic pancreatitis, according to a new report. In addition, the risk of developing the disease may be higher in those who smoke more.

The occurrence of pancreatitis (an inflammation of the pancreas usually characterized by abdominal pain) has increased in recent decades, according to background information in the article. Acute and chronic pancreatitis are believed to be commonly caused by gallstone disease and excessive alcohol use, respectively. Studies have suggested that smoking may be associated with damage to the pancreas, but since smoking may be associated with alcohol use and risk of gallstone disease, it is difficult to note whether smoking is an independent risk factor for the disease.

Janne Schurmann Tolstrup, M.Sc., Ph.D., of the National Institute of Public Health, University of Southern Denmark, Copenhagen, and colleagues analyzed results from physical examinations and lifestyle habit self-administered questionnaires of 17,905 participants (9,573 women and 8,332 men) to determine if smoking was associated with an increased risk of acute or chronic pancreatitis independent of alcohol consumption and gallstone disease. Participants were followed up for an average of 20.2 years.

“Overall, 58 percent of the women and 68 percent of the men were current smokers, 15 percent of the women and 19 percent of the men were ex-smokers and 28 percent of the women and 13 percent of the men had never smoked,” the authors write. “Participants who at baseline reported smoking or being previous smokers had higher risks of developing acute and chronic pancreatitis compared with non-smokers.” By the end of the study, 235 participants (113 women and 122 men) had developed acute (160 cases) or chronic (97 cases) pancreatitis, with some participants having developed both. About 46 percent of pancreatitis cases were attributable to smoking in this group.

Although alcohol intake was associated with increased risk of pancreatitis, the risk of pancreatitis associated with smoking was independent of alcohol and gallstone disease.
“Apart from the epidemiologic evidence of an association between smoking and development of acute and chronic pancreatitis, a biological effect of smoking seems plausible because both animal studies and human studies have demonstrated changes of the pancreas and in pancreatic functioning after exposure to tobacco smoke,” they conclude.
This study was supported by grants from the Danish National Board of Health and the Danish Medical Research Council.

Source: Tolstrup et al. Smoking and Risk of Acute and Chronic Pancreatitis Among Women and Men: A Population-Based Cohort Study. Archives of Internal Medicine, 2009; 169 (6): 603 DOI: 10.1001/archinternmed.2008.601 ScienceDaily (Mar. 28, 2009)

Filed under: Health,Nicotine :

ScienceDaily (Jan. 29, 2005) — Children who are exposed to environmental tobacco smoke (passive smoking) are at a higher risk of developing lung cancer as adults, says a paper in this week’s BMJ.

Those children exposed to passive smoking on a daily basis and for many hours are the most vulnerable – facing over treble (3.63) the risk of those who grew up in smoke-free environments.
Children experiencing passive smoke a few times a week are one and a half (1.45) times more likely to develop lung cancer, and those exposed daily but not for many hours faced twice (2.08) the risk.
In one of the most comprehensive studies into passive smoking of its kind, researchers looked at 303,020 people across Europe who had never smoked, or had stopped smoking by at least ten years. Within this group, 123,479 provided information on exposure to passive smoke, and researchers followed these participants’ progress for an average of seven years.
Of those who had known exposure to passive smoke (but were not smokers themselves), 97 had developed lung cancer, 20 more had upper respiratory cancers such as cancer of the larynx, and 14 died from chronic obstructive pulmonary disease during the seven follow-up years.
Former smokers faced up to twice the risk of respiratory diseases from passive smoke than those who’d never smoked. This may be because their lungs are already damaged, making them more at risk to the effects of environmental tobacco smoke, say the researchers.
This study significantly reinforces previous research into the cancerous effects of passive smoke, the authors conclude.

Source: British Medical Journal (2005, January 29). Passive Smoking In Childhood May Increase Risk Of Lung Cancer In Later Life. ScienceDaily. Retrieved May 12, 2009, from http://www.sciencedaily.com¬ /releases/2005/01/050128223746.htm

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

A new report from Perth’s Telethon Institute for Child Health Research has found a strong link between childhood ear infections and exposure to tobacco smoke.

The families of 100 Aboriginal children and 180 non-Aboriginal children participated in the Kalgoorlie Otitis Media Research Project, allowing the collection of social, demographic, environmental and biological data to investigate the causes of otitis media (middle ear infections). The children had regular ear examinations from birth until 2 years of age.
Chief Investigator Dr Deborah Lehmann, who heads the Institute’s infectious diseases research, said ear infections were the most common reason that young children see a doctor and can cause life-long problems.

“Up to 20 per cent of children have more than three ear infections between 1 and 2 years of age. If their hearing is damaged, it can seriously affect their educational outcomes and social circumstances in adulthood,” Dr Lehmann said.
“In Aboriginal children, these ear infections typically start at a younger age, are much more common and more likely to result in hearing loss.”
Key findings from the project include:
  Otitis media was diagnosed at least once in 74% of Aboriginal children and 45% of non-Aboriginal children.
  64% of Aboriginal children and 40% of non-Aboriginal children were exposed to environmental tobacco smoke.
  If we eliminated exposure to tobacco smoke we estimate that we could reduce ear infections by 27% in Aboriginal children and 16% in non-Aboriginal children
  The impact of passive smoking in the home on ear infections was reduced if the children also attended day care.
Dr Lehmann said there is evidence that passive smoking can increase the adherence of bacteria in the respiratory passages and depress the immune system.
“These results highlight the importance of reducing children’s exposure to passive smoking, and this is particularly important for Aboriginal people where the rates of both smoking and otitis media are high,” she said.

“Few Aboriginal children have access to formal childcare despite studies showing that it is an effective way to improve early development and educational outcomes for disadvantaged children. The fact that it could also reduce the burden of ear infections in Aboriginal children adds weight to calls for appropriate childcare facilities to be provided.”
The results are published in the latest edition of the Medical Journal of Australia.

Source: Telethon Institute for Child Health Research (2008, May 19). Ear Infections In Children Linked To Passive Smoking. ScienceDaily. Retrieved May 12, 2009, from http://www.sciencedaily.com¬ /releases/2008/05/080519110703.htm

Filed under: Drug use-various effects on foetus, babies, children and youth,Health,Nicotine :

