Klipspringer:Asmodeus:
Fact is it doesn't kill or even really hurt people in itself (whereas tobacco and alcohol do very much). The harm from cannabis comes because it is illegal and therefore unregulated and supplied by criminals.
Maybe you should tell these guys because it seems you know something they dont:The British Lung Foundation has commissioned a survey into tobacoo and cannabis usage amongst 1,045 people in Britain, and has found that smoking cannabis presents a much greater risk of lung cancer than does tobacco – 20 times more, in fact
That's a lovely piece of non-peer-reviewed anti-cannabis propaganda you have there from a biased organisation using cherry-picked data :)
Proper peer-reviewed Medline indexed studies from respected medical journals are the only source of good information. Unfortunately, even the majority of those have poor study designs.
In addition to that, cannabis does not have to be smoked, It can be vapourised eaten or used as a tincture. There is no evidence for non-smoked cannabis causing cancer. Any smoke is bad for you, but the frequency and amounts smoked by the typical non-cigarette smoking cannabis user are small.
Here's a few proper studies refuting what you posted:
http://www.ncbi.nlm.nih.gov/pubmed/16054989
Alcohol. 2005 Apr;35(3):265-75.Epidemiologic review of marijuana use and cancer risk.Hashibe M, Straif K, Tashkin DP, Morgenstern H, Greenland S, Zhang ZF.SourceInternational Agency for Research on Cancer, 69008 Lyon, France.
AbstractMarijuana is the most commonly used illegal drug in the United States and is considered by young adults to be the illicit drug with the least risk. On the other hand, marijuana smoke contains several of the same carcinogens and co-carcinogens as the tar from tobacco, raising concerns that smoking of marijuana may be a risk factor for tobacco-related cancers. We reviewed two cohort studies and 14 case-control studies with assessment of the association of marijuana use and cancer risk. In the cohort studies, increased risks of lung or colorectal cancer due to marijuana smoking were not observed, but increased risks of prostate and cervical cancers among non-tobacco smokers, as well as adult-onset glioma among tobacco and non-tobacco smokers, were observed. The 14 case-control studies included four studies on head and neck cancers, two studies on lung cancer, two studies on non-Hodgkin's lymphoma, one study on anal cancer, one study on penile cancer, and four studies on childhood cancers with assessment of parental exposures. Zhang and colleagues reported that marijuana use may increase risk of head and neck cancers in a hospital-based case-control study in the United States, with dose-response relations for both frequency and duration of use. However, Rosenblatt and co-workers reported no association between oral cancer and marijuana use in a population-based case-control study. An eightfold increase in risk among marijuana users was observed in a lung cancer study in Tunisia. However, there was no assessment of the dose response, and marijuana may have been mixed with tobacco. Parental marijuana use during gestation was associated with increased risks of childhood leukemia, astrocytoma, and rhabdomyosarcoma, but dose-response relations were not assessed. In summary, sufficient studies are not available to adequately evaluate marijuana impact on cancerrisk. Several limitations of previous studies include possible underreporting where marijuana use is illegal, small sample sizes, and too few heavy marijuana users in the study sample. Recommendations for future studies are to (1) focus on tobacco-related cancer sites; (2) obtain detailed marijuana exposure assessment, including frequency, duration, and amount of personal use as well as mode of use (smoked in a cigarette, pipe, or bong; taken orally); (3) adjust for tobacco smoking and conduct analyses on nonusers of tobacco; and (4) conduct larger studies, meta-analyses, or pooled analyses to maximize statistical precision and investigate sources of differences in results. Despite the challenges, elucidation of the association between marijuana use and cancer risk is important in weighing the benefits and risks of medical marijuana use and to clarify the impact of marijuana use on public health.
http://www.ncbi.nlm.nih.gov/pubmed/18235388
Rev Mal Respir. 2007 Oct;24(8 Pt 2):6S10-5.[Novel epidemiology in lung cancer - non-smokers, women and cannabis].[Article in French]Quoix E.SourceDépartement de pneumologie, Hôpitaux Universitaires, Strasbourg cedex, France. elisabeth.quoix@chru-strasbourg.fr
AbstractActive tobacco-smoking is the main risk factor of developing a lung cancer and the increase in smoking since the end of the sixties among French women partly explains the increase in lung cancer that has been observed in this group recently. However the part of the risk attributable to active tobacco-smoking is less in women than men and other aetiological factors need to be considered. There are some suggestions that females have a higher susceptibility to the carcinogenic effects of tobacco smoke even if the intrinsic risk of developing lung cancer is lower than in males. The incidence of lung cancer in non-smokers seems to be increasing and this may be partly due to the ageing of the general population. This incidence is variable according to continents, non-smokers with lung cancer being more frequent in Asia compared to Europe or North-America with the difference being even more pronounced in females. Histological subtype also differs according to sex and smoking habits. Adenocarcinoma is the most important histological subtype in females but also in the youngest cohorts of lung cancer patients probably linked to the modification of smoking habits (use of filters and blond tobacco). The role of cannabis as a risk factor of lung cancer is difficult to assess as most cannabis smokers are also tobacco-smokers but recent epidemiological studies suggest that cannabis is not carcinogenic.
