(J Thorac Oncol. (2008 Dec 3) P| 1371-2.)
Cannabis smoking and risk of lung cancer in men: a pooled analysis of three studies in Maghreb.Cannabis is the most widely consumed illicit drug worldwide and the relation between cannabis smoking and lung cancer is suggestive, albeit inconclusive. METHOD: We conducted three hospital based case-control studies in Tunisia, Morocco, and Algeria, three areas of high prevalence of cannabis consumption as well as production. This paper presents the pooled analysis of these three studies restricted to men with a total of 430 cases and 778 controls.
RESULTS: Ninety-six percent of the cases and 67.8% of the controls were tobacco smokers and 15.3% of the cases and 5% of the controls were ever cannabis smokers. All cannabis smokers were tobacco users. Adjusting for country, age, tobacco smoking, and occupational exposure, the odds ratio (OR) for lung cancer was 2.4 (95% confidence interval [CI]: 1.6-3.8) for ever cannabis smoking. This association remained after adjustment for lifetime tobacco packyears as continuous variable, OR = 2.3 (95% CI: 1.5-3.6). The OR adjusted for intensity of tobacco smoking (cigarette/d) among current tobacco smokers and never cannabis smokers was 10.9 (95% CI: 6.0-19.7) and the OR among current tobacco users and ever cannabis smokers was 18.2 (95% CI: 8.0-41.0). The risk of lung cancer increased with increasing joint-years, but not with increasing dose or duration of cannabis smoking.
CONCLUSION: Our results suggest that cannabis smoking may be a risk factor for lung cancer. However, residual confounding by tobacco smoking or other potential confounders may explain part of the increased risk
Division of Pulmonaiy & Critical Care Medicine, Department of Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095-1690, USA. [email protected]
In many societies, marijuana is the second most commonly smoked substance after tobacco. While delta9-tetrahydrocannabinol (THC) is unique to marijuana and nicotine to tobacco, the smoke of marijuana, like that of tobacco, consists of a toxic mixture of gases and particulates, many of which are known to be harmful to the lung. Although far fewer marijuana than tobacco cigarettes are generally smoked on a daily basis, the pulmonary consequences of marijuana smoking may be magnified by the greater deposition of smoke particulates in the lung due to the differing manner in which marijuana is smoked. Whereas THC causes modest short-term bronchodilation, regular marijuana smoking produces a number of long-term pulmonary consequences, including chronic cough and sputum, histopathologic evidence of widespread airway inflammation and injury and immunohistochemical evidence of dysregulated growth of respiratory epithelial cells, that may be precursors to lung cancer. The THC in marijuana could contribute to some of these injurious changes through its ability to augment oxidative stress, cause mitochondrial dysfunction, and inhibit apoptosis. On the other hand, physiologic, clinical or epidemiologic evidence that marijuana smoking may lead to chronic obstructive pulmonary disease or respiratory cancer is limited and inconsistent. Habitual use of marijuana is also associated with abnormalities in the structure and function of alveolar macrophages, including impairment in microbial phagocytosis and killing that is associated with defective production of immunostimulatory cytokines and nitric oxide, thereby potentially predisposing to pulmonary infection. In view of the growing interest in medicinal marijuana, further epidemiologic studies are needed to clarify the true risks of regular marijuana smoking on respiratory health.
Tobacco and Cancer Group, International Agency for Research on Cancer, Lyon, France.
The association between the use of cannabis and the risk of lung cancer is unclear. A hospital-based case-control study was conducted among men in Tunisia and included 149 incident lung cancer cases and 188 controls. Tobacco smoking was significantly associated with an increased risk of lung cancer with odds ratios increasing linearly (p for trend < 0.0001) from 3.9 (95% confidence interval [CI], 1.4-10.9) for former smokers to 17.1 (95% CI: 6.3-46.3) among current smokers who had smoked for >35 years. The odds ratio for the past use of cannabis and lung cancer was 4.1 (95% CI: 1.9-9.0) after adjustment for age, tobacco use, and occupational exposures. No clear dose-response relationship was observed between the risk of lung cancer and the intensity or duration of cannabis use. This study suggests that smoking cannabis may be a risk factor for lung cancer.
D'Souza, Deepak Cyril et al. (2009) "PSYCHOPHARMACOLOGY" P|569-578
Acute and chronic exposure to cannabinoids has been associated with cognitive deficits, a higher risk for schizophrenia and other drug abuse. However, the precise mechanism underlying such effects is not known. Preclinical studies suggest that cannabinoids modulate brain-derived neurotrophic factor (BDNF). Accordingly, we hypothesized that Delta(9)-tetrahydrocannabinol (Delta(9)-THC), the principal active component of cannabis, would alter BDNF levels in humans.
Healthy control subjects (n = 14) and light users of cannabis (n = 9) received intravenous administration of (0.0286 mg/kg) Delta(9)-THC in a double-blind, fixed order, placebo-controlled, laboratory study. Serum sampled at baseline, after placebo administration, and after Delta(9)-THC administration was assayed for BDNF using ELISA.
Delta(9)-THC increased serum BDNF levels in healthy controls but not light users of cannabis. Further, light users of cannabis had lower basal BDNF levels. Delta(9)-THC produced psychotomimetic effects, perceptual alterations, and "high" and spatial memory impairments.
The effects of socially relevant doses of cannabinoids on BDNF suggest a possible mechanism underlying the consequences of exposure to cannabis. This may be of particular importance for the developing brain and also in disorders believed to involve altered neurodevelopment such as schizophrenia. Larger studies to investigate the effects of cannabinoids on BDNF and other neurotrophins are warranted.
Gudlowski, Y et al. (2008) "GESUNDHEITSWESEN" p|653-657
Cannabis consumption has varying effects over the whole life span, especially on achievements in the areas of schooling, professional life and performance in a social environment. Data from Studies oil remission from neurocognitive deficits following chronic cannabis consumption are ambiguous. The outcome range included everything from complete remission over considerable lasting deficits up to even chronic psychotic disorders. The data seem to be consistent however, when a differentiation between early begin of consumption (before the age of 16) and late begin of consumption is taken into account. Mainly those cannabis users with an early begin of consumption are prone to developing lasting neurocognitive deficits and even a decrease in grey Substance volume, as well as an increase in the risk of psychosis. The correlation of this outcome with cannabis Consumption during a phase of brain development that includes the consolidation of higher cognitive functions, awareness of social cues, planning of concepts and motivation as well as tools of functional control, is highly convincing. The endocannabinoid system reaches the point of highest receptor density during this age of 16/17 years, and many of the above-mentioned developmental processes are modulated by this system. A chronic damage to this system (e.g., down-regulation or desensitisation of CB1receptors by exogenous cannabinoids) therefore holds the potential for permanent neurophysiological as well as neurocognitive deficits, and also for the development of psychotic disorders.