Marijuana worsens breathing problems in current smokers with chronic obstructive pulmonary disease (COPD), according to a new study. The study found that among people 40 and older, smokers were two-and-a-half times as likely as nonsmokers to develop COPD, while smoking cigarettes and marijuana together boosted the odds of developing COPD to three-and-a-half times the risk of someone who did not smoke either cigarettes or marijuana–in other words, adding marijuana smoking to cigarette smoking increased the risk by one-third, says Wan Tan, M.D., of St. Paul’s Hospital in Vancouver, British Columbia.
The odds of cigarette smokers having any respiratory symptoms was 2.36 times that of nonsmokers, while the odds of someone who smoked both cigarettes and marijuana having respiratory symptoms was 18 times that of someone who smoked neither–an eightfold jump in risk, Dr. Tan says.
“This study suggests an interaction between cigarettes and marijuana smoking. These findings have not been reported before, and they have a big public health implication,” Dr. Tan says.
A majority of cigarette smokers in the study were also marijuana smokers. In both younger and older adults in the study, 30% smoked both cigarettes and marijuana. Among younger cigarette smokers, 76% also smoked marijuana, while 58% of older cigarette smokers also smoked marijuana.
The findings come from a study of 648 adults ages 18 and older who answered questions on smoking, including their cigarette and marijuana use, and respiratory symptoms. Study subjects ages 40 and older had lung function tests.
The Vancouver researchers decided to study both marijuana and cigarette smoking because both cigarette and marijuana smoking is prevalent in their area, says Dr. Tan. They found that 49% of participants ages 18 to 39 and 46% of those 40 and older had smoked marijuana at least once. Among 18-39 year-olds, 17% said they currently smoked marijuana, compared with 13% in the 40+ age group. In the younger group, 31% said they had ever smoked cigarettes, and 16% were current smokers. In the 40+ group, 52% were ever-smokers while 16% were current smokers.

Source: American Thoracic Society (2007, May 23). Marijuana Worsens COPD Symptoms In Current Cigarette Smokers. ScienceDaily. Retrieved May 12, 2009

Filed under: Cannabis/Marijuana,Nicotine :

A new study finds that the development of bullous lung disease occurs in marijuana smokers approximately 20 years earlier than tobacco smokers. A condition often caused by exposure to toxic chemicals or long-term exposure to tobacco smoke, bullous lung disease (also known as bullae) is a condition where air trapped in the lungs causes obstruction to breathing and eventual destruction of the lungs.
At present, about 10% of young adults and 1% of the adult population smoke marijuana regularly. Researchers find that the mean age of marijuana-smoking patients with lung problems was 41, as opposed to the average age of 65 years for tobacco-smoking patients.
The study “Bullous Lung Disease due to Marijuana” also finds that the bullous lung disease can easily go undetected as patients suffering from the disease may show normal chest X-rays and lung functions. High-resolution CT scans revealed severe asymmetrical, variably sized bullae in the patients studied. However, chest X-rays and lung functions were normal in half of them.
Lead author Dr. Matthew Naughton says, “What is outstanding about this study is the relatively young ages of the lung disease patients, as well as the lack of abnormality on chest X-rays and lung functions in nearly half of the patients we tested.”
He added, “Marijuana is inhaled as extremely hot fumes to the peak inspiration and held for as long as possible before slow exhalation. This predisposes to greater damage to the lungs and makes marijuana smokers are more prone to bullous disease as compared to cigarette smokers.”
Patients who smoke marijuana inhale more and hold their breath four times longer than cigarette smokers. It is the breathing manoeuvres of marijuana smokers that serve to increase the concentration and pulmonary deposition of inhaled particulate matter – resulting in greater and more rapid lung destruction.

Source: Respirology .Blackwell Publishing (2008, January 27). Marijuana Smokers Face Rapid Lung Destruction — As Much As 20 Years Ahead Of Tobacco Smokers. ScienceDaily. Retrieved May 12, 2009

Filed under: Cannabis/Marijuana,Health,Nicotine :

New research suggests that smoking increases the production of osteopontin in the lungs, which contributes to the development of smoking-related lung disease.
Prasse et al. report their findings in the May 2009 issue of The American Journal of Pathology. Nearly one billion people worldwide smoke tobacco products. Long-term exposure to compounds found in smoke can lead to both cardiovascular and lung disease. Although lung exposure to cigarette smoke leads to immune cell recruitment and tissue fibrosis, how cigarette smoke causes these changes is largely unknown.
To determine if osteopontin, a molecule that attracts immune cells, mediates cell recruitment in smokers, Prasse et al. compared osteopontin levels from smokers with different types of lung diseases, healthy smokers, and healthy non-smokers. They found high levels of osteopontin expression in patients with interstitial lung disease, whereas healthy smokers had lower levels, and healthy non-smokers produced no osteopontin. Osteopontin expression could be stimulated directly by nicotine treatment.
In addition, expressing osteopontin in rat lung resulted in recruitment of immune cells, resulting in symptoms similar to smoking-related interstitial lung diseases. These results indicate that osteopontin may be pathogenic in smoking-initiated lung disease.
The article from Prasse et al “suggest[s] that chronic nicotine stimulation induced by cigarette smoking promotes macrophage and Langerhans cell accumulation in the lung via an increase in [osteopontin production].” Osteopontin and cellular receptors for nicotine may therefore be new targets for treating smoking related lung disease.

Source: American Journal of Pathology (2009, May 2). New Mediator Of Smoking Recruits. ScienceDaily. Retrieved May 12, 2009,

Filed under: Health,Nicotine :

Alcoholics who smoke appear to lose more brain mass than alcoholics who don’t smoke, according to a study at the San Francisco VA Medical Center.

It is already well-known that the brains of long-term alcoholics atrophy and shrink, the study authors say, but the new findings are the first evidence that cigarette smoking might contribute to that atrophy, particularly in grey matter of the parietal and temporal lobes.
Fifty to 90 percent of alcoholics also are smokers, according to Dieter Meyerhoff, PhD, a radiology researcher at SFVAMC and the principal investigator of the study
“Just looking at the amount of tissue mass lost due to either drinking or smoking, alcoholics who smoke show a greater loss in some regions of the brain compared to alcoholics who don’t smoke,” says Meyerhoff, who also is a professor of radiology at the University of California, San Francisco.
The study, which was published in the August 2005 issue of Alcoholism: Clinical and Experimental Research, compared 37 recovering alcoholics between the ages of 26 and 66 with a control group of 30 healthy light drinkers. The researchers used magnetic resonance imaging, a safe, non-invasive imaging technique, to measure brain volumes of the study participants.
They discovered that the more severe the tobacco habit, the greater the brain injury. “In smoking alcohol-dependent individuals, smaller regional [brain] volumes are related to greater cigarette-smoking severity,” according to the study findings, with severity measured by level of nicotine dependence, cigarettes smoked per day, and years of smoking.
The alcoholics (24 smokers and 13 non-smokers) averaged around 400 drinks per month for three years prior to the study; the light drinkers (seven smokers and 23 non-smokers) averaged between four and 11 drinks per month before the study and had no history of alcohol abuse or dependence. The alcoholics were sober for approximately one week before the study began.
The study uncovered no apparent differences in brain volume between smoking and non-smoking light drinkers.
Another key finding was that among non-smoking alcoholics, there was a direct relationship between brain volume and cognitive function: the higher the volume, the better the function. However, no such relationship was apparent among smoking alcoholics, according to co-author Timothy Durazzo, PhD, an associate radiology researcher at SFVAMC. Nor has such a relationship been measured before in previous studies on alcohol abuse and brain volume, he says.
“And this makes us wonder if what has been reported in the literature of alcoholism could have been obscured or distorted by combining smokers and non-smokers in the same studies,” Durazzo adds.
In their paper, the researchers speculate that smoking “disrupts these [brain] structure-function relationships,” possibly through its detrimental effects on brain volume or on brain neurochemistry.
Meyerhoff and his co-authors emphasize that their results are retrospective — that is, they discovered the apparent effects of smoking during statistical analysis of the participants in an earlier study they conducted on alcoholism and its effects on the brain. They then went back, re-classified each study participant as smoking or non-smoking, and analyzed brain volumes accordingly.
The authors say that if replicated in other studies, their results will raise several potentially important questions. The first is whether recovering alcoholics should also be treated for smoking — and if so, at what point during their treatment. At present, alcohol treatment programs such as Alcoholics Anonymous do not discourage smoking or even address the issue, they say.
Beyond that, says Durazzo, there is the potential effect of smoking on cognitive dysfunction, which is common among older long-term alcoholics. “Right now, our study participants are relatively young, around 50,” he notes. “But will the combination of smoking and drinking, or continued smoking during abstinence from alcohol, put them at greater risk for cognitive dysfunction as they age?” Finally, says Meyerhoff, there is the question of whether smoking has an effect on physical recovery from alcohol abuse. “In alcoholics who stop drinking, we know that there is recovery from at least some of these injuries to the brain — but is this recovery affected by continued smoking?” Meyerhoff and his team are conducting a study to explore that question right now.
In the future, the researchers plan a prospective study that will use MRI to compare brain volumes between smoking and non-smoking light drinkers and smoking and non-smoking alcoholics, with the hope of replicating the results of their current retrospective study.