http://www.ncbi.nlm.nih.gov/pubmed/21462790
Prescrire Int. 2011 Jan;20(112):18-23.Adverse effects of cannabis.[No authors listed]AbstractCannabis, Cannabis sativa L., is used to produce a resin that contains high levels of cannabinoids, particularly delta9-tetrahydrocannabinol (THC), which are psychoactive substances. Although cannabis use is illegal in France and in many other countries, it is widely used for its relaxing or euphoric effects, especially by adolescents and young adults. What are the adverse effects of cannabis on health? During consumption? And in the long term? Does cannabis predispose users to the development of psychotic disorders? To answer these questions, we reviewed the available evidence using the standard Prescrire methodology. The long-term adverse effects of cannabis are difficult to evaluate. Since and associated substances, with or without the user's knowledge. Tobacco and alcohol consumption, and particular lifestyles and behaviours are often associated with cannabis use. Some traits predispose individuals to the use of psychoactive substances in general. The effects of cannabis are dosedependent.The most frequently report-ed adverse effects are mental slowness, impaired reaction times, and sometimes accentuation of anxiety. Serious psychological disorders have been reported with high levels of intoxication. The relationship between poor school performance and early, regular, and frequent cannabis use seems to be a vicious circle, in which each sustains the other. Many studies have focused on the long-term effects of cannabis on memory, but their results have been inconclusive. There do not * About fifteen longitudinal cohort studies that examined the influence of cannabis on depressive thoughts or suicidal ideation have yielded conflicting results and are inconclusive. Several longitudinal cohort studies have shown a statistical association between psychotic illness and self-reported cannabis use. However, the results are difficult to interpret due to methodological problems, particularly the unknown reliability of self-reported data. It has not been possible to establish a causal relationship in either direction, because of these methodological limitations. In Australia, the marked increase in cannabis use has not been accompanied by an increased incidence of schizophrenia. On the basis of the available data, we cannot reach firm conclusions on whether or not cannabis use causes psychosis. It seems prudent to inform apparently vulnerable individuals that cannabis may cause acute psychotic decompensation, especially at high doses. Users can feel dependent on cannabis, but this dependence is usually psychological. Withdrawal symptoms tend to occur within 48 hours following cessation of regular cannabis use, and include increased irritability, anxiety, nervousness, restlessness, sleep difficulties and aggression. Symptoms subside within 2 to 12 weeks. Driving under the influence of cannabis doubles the risk of causing a fatal road accident. Alcohol consumption plays an even greater role. A few studies and a number of isolated reports suggest that cannabis has a role in the occurrence of cardiovascular adverse effects, especially in patients with coronary heart disease. Numerous case-control studies have investigated the role of cannabis in the incidence of some types of cancer. Its role has not been ruled out, but it is not possible to determine whether the risk is distinct from that of the tobacco with which it is often smoked. Studies that have examined the influence of cannabis use on the clinical course of hepatitis C are inconclusive. Alcohol remains the main toxic agent that hepatitis C patients should avoid. In practice, the adverse effects of low-level, recreational cannabis use are generally minor, although they can apparently be serious in vulnerable individuals. The adverse effects of cannabis appear overall to be less serious than those of alcohol, in terms of neuropsychological and somatic effects, accidents and violence.
http://www.ncbi.nlm.nih.gov/pubmed/9358987Clin Rev Allergy Immunol. 1997 Fall;15(3):243-69.Marijuana. Respiratory tract effects.Van Hoozen BE, Cross CE.SourceDivision of Pulmonary and Critical Care Medicine, University of California at Davis, Sacramento 95817, USA.
