THE REAL DANGER OF CANNABIS

What's Wrong With Permiting The Use of Smoked Marijuana

Simply put, the smoked form of marijuana is not considered modern medicine. On April 20th, 2006, the FDA issued an advisory concluding that no sound scientific studies have supported medical use of smoked marijuana for treatment in the United States, and no animal or human data support the safety or efficacy of smoked marijuana for general medical use.

A number of states have passed voter referenda or legislative actions making smoked marijuana available for a variety of medical conditions upon a doctor's recommendation. According to the Food and Drug Administration (FDA), these measures are inconsistent with efforts to ensure medications undergo the rigorous scientific scrutiny of the FDA approval process and are proven safe and effective under the standards of the FD&C Act.

While smoking marijuana may allow patients to temporarily feel better, the medical community makes an important distinction between inebriation and the controlled delivery of pure pharmaceutical medication. The raw (leaf ) form of marijuana contains a complex mixture of compounds in uncertain concentrations, the majority of which have unknown pharmacological effects.

The Institute of Medicine (IOM) has concluded that smoking marijuana is not recommended for any long-term medical use, and a subsequent IOM report declared that, “marijuana is not modern medicine.” Additionally, the American Medical Association, the National Cancer Institute, the American Cancer Society, and the National Multiple Sclerosis Society do not support the smoked form of marijuana as medicine.

Smoking Marijuana May Unintentionally Cause Serious Harm to Patients

The delicate immune systems of seriously ill patients may become compromised by the smoking of marijuana. Additionally, the daily use of marijuana compromises lung function and increases the risk for respiratory diseases, similar to those associated with nicotine cigarettes.

Marijuana has a high potential for abuse and can incur addiction. Frequent use of marijuana leads to tolerance to the psychoactive effects and smokers compensate by smoking more often or seeking higher potency marijuana.

In people with psychotic or other problems, the use of marijuana can precipitate severe emotional disorders. Chronic use of marijuana may increase the risk of psychotic symptoms in people with a past history of schizophrenia. Marijuana smoking by young people may lead to severe impairment of higher brain function and neuropsychiatric disorders, as well as a higher risk for addiction and polydrug abuse problems.

Existing Legal Drugs Provide Superior Treatment for Serious Medical Conditions

The FDA has approved safe and effective medication for the treatment of glaucoma, nausea, wasting syndrome, cancer, and multiple sclerosis.

Marinol, the synthetic form of THC (the psychoactive ingredient contained in marijuana), is already legally available for prescription by physicians whose patients suffer from pain and chronic illness.

“Medical marijuana was supposed to be for the truly ill cancer victims and AIDS patients who could use the drug to relieve pain or restore their appetites. Yet the number of dispensaries has skyrocketed from five in 2005 to 143 by the end of 2006. In North Hollywood alone, there are more pot clinics than Starbucks.”
–Pasadena Star-News, January 21st, 2007



In Their Words: What the Experts Say:

The American Academy of Ophthalmology:

“Based on reviews by the National Eye Institute (NEI) and the Institute of Medicine and on available scientific evidence, the Task Force on Complementary Therapies believes that no scientific evidence has been found that demonstrates increased benefits and/or diminished risks of marijuana use to treat glaucoma compared with the wide variety of pharmaceutical agents now available.”
Complementary Therapy Assessment: Marijuana in the Treatment of Glaucoma, American Academy of Ophthalmology, May 2003

The American Medical Association:

“...AMA recommends that marijuana be retained in Schedule I of the Controlled Substances Act...AMA believes that the NIH should use its resources and influence to support the development of a smoke-free inhaled delivery system for marijuana or delta-9-tetrahydrocannabinol (THC) to reduce the health hazards associated with the combustion and inhalation of marijuana...”
Policy Statement H-95.952, American Medical Association, http://www.ama-assn.org

The National Multiple Sclerosis Society:

“Studies completed thus far have not provided convincing evidence that marijuana or its derivatives provide substantiated benefits for symptoms of MS.”
The MS Information Sourcebook, Marijuana (Cannabis), National Multiple Sclerosis Society, September 18th, 2006

The Institute of Medicine (IOM):

“Because of the health risks associated with smoking, smoked marijuana should generally not be recommended for long-term medical use.”
Marijuana and Medicine: Assessing the Science Base, Institute of Medicine, 1999

link---http://www.whitehousedrugpolicy.gov/drugfact/factsht/medical_marijuana.html

Peregrine(Endangered) wrote: others could die wheter they used alot or little

Die?

You do know that you would have to smoke 40,000, yep THOUSAND, times the quantity it would take to get stoned for that to come close to even being the case. And since I would consider that amount physically impossible.....

Marijuana affects your brain. THC (the active ingredient in marijuana) affects the nerve cells in the part of the brain where memories are formed.

Marijuana affects your self-control. Marijuana can seriously affect your sense of time and your coordination, impacting things like driving. In 2002, nearly 120,000 people were admitted to emergency rooms suffering from marijuana-related problems, an increase of more than 139 percent since 1995.1

Marijuana affects your lungs. There are more than 400 known chemicals in marijuana. A single joint contains four times as much cancer-causing tar as a filtered cigarette.2

Marijuana affects other aspects of your health. Marijuana can limit your body's ability to fight off infection.3 Long-term marijuana use can even increase the risk of developing certain mental illnesses.4

Marijuana is not always what it seems. Marijuana can be laced with other dangerous drugs without your knowledge. "Blunts"--hollowed-out cigars