Source: University of California – San Francisco (2005, September 29). Smoking Seems To Increase Brain Damage In Alcoholics. ScienceDaily. Retrieved May 31, 2009, from http://www.sciencedaily.com¬ /releases/2005/09/050929081514.htm

Filed under: Alcohol,Brain and Behaviour,Nicotine :

A new global study has found that lifestyle risk factors such as alcohol consumption and cigarette smoking are important risk factors for bowel cancer. Researchers have shown that people who consume the largest quantities of alcohol (equivalent to > 7 drinks per week) have 60% greater risk of developing the cancer, compared with non-drinkers.

Smoking, obesity and diabetes were also associated with a 20% greater risk of developing bowel cancer – the same risk linked with consuming high intakes of red and processed meat.
Approximately one million new cases of bowel (colorectal) cancer are diagnosed worldwide each year, and more than half a million people die from this type of cancer. In Australia alone, it is the most commonly occurring cancer with more than 12,000 new cases diagnosed each year.
According to lead researcher Associate Professor Rachel Huxley at The George Institute, the most startling finding of this study was, “The strong, and largely, unknown association between high intakes of alcoholic beverages with risk of colorectal cancer. Most people probably know that being overweight and having poor dietary habits are risk factors for the disease, but most are probably unaware that other lifestyle risk factors such as alcohol consumption, cigarette smoking and diabetes are also important culprits.”
Australia’s National Health and Medical Research Council recommend individuals shouldn’t be drinking more than two standard drinks per day.
On a positive note, researchers also demonstrated that physical activity lowered an individual’s risk of the disease but surprisingly, there was little evidence to indicate that high intakes of fruit and vegetables were protective against bowel cancer.
“These findings strongly suggest that a large proportion of colorectal cancer cases could potentially be avoided by making relatively modest lifestyle adjustments such as drinking less, quitting smoking, eating healthily and being a little more active”, said Associate Professor Huxley. “Such changes would also have huge benefits in terms of reducing an individuals’ risk of developing other major forms of illness including cardiovascular disease.”
The study reviewed more than 100 published studies that had reported on the association between major and modifiable risk factors for colorectal cancer including alcohol, smoking, diabetes, physical activity and various dietary components.

Source: Parkin DM, Bray F, Ferlay J, et al. Global cancer statistics, 2002. CA Cancer J Clin 2005;55:74-108.

Filed under: Alcohol,Health,Nicotine :

New research suggests that the combination of drinking alcohol and smoking cigarettes increases the risk of throat and stomach cancers.
Researchers investigated risk factors for three kinds of cancers: esophageal adenocarcinoma (throat cancer), gastric cardia adenocarcinoma (stomach cancer) and esophageal squamous cell carcinoma (which resembles head and neck cancer).
Past studies have linked cancer of the esophagus to drinking and smoking, but the new research found that people who drank four glasses of alcohol daily had five times the risk of developing esophageal squamous cell carcinoma than nondrinkers. Smoking was related to increased risk of developing all three types of cancer, with risk of throat cancer the most elevated.
“It appeared that current smokers have the highest risks, and former smokers have an intermediate risk compared with never-smokers,” said study author Jessie Steevens, an epidemiologist at Maastricht University in the Netherlands.
The findings were presented at a meeting of the American Association for Cancer Research.
Source: Reuters November 17, 2008

Filed under: Alcohol,Health,Nicotine :

Researchers led by Debapriya Ghosh and Anirban Basu of the Indian National Brain Research Center (NBRC) said that the compound NNK, found in tobacco, incites white blood cells in the central nervous system to attack healthy cells, leading to severe brain damage.
The research focused primarily on the NNK compound that is found in all forms of tobacco. NNK is a chemical substance that becomes carcinogenic during the body’s metabolic process.
In their tests, the Indian researchers found that NNK provoked an errant response from microglia, immune cells in the brain that normally attack damaged or unhealthy cells.
“This research sheds light on the processes that lead to nerve-cell damage in those who smoke cigarettes or consume tobacco products on a regular basis,” said Ghosh.
Researchers believe the neuroinflammation caused by NNK may lead to disorders like multiple sclerosis.
The findings will be published in the July 2009 issue of the Journal of Neurochemistry.

Filed under: Health,Nicotine :

Nicotine is thought to exert its effects on the brain by binding to receptors in the brain called nicotinic acetylcholine receptors (nAChRs). However, tobacco smoke contains thousands of chemicals besides nicotine, some of which may also bind to the nAChRs or cause molecules normally found in the body to bind to these receptors. To study the effects of denicotinized cigarettes—cigarettes from which nicotine has been removed—on a specific type of nAChR (a4b2* nAChRs), researchers funded in part by NIDA used a brain imaging technique known as positron emission tomography (PET) to visualize these receptors in the brains of smokers during withdrawal and after smoking either low-nicotine or denicotinized cigarettes. Before the PET imaging, all volunteers stopped smoking for approximately 2 days. The volunteers underwent an hour of PET imaging while still undergoing withdrawal and then were assigned to perform one of three activities: smoke a low-nicotine cigarette, smoke a denicotinized cigarette, or not smoke; they then underwent approximately 4 more hours of PET imaging. Withdrawal symptoms were monitored during all imaging sessions. The imaging results showed not only that “inhalation of nicotine during cigarette smoking is solely responsible for occupancy of brain a4b2* nAChRs,” but also that the imaging “demonstrated significant a4b2* nAChR occupancy from smoking a denicotinized cigarette,” state the authors. This result challenges the assumption that denicotinized cigarettes do not affect the brain’s nicotine receptors, the authors further explain. Interestingly, whether or not the receptors were occupied did not correlate with withdrawal symptoms, indicating that factors other than nicotine binding to the receptors play a role in the relief of withdrawal symptoms provided by smoking.