AbstractDaily marijuana smoking has been clearly shown to have adverse effects on pulmonary function and produce respiratory symptomatology (cough, wheeze, and sputum production) similar to that of tobacco smokers. Based on the tobacco experience, decrements in pulmonary function may be predictive of the future development of chronic obstructive pulmonary disease (COPD). However, in the absence of alpha-1-antitrypsin deficiency, the habitual marijuana-only smoker would likely have to smoke 4-5 joints per day for a span of at least 30 yr in order to develop overt manifestations of COPD. The mutagenic/carcinogenic properties of marijuana smoke are also well-established. The potential for induction of laryngeal, oropharyngeal, and possibly bronchogenic carcinoma from marijuana has been documented by several case reports and observational series. Despite this, a relative risk ratio for the development of these tumors has not yet been quantified. Based on a higher frequency of case reports for upper airway cancercompared to bronchogenic carcinoma, marijuana smoking may have a more deleterious effect on the upper respiratory tract. However, this hypothesis remains speculative at best, pending confirmation by longitudinal studies.
http://www.ncbi.nlm.nih.gov/pubmed/3520605Pharmacol Rev. 1986 Mar;38(1):1-20.Health aspects of cannabis.Hollister LE.AbstractMarijuana seems firmly established as another social drug in Western countries, regardless of its current legal status. Patterns of use vary widely. As with other social drugs, the pattern of use is critical in determining adverse effects on health. Perhaps the major area of concern about marijuana use is among the very young. Using any drug on a regular basis that alters reality may be detrimental to the psychosocial maturation of young persons. Chronic use of marijuana may stunt the emotional growth of youngsters. Evidence for an amotivational syndrome is largely based on clinical reports; whether marijuana use is a cause or effect is uncertain. A marijuana psychosis, long rumored, has been difficult to prove. No one doubts that marijuana use may aggravate existing psychoses or other severe emotional disorders. Brain damage has not been proved. Physical dependence is rarely encountered in the usual patterns of social use, despite some degree of tolerance that may develop. The endocrine effects of the drug might be expected to delay puberty in prepubertal boys, but actual instances have been rare. As with any material that is smoked, chronic smoking of marijuana will produce bronchitis; emphysema or lung cancer have not yet been documented. Cardiovascular effects of the drug are harmful to those with preexisting heart disease; fortunately the number of users with such conditions is minimal. Fears that the drug might accumulate in the body to the point of toxicity have been groundless. The potential deleterious effects of marijuana use on driving ability seem to be self-evident; proof of such impairment has been more difficult. The drug is probably harmful when taken during pregnancy, but the risk is uncertain. One would be prudent to avoid marijuana during pregnancy, just as one would do with most other drugs not essential to life or well-being. No clinical consequences have been noted from the effects of the drug on immune response, chromosomes, or cell metabolites. Contamination of marijuana by spraying with defoliants has created the clearest danger to health; such attempts to control production should be abandoned. Therapeutic uses for marijuana, THC, or cannabinoid homologs are being actively explored. Only the synthetic homolog, nabilone, has been approved for use to control nausea and vomiting associated with cancer chemotherapy.
On non-smoked cannabis:
http://www.ncbi.nlm.nih.gov/pubmed/18286801
Cannabis sativa L. preparations have been used in medicine for millenia. However, concern over the dangers of abuse led to the banning of the medicinal use of marijuana in most countries in the 1930s. Only recently, marijuana and individual natural and synthetic cannabinoid receptor agonists and antagonists, as well as chemically related compounds, whose mechanism of action is still obscure, have come back to being considered of therapeutic value. However, their use is highly restricted. Despite the mild addiction to cannabis and the possible enhancement of addiction to other substances of abuse, when combined with cannabis, the therapeutic value of cannabinoids is too high to be put aside. Numerous diseases, such as anorexia, emesis, pain, inflammation, multiple sclerosis, neurodegenerative disorders (Parkinson's disease, Huntington's disease, Tourette's syndrome, Alzheimer's disease), epilepsy, glaucoma, osteoporosis, schizophrenia, cardiovascular disorders, cancer, obesity, and metabolic syndrome-related disorders, to name just a few, are being treated or have the potential to be treated by cannabinoid agonists/antagonists/cannabinoid-related compounds. In view of the very low toxicity and the generally benign side effects of this group of compounds, neglecting or denying their clinical potential is unacceptable--instead, we need to work on the development of more selective cannabinoid receptor agonists/antagonists and related compounds, as well as on novel drugs of this family with better selectivity, distribution patterns, and pharmacokinetics, and--in cases where it is impossible to separate the desired clinical action and the psychoactivity--just to monitor these side effects carefully.
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