Source: Brody et al. Brain nicotinic acetylcholine receptor occupancy: Effect of smoking a denicotinized cigarette. Int J Neuropsychopharmacol. 2009;12(3):305–316.

Filed under: Brain and Behaviour,Nicotine :

Filed under: Alcohol,Health,Nicotine :

A new Harvard study concludes that smokers with multiple sclerosis (MS) experience more rapid progression of the disease than non-smokers, Reuters reported July 14.
Smokers also were 2.4 times more likely to have a progressive form of MS rather than the relapsing/remitting type, and 2.5 times more likely to have developed secondary progressive MS after an initial diagnosis of the relapsing/remitting version of the disease. Researchers found that smokers had more disability, severe disease and brain atrophy than non-smokers with MS, and had a greater degree of damaged brain tissue and brain atrophy over time.
Researcher Alberto Ascherio of the Harvard School of Public Health put a positive spin on the findings, noting that MS patients who quit smoking could slow progression of the disease.
Source: Archives of Neurology. July 2009

Filed under: Health,Nicotine :

By Patrick Zickler
NIDA NOTES Staff Writer

Smokers who want to quit can get help with a variety of treatments, including counselling, nicotine replacement therapy (patches, gum, lozenges, or inhalers and medications. Some smokers use these treatments and succeed; for many. however, the discomfort of withdrawal and craving for nicotine lead to relapse. Recent NIDA funded research suggests that our genes may partly explain this variable success.

The research evaluated the effect of an enzyme, designated CYP2B6, on craving and relapse. This enzyme breaks down nicotine in the brain. Some peoples’ genes produce a more active form of the enzyme. while others have a less active form. Dr. Caryn Lerman at the NIDA- and NCI supported Transdisciplinary Tobacco Use Research Centre (TTURC) at the University of Pennsylvania, found that among smokers enrolled in a smoking cessation program, those with the genetic variant that decreases activity of CYP2B6 reported greater craving than did those with the more active form of the enzyme. Moreover, those with the less active enzyme were 1.5 times more likely to resume smoking during treatment.

The same enzyme helps break down bupropion, an antidepressant medication that acts on the brain’s dopamine system—where nicotine exerts much of its addictive influence—and helps some smokers quit. Dr. Lerman, along with colleagues at Georgetown University in Washington, DC., the State University of New York at Buffalo, and Brown University in Providence, Rhode Island, also investigated the relationship of CYP2B6 activity with bupropion treatment. They found that bupropion nearly tripled the success rate for women with the less active enzyme.

These findings provide initial evidence that smokers who have decreased CYP2B6 activity experience greater craving for nicotine than those with the more active form of this enzyme,” Dr. Lerman says. “Perhaps of greater interest is the preliminary evidence that, among women, bupropion may overcome the effect this genetic predisposition has on relapse.”

Genes, Treatment, and Abstinence

Most people—about 70 percent of the U.S. population—inherit two copies of the ‘C’ variant of the gene that influences CYP2B6 activity. The rest of the population inherits from one or both parents the less common form of the gene—the “T’ variant associated with decreased CYP2B6 activity. Among the 426 participants (232 men, 194 women) in the TTURC study, 128 (29.6 percent) had one or two copies of the T form of the gene. All participants received counselling to quit smoking; 229 received bupropion (300 mg/day) and 197 received placebo throughout the 10-week study. The participants provided weekly reports on craving and smoking rates. Abstinence (7 consecutive days without smoking) was verified with blood tests. At the end of treatment, participants who received counselling and bupropion had higher abstinence rates than those who received counselling and placebo. With one exception. participants with the less active enzyme had lower abstinence rates than those with the more active enzyme. Women with the less active enzyme who received bupropion showed the largest treatment effect, with 54 percent achieving abstinence, up from a 19-percent rate among women in the placebo group, notes Dr. Lerman.

This study suggests that properly selected treatment matched to a patient’s characteristics can improve a smoker’s chance of quitting

Theories To Explain Outcomes

The higher abstinence rate with bupropion for women with the lower activity enzyme may he due, in part, to reduced susceptibility to low moods that accompany nicotine withdrawal; overall. women reported more negative feelings than did men when asked to rate their mood during withdrawal. “This rate may reflect better management of the negative moods and craving that abstinence can create. But more study is needed to clarify the mechanisms by which bupropion influences smokers’ success in quitting”, Dr. Lerman says.
Researchers theorize that the association between the less active enzyme and increased craving could be the result of nicotine’s remaining longer in the brains of smokers with the less active enzyme. When nicotine lingers in the brains of these smokers, it may change their brain cells more profoundly than those of smokers with the more active enzyme. If so, the changes might produce more severe addiction marked by more intense craving during abstinence and increased risk of relapse.

“This study offers additional evidence of the important role genes play in smoking and treatment,” says Dr. Joni Rutter of NIDAs Division of Neuroscience and Behavioural Research, ‘While illustrating the increased craving and vulnerability to relapse that may be associated with inherited traits, it also suggests that properly selected treatment matched to a patient’s characteristics in this case, Bupropion for some women can improve a smoker’s chance of quitting.’

Source:Lerman, C., et al. Pharmacogenetic investigation of smoking cessation treatment, Pharmacogenetics
12(8):627-634, 2002.

Filed under: Addiction,Brain and Behaviour,Nicotine :

A comprehensive report on smoking and health released by the U.S. Surgeon General finds that smoking causes diseases in nearly every organ of the body.

When the first Surgeon General’s report on smoking was published 40 years ago, it concluded that smoking was a definite cause of cancers of the lung and larynx in men and chronic bronchitis in both men and women. Later reports concluded that smoking caused cancers of the bladder, esophagus, mouth and throat; cardiovascular diseases; and reproductive effects.

The new report, “The Health Consequences of Smoking: A Report of the Surgeon General,” finds that cigarette smoking is also linked to leukemia, cataracts, periodontitis, pneumonia, acute myeloid, abdominal aortic aneurysm, and cancers of the cervix, kidney, pancreas, and stomach.

“We’ve known for decades that smoking is bad for your health, but this report shows that it’s even worse than we knew,” said U.S. Surgeon General Richard Carmona. “The toxins from cigarette smoke go everywhere the blood flows. I’m hoping this new information will help motivate people to quit smoking and convince young people not to start in the first place.”

According to the report, smoking kills an estimated 440,000 Americans each year. Furthermore, the economic toll linked to smoking is $157 billion each year, with $75 billion spent on direct medical costs and $82 billion in lost productivity.

“We need to cut smoking in this country and around the world,” said HHS Secretary Tommy Thompson. “Smoking is the leading preventable cause of death and disease, costing us too many lives, too many dollars, and too many tears. If we are going to be serious about improving health and preventing disease, we must continue to drive down tobacco use. And we must prevent our youth from taking up this dangerous habit.”

Source:“The Health Consequences of Smoking: A Report of the Surgeon General,” May 2004

Filed under: Health,Nicotine :

NEW YORK (Reuters Health) – Watching a favorite movie star smoke appears to encourage teen girls to adopt the habit themselves, according to new findings released Tuesday.

Investigators found that girls who said their favorite celebrity was someone who had smoked in at least two recent movies were almost twice as likely to start smoking within the next three years as girls whose favorite stars did not smoke in films.

“Really, smoking in movies is just an effective form of marketing,” study author Dr. John Pierce told Reuters Health .

Pierce, based at the University of California in San Diego, added that it is also common for teens to copy their favorite stars’ clothing, hair and jewelry. Those habits are easy to alter as styles evolve, he said, but once teens become hooked on smoking, “that is something that’s very hard to change.”

Pierce noted that the tobacco industry has argued that it does not pay for actors to smoke on screen, and actors do it simply because it makes them feel more comfortable.

If that is the case, then one could argue that the stars themselves are responsible for encouraging teens to smoke, and should be held accountable for that, Pierce noted.

“If it’s the stars, and they’re liable, then they’d better watch out,” he said.

To investigate whether watching stars smoke on-screen influences teens to do the same, Pierce and his colleagues asked 3104 never-smokers between the ages of 12 and 15 to name their two favorite female stars and two favorite male movie stars.

The researchers reviewed the stars’ movies during the past 3 years, and counted them as smokers if they puffed during at least two films. They then re-interviewed teens three years later, to see how many had started smoking.

When Pierce and his team first contacted teens in 1996, the most popular stars among teen girls were Brad Pitt, Sandra Bullock and Leonardo DiCaprio. Favorite actors for boys were Pamela Anderson, Sandra Bullock and Demi Moore. More than 40 percent of girls and 30 percent of boys had favorite stars who smoked.

Favorite stars who did not smoke on-screen included Jim Carrey, Tom Hanks and Tom Cruise.

Although girls appeared to be influenced by the smoking habits of favorite stars, boys were not, the authors report in the American Journal of Public Health.

They note that research has shown that boys tend to prefer action movies, which tend to include less smoking by stars, while girls prefer more smoke-filled romances and dramas.

Pierce explained that his team also measured each child’s susceptibility to smoking — defined as being unwilling to rule out the option of future smoking. This removed the possibility that only those who were susceptible to smoking would have a favorite star who smoked on-screen, he said.

Dr. Stanton Glantz of the University of California in San Francisco, who was not an author of the paper, noted that research shows that the more teens see people smoke, the more likely they are to pick up the habit. The latest findings suggest that policymakers should strictly limit teens’ exposure to on-screen smoking, he said.

Restricting smoking to R-rated movies would apply “the same rules that Hollywood applies to saying the F-word,” Glantz said.

SOURCE: American Journal of Public Health, July 2004.

Filed under: Nicotine,Prevention and Intervention,Youth :

Almost a third (29%) of Welsh girls aged 15 to 16 admit they smoke on a weekly basis, a new study by the National Public Health Service for Wales has revealed. Among boys of the same aged, 20% admitted to smoking regularly. The report examined a range of determinants of health including alcohol, drug use, socio-economic background, exercise and diet.

The South Wales Echo report includes a case study of one 28-year old who started smoking at the age of 14. She comments: “When I was 16 I was going out more and I would smoke about a pack a week. By the time I was 19 I was smoking about five packs a week. Of course I regret it now – my face is a prune! I wish I had never smoked because it’s really hard to stop and I could die of lung cancer.”

South Wales Echo, 3/8/04

Filed under: Nicotine,Youth :

Merseyside’s first non-smoking pub has registered “record breaking-profits.” The Ring O’Bells in West Kirby barred smoking in June 2003.

Since then alcohol sales have risen 60 percent and food takings have doubled. The pub’s kitchen had to be refitted to cater for the demand.

Landlord Alan Jones said: “We lost some custom, which was a concern. But our profits have proved us right.”

Source: Liverpool Echo, 18 August 2004

Filed under: Nicotine,Prevention and Intervention :

A new survey reveals that one in five mothers smoke while pregnant. The habit causes low birth-weight babies with dramatically increased chances of mental impairment, disability and sudden death as infants. Baby health charity Tommy’s conducted the poll.

Smoking is also linked to ectopic pregnancy.

Source: The Sun, September 6, 2004

Filed under: Drug use-various effects,Nicotine :

Children with asthma who have at least one parent who smokes are twice as likely to have asthma symptoms all year long compared with children of non-smokers, according to researchers from the University of Michigan (U-M) Health System.The involved in-depth telephone interviews with 896 parents of asthmatic children ages 2 to 12 years old in 10 states. “We set out to look at children who have seasonal asthma symptoms, but found that a substantial percentage have symptoms year-round,” said Kathryn Slish, a researcher in the U-M Department of Pediatrics. “We looked more closely and found a strong relationship between parents’ smoking status and the likelihood that their child would have problems all year long.”

“The only other factor that was associated with year-round symptoms was Medicaid insurance coverage,” added Cabana.

With well-publicized information that secondhand smoke can trigger asthma in children, Slish said, “it’s astounding that so many parents smoke around their asthmatic kids, and don’t stop even though their children are having trouble breathing all year.”

The researchers recommended that pediatricians, family physicians, and nurses address the subject of smoking with the parents of any child diagnosed with asthma and to provide resources to encourage them to quit.

The study’s findings were presented May 4 at the Pediatric Academic Societies annual meeting.

Source: University of Michigan (U-M) Health System.

Filed under: Drug use-various effects on foetus, babies, children and youth,Nicotine,Parents :

The research concluded that cigarette smoking and a poor ratio of bad to good cholesterol contribute to two-thirds of all heart attacks worldwide.

The study’s findings are published in issue of the British medical journal

Source: The Lancet. Sept. 11 2004

Filed under: Health,Nicotine :

New research from the University of California (UC) Davis School of Medicine and Medical Center found that cancer death rates among African-American males would decline by almost two-thirds if their exposure to cigarette smoke was eliminated.

“African-American men have had the highest cancer burden of any group in this country for decades,” said study author Bruce Leistikow, associate professor of epidemiology and preventive medicine at the UC Davis School of Medicine and Medical Center. “This study demonstrates, for the first time, that this excess cancer burden can be clearly linked to smoking. Smoke exposure appears responsible for African-American males’ high overall cancer mortality rates, not just their lung cancers.”

By analyzing data, Leistikow determined a correlation between annual smoke exposure and non-lung-cancer death rates for black males in the United States for the years 1969 through 2000. “During two decades of a steep rise, and a subsequent decade of steep fall, U.S. black male smoke exposures and non-lung-cancer death rates have moved in near-perfect lockstep up and down. The associations are very strong and have been consistent year-by-year for over 30 years,” Leistikow said.

Leistikow’s research found that smoking exposure is responsible for more than half the non-lung-cancer death rate in African-American males, and up to two thirds of their overall cancer death rate.

“This means that if black-male smoking exposures fall dramatically, that alone is likely to erase the great majority of their cancer burden,” said Leistikow. “Going back to the low black-male cancer burdens seen before the cigarette epidemic appears possible. Indeed, New York and, less so, California appear to be well on their way there.”

The study’s findings are published in the May 2004 issue of the journal Preventive Medicine.

Source:University of California (UC) Davis School of Medicine and Medical Center; Apr 2004.

Filed under: Health,Nicotine :

New research from Sweden has shown that smokers puff clouds of poison in to the air which can seriously affect the breathing around them. The discovery has prompted ASH to urge the government to ban indoor smoking in workplaces. Swedish scientists found that endotoxins, which are made by bacteria and occur naturally in the air, are produced by tobacco smoke in high concentrations. Tobacco is known to contain over 4,000 chemicals, including 50 substances known to cause cancer. Low concentrations of endotoxins are not harmful and may even play a role in protecting people against allergies. However, in high concentrations, endotoxins can cause serious inflammatory reactions in the respiratory tract, leading to bronchitis and asthma. The researchers also concluded that tobacco endotoxins appeared to be the most aggressive among the various types that exist. ASH spokeswoman Amanda Sandford noted that the research could lead to a greater understanding of how tobacco smoke can trigger respiratory diseases such as asthma: “There are lots of sources of pollution we don’t have much control over, but we can control tobacco smoke in enclosed areas,” she said. She added that the study reinforced the need for a ban on smoking ban on indoor places.

Source: Morning Star, Times, 23 August, 2004

Filed under: Drug use-various effects,Nicotine :

For recovering alcoholics and ex-smokers, as well as former users of illicit drugs, the mundane trappings of their addictions—ice cubes, ashtrays, straws, needles—exert a strong, long-lasting power to trigger relapse. A new University of Michigan study, published in the current (October 2001) issue of the Journal of Neuroscience, provides experimental evidence supporting a neurological explanation for why cues as innocent as the sound of ice cubes tinkling in a glass can cause “recovered” addicts to experience dangerous drug cravings. “Drug use is known to sensitize’ certain neural systems within the brain, causing changes that are relatively permanent,” says U-M psychologist Kent C. Berridge, co-author of the study with U-M psychologist Cindy L. Wyvell. “This study shows that the brain is vulnerable to cues that trigger irrational ‘wanting,’ even after a long period of remaining drug-free, once sensitized by prior drug use or exposure.” The research was supported by the National Science Foundation and by the National Institute on Drug Abuse.
For the study, Wyvell and Berridge designed an experiment with rats that eliminated several alternative explanations, such as withdrawal symptoms, learned habits or drug pleasure, for the increase in compulsive drug-seeking that is commonly triggered in human addicts by encounters with drug cues.

First, in order to avoid withdrawal symptoms, they trained the rats to press a lever to get a reward of sugar pellets, not an addictive drug. They also taught the rats to associate a 30-second tone with getting sugar pellets, without needing to press the lever. Then they sensitized one group of rats by administering a series of amphetamine injections, while injecting controls with a saline solution. Next, the researchers waited 10 to 14 days to make sure both groups were drug-free, then resumed the experiment. While the rats pressed the lever in hope of getting the sugar reward, they were presented intermittently with the sound cue, to assess the cue’s ability to trigger excessive pursuit of reward.

In the sensitized rats, the cue triggered excessive wanting,” says Berridge. “Whenever a sugar cue (a sound) occurred, rats pressed in a frenzy on a lever that had previously earned them a sugar reward.” In fact, the researchers found that sensitized rats pressed the lever 200 percent more than rats in the control group, an increase equivalent to the behaviour produced in other rats by injecting amphetamine directly into their brains. This showed that sensitization of the brain and direct drug activation of the brain’s dopamine reward-craving system amplified equally the ability of reward cues to trigger excessive ‘wanting.” “Much more remains to be done before we understand how this process works in humans, with drug rewards such as cocaine and heroin, and to a lesser extent, alcohol or nicotine,” says Berridge. ‘But this study is an important step, because it provides the first pure demonstration that neural sensitization causes a specific process— irrational cue-triggered ‘wanting’ for reward—that is a plausible psychological mechanism for relapse. These results from animals based on a natural sugar reward this may be a useful step toward understanding brain mechanisms of cue-triggered relapse in human drug addiction”

Source: Cindy L. Wyvell. Journal of Neuroscience , Oct 2001.

Filed under: Alcohol,Brain and Behaviour,Drug use-various effects,Nicotine :

New research suggests that a combination of two genes is linked to whether a person can quit smoking and remain tobacco-free through the years.The study by researchers from the Tobacco Use Research Center of the University of Pennsylvania School of Medicine involved 418 smokers who received either bupropion or a placebo with seven sessions of behavioral group counseling. The researchers tracked the smoking status, abstinence symptoms and side effects of participants weekly, as well as at the end of treatment and six months later.The study found that certain variants of the SLC6A3 dopamine transporter gene and the DRD2 dopamine receptor gene resulted in higher abstinences rates and longer relapse times than other variants of these genes.

“While previous research has examined the effects of genes related to dopamine, a chemical in the brain associated with reinforcing the effects of nicotine, this study provides the first evidence that genes that alter dopamine function may influence smoking cessation and relapse during treatment,” said lead author Caryn Lerman, Ph.D., associate director for Cancer Control and Population Science at the Abramson Cancer Center of the University of Pennsylvania and professor in Penn’s School of Medicine and the Annenberg Public Policy Center.

Lerman said the study’s findings could lead to more effective smoking cessation methods. “Future smoking cessation studies should evaluate genetic predisposition, as well as the influence of psychological and environmental factors that may promote relapse,” she said.

The study’s findings are published in the October issue of Health Psychology. 2003

Source: Science Daily reported Oct. 3.2003

Filed under: Nicotine :

Nursing students are more likely to smoke cigarettes and to be nicotine dependent than medical students, says a study published in Chest (2003;124: 1415 – 20). A survey of more than 500 students in Philadelphia, USA, showed that four times as many nursing students smoked cigarettes as medical students, and twice as many students were former smokers. The rate of smoking among medical students had fallen in the past decade, and those who did smoke were less nicotine dependent than their nursing counterparts.

Source: The Lancet, 18 October 2003

Filed under: Nicotine :

US researchers investigated 3,122 patients with previous MI or stable angina and found that those who smoked were two and a half times more likely to suffer sudden cardiac death than those who had never smoked. However those who had given up were not at increased risk.

Source: General Practitioner, 3 November 2003

Filed under: Health,Nicotine :

A government report on America’s children shows that violent crime, smoking, and heavy drinking among U.S. teenagers are all on the decline, Reuters reported July 18.
However, more children are overweight than ever, the report found. “Most people, about two-thirds, believe that crime is going up among America’s children,” said Dr. Duane Alexander, director of the National Institute of Child Health and Human Development. “The picture painted by this report, based on actual data, paints the opposite picture. “According to the report released by the National Institutes of Health, the Census Bureau, and other agencies, victims reported 413,000 juvenile crimes in 2002, which translates into 17 violent crimes per 1,000 juveniles aged 12 to 17.”This is a 67-percent drop from the 1993 high, and the lowest rate recorded since the national victimization survey began in 1973,” the report stated.The report also found that fewer children are being killed by guns. Last year, firearms were involved in 19 percent of deaths among 15- to 19-year-olds.Exposure to secondhand smoke also fell, the report said, and fewer teens smoked. As recently as 1994, 88 percent of children ages 4 to 11 were exposed to secondhand smoke. The latest report found that rate had dropped to 64 percent. Daily smoking by youth dropped to the lowest rate since 1975, and heavy drinking among teens also declined.source:Reported in Join Together Online. 7.21.2003

Filed under: Alcohol,Nicotine,Youth :

Women who smoke are more likely to go through an early menopause, new research has confirmed. Women smokers may experience the change of life more than two years earlier than non-smokers. The latest study, published in the journal Reproductive Biomedicine Online, suggest smoking actually harms a woman’s ovaries and affects her fertility.
Researchers from the Civitanova Marche General Hospital in Italy studied 350 women attending the hospital’s menopause clinic.They found that the menopause started at around 47 years of age for smokers compared with 49 years, six months, for non-smokers.Women who had stopped producing eggs before the age of 46 were more likely to be smokers.

Source: Daily Mail, 6/2/04. http://www.rbmonline.com/4DCGI/Article/Detail?38%091%09=%201149%09

Filed under: Nicotine :

The Observer notes growing concern over the impact of cigarette smoking in films. Anti-smoking campaigners, backed by Britain’s largest cancer charity, claim the age classification of films should be as sensitive to smoking as to offensive language and obscenities.

‘We are not arguing for a total ban on smoking in films,’ said Deborah Arnott, director of ASH. ‘But there is strong evidence of a causal link between stars’ smoking behaviour and teenage smoking.’

Some of Hollywood’s biggest names, including Zeta-Jones, Nicole Kidman and Pierce Brosnan, have been criticised after recent research showed that smoking on screen is at its most prevalent for 50 years. Nearly 80 per cent of Hollywood films given a 12 rating feature some form of tobacco use while half of all children’s and PG-rated films depict smoking, according to a survey of 775 Hollywood films.

British Board of Film Classification guidelines now say films with a PG rating must not contain references to illegal drugs or drug use. It also forbids films with a 15 classification from depicting ‘imitable techniques’ such as emphasising fighting or easily accessible lethal weapons, like knives. However, the guidelines contain no references to cigarettes, which kill 120,000 people each year in the UK. ‘There is surely a strong case for upgrading the age classification of a film to at least 15 if it features smoking by aspirational role models for young people, as this is clearly imitable and dangerous behaviour,’ said Arnott.

Source:http://observer.guardian.co.uk/uk_news/story/0,6903,1168901,00.html

Filed under: Nicotine :

Seeing actors smoke on-screen can raise the risk of young people starting to smoke, suggests a new study that also concludes that many kids decide to smoke based solely on the behaviour of cinematic role models. The Associated press reported June 9 that researchers from Dartmouth Medical School studied 2,600 children ages 10 to 14, all nonsmokers when the study started in 1999. Each was rated by their exposure to smoking in movies. A follow-up survey found that even when controlling for other factors, the youths who were highly exposed to smoking in movies were three times more likely to start smoking themselves, compared to those students whose exposure to on-screen smoking was rated as low.

The researchers said that 52 percent of those who started smoking seemed to have been primarily influenced in their decision by on-screen smoking. In an accompanying commentary, researcher Stanford Glantz said that movies that depict smoking should be rated R by the Motion Picture Association of America.

Source:Dalton, M., Sargent, J., Beach, M., Titus-Ernstoff, L., Gibson, J., Ahrens, M., Tickle, J., & Heatherton, T. (2003)

Effect of viewing smoking in movies on adolescent smoking initiation: a cohort study. The Lancet, 361(9373).

Filed under: Nicotine :

Smoking among U.S. high school students has fallen to about one in five the lowest level in at least a generation in a drop-off the government attributes to anti-smoking campaigns and higher cigarette taxes.The Centers for Disease Control and Prevention reported Thursday that nearly 22 percent of high school students said they were smokers in 2003. That is down from more than 36 percent in 1997, and the lowest level since the CDC began keeping track in 1975. The drop was so dramatic that for the first time in more than two decades, the percentage of high school smokers is lower than the percentage of adult smokers. That was seen as an especially encouraging sign by the government.

In fact, the CDC study found that anti-tobacco efforts have been successful across the board, from curbing the number of first-time smokers to reducing the ranks of the heaviest smokers.”We are reaching all the youth. If we can stop youth from becoming addicted smokers, eventually we can stop this epidemic,” said Terry Pechanek, associate director of science for the CDC’s Office on Smoking and Health. “We’re making the progress we’ve been working toward for the last 40 years.”

Dr. John Banzhaf III, who helped mastermind lawsuits against the tobacco industry, said the study illustrates “probably the most dramatic progress which has been made in terms of any public health problem, at least in recent memory.” “The question would be whether we have the political will to continue to do it,” said Banzhaf, executive director of Action on Smoking and Health and professor of public interest law at George Washington University Law School.The CDC said that anti-tobacco efforts such as TV ads and school campaigns have been highly successful. Some of the programs were funded by the $206 billion settlement that tobacco companies and states reached in 1998.

Another big reason fewer teenagers are lighting up is the cost of a pack of cigarettes, the CDC said. The agency said cigarette prices went up 90 percent from 1997 to 2003, mostly because of tax increases. Students were classified as current smokers if they had lit up in the preceding 30 days.The study found that the percentage of heavy smokers those who lit up 20 days or more per month fell to 9.7 percent from 16.8 percent in 1999.Also, fewer students are trying cigarettes: A little more than 58 percent of students in 2003 said they had tried smoking, down from more than 70 percent in 1999.Still, the government noted that other studies recently have warned that the rate of decline in student smoking may be slowing.

The CDC blamed that on several factors, including more depictions of smoking in movies and a near doubling of spending on
tobacco advertising from cigarette makers ($5.7 billion in 1997 to $11.2 billion in 2001). Also, states are spending less money from the tobacco settlement on smoking prevention.Trend-setting states that had well-funded programs and subsequent decreases in student smoking now have had those programs crippled by budget cuts, causing a rise in student smoking rates in those areas, said Matt Barry of the Campaign for Tobacco-Free Kids.Philip Morris spokeswoman Jennifer Golisch said the nation’s No. 1 cigarette maker is “very happy” about the study’s results. “As a manufacturer of a product intended for adults, we believe we have a responsibility to help prevent kids from smoking,” she said.

Golisch said Philip Morris does not place its cigarettes in movies or on TV, though some filmmakers or TV producers have used
Philip Morris products without its permission. She also said the company is spending less on cigarette advertising, in part because of restrictions contained in the tobacco settlement.

Source:http://abcnews.go.com/wire/Living/ap20040618_504.html; 18/Jun/2004

Filed under: Nicotine :

Wearing a nicotine patch can boost memory and stop forgetfulness in older people according to a new study by researchers in to old age. Previous evidence found that nicotine might benefit people with a variety of disorders, including schizophrenia, Alzheimer’s, and attention deficit hyperactivity disorder. The latest study is the first to examine the effect of the drug on people with age-associated memory impairment (AAMI), a common condition among the elderly.
In a small study of over 60s the researchers found that using a standard memory test, four weeks of nicotine treatment halved decision times. Doctors point out that none of the people on the trial had any form of dementia, such as Alzheimer’s, but some memory loss is normal with ageing. While receiving nicotine, patients assessments of their own memories also showed a small but significant improvement, say researchers at Duke University in Durham, USA. Experts think patches could be used over short periods of time for memory enhancement, without a person having to wear a patch regularly.

Source: Daily Mail, 27 January 2004

Filed under: Nicotine :

In an experiment to test the availability of cigarettes online, four adolescents were able to buy tens of thousands of cigarettes online from dozens of websites, the Durham Herald-Sun reported Sept. 9. The four children, ages 11 to 15, were taking part in a University of North Carolina at Chapel Hill study when they used credit cards and money orders to try to buy cigarettes from 55 Internet vendors. Over a four-month period in 2001, they succeeded 94 percent of the time using credit cards and 90 percent of the time using money orders. Just one package was marked as containing tobacco products, and only one required an adult signature for delivery. A number of vendors sent free cigarettes and promotional materials to the children.

“Although it is against the law for stores to sell cigarettes to minors in every state in America, there is currently no federal law that bans Internet and mail-order cigarette sales to minors,” lead study author Kurt Ribisl said. “Congress has been considering legislation to ban cigarette sales to minors for more than four years. This study clearly shows that Internet cigarette vendors are not adequately verifying the age of their customers and that federal action is urgently needed.” In the wake of the report, Rep. Marty Meehan (D-Mass.) introduced legislation to regulate Internet cigarette sales and collect excise takes on such sales.

There are now at least 353 online cigarette retailers, and their sales could top $5 billion by the end of 2005, Ribisl said. Most are located in low-tax states like Virginia, North Carolina. One of the biggest online retailers is New York‘s Seneca Indian tribe, which sells cigarettes tax-free from its reservation.

Source: Ribisl, K., Williams, R., & Kim, A. (2003) Internet Sales of Cigarettes to Minors,
Journal of the American Medical Association, 290(10): 1356-1359.

Filed under: Nicotine,Youth :

New data indicates that youth in Washington are taking the advice offered in the anti-tobacco ads being run by the Washington State Department of Health. According to the latest report from Sedgwick Rd., the Seattle advertising agency that created the ads, 80 percent of Washington youth had seen the anti-smoking advertisements. Furthermore, 94 percent of those who had seen the ads said they gave them good reasons not to smoke.

“The effectiveness of our advertising efforts lies in the extensive investigation we did with Washington state youth about what catches their attention most,” said Terry Reid, manager of the state Department of Health Tobacco Prevention and Control Program. “Our ads speak directly to youth who are at risk for smoking, with messages specifically designed to get their attention and give them the hard facts.”
The ads are part of the state’s comprehensive Tobacco Prevention and Control Program, which began in July 2000. The campaign also includes radio, print, and Web-based ads, community outreach, support services, and school-based education programs. Since the start of the state wide campaign, the number of Washington 10th-graders who smoke has dropped by 40 percent. “We’re creating real and lasting change in Washington,” said Secretary of Health Mary Selecky. “Still, we have more work to do; about 55 kids start smoking every day in our state. Our new ad campaign will help us reach more youth so we can convince them to quit smoking or never start.”

Source: JTO Online May 2004

Filed under: Nicotine,Youth :

Britain‘s largest tobacco company British American Tobacco (BAT) stands accused of adding sweeteners to cigarettes in an underhand attempt to entice youngsters to smoke, reports the Independent. Apparently, BAT whose products include Lucky Strike and Rothmans has been conducting scientific trials on animals in Canada. The additives that are believed to have been tested include chocolate, wine, cocoa, maple syrup and vanilla.
The experiment has drawn a furious response from Director of ASH, Deborah Arnott. “Adding sweets to tobacco is appalling. It shows that we need more tobacco regulation to prevent anything being added that could make tobacco more attractive, or smother, or easier to use. These are the sort of ingredients that could make cigarettes more attractive to children, why would they want to test these sort of additives?” she asked.

The controversial trials were outlined in the journal Food and Chemical Toxicology. BAT admitted it had indeed commissioned the work to see if cigarettes with additional ingredients had different effects on health compared to cigarettes without additives. The study, conducted over a 90 day duration and used laboratory rats in Canada because testing tobacco on live animals in Britain has been outlawed since 1997.

A BAT spokesman admitted that food additives such as cocoa butter and liquorice are already used in brands such as Lucky Strike to add a subtle taste. The spokesman added: “The amounts are tiny but they allow you to play very subtly with the taste of cigarettes. They (the additives) are handy, they are useful, they are food-type ingredients.”

Source: The Independent, 3 June 2004.

Link: http://news.independent.co.uk/uk/health_medical/story.jsp?story=527695

Filed under: Nicotine :

Nicotine

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— Effect on sperm quality, testicular function worse than cigarettes

Kevin Sabet was a drug control policy adviser in the White House for both Republicans and Democrats

Big investors lining up to cash-in on pot

‘Not your Woodstock weed’

Potent pot and drug-induced psychosis

Most e-cigs contain toxic metals, and using them may increase the risk of a heart attack

A new survey suggests that teens who use Juul e-cigs aren’t aware of these risks

Abstract

Conflict of interest statement

Study finds combined use of cigarettes and marijuana may increase children’s exposure to second-hand smoke

FEATURED ADDICTION EXPERT: Daniel M. Blumenthal, MD, MBA Attending Physician, Division of Cardiology, Massachusetts General Hospital Instructor of Medicine at Harvard Medical School Associate Chief Medical Officer at Devoted Health

FEATURED ADDICTION EXPERT: Frederick S. Southwick, MD Professor of Internal Medicine and Former ​Chief of Infectious Diseases at the University of Florida 2010 Harvard University Advanced Leadership Fellow Expert in Medicine, Infectious Disease and Medical Errors​

Links:

FEATURED ADDICTION EXPERT:
Daniel M. Blumenthal, MD, MBA
Attending Physician, Division of Cardiology, Massachusetts General Hospital
Instructor of Medicine at Harvard Medical School
Associate Chief Medical Officer at Devoted Health

FEATURED ADDICTION EXPERT:
Frederick S. Southwick, MD
Professor of Internal Medicine and Former Chief of Infectious Diseases at the University of Florida
2010 Harvard University Advanced Leadership Fellow
Expert in Medicine, Infectious Disease and Medical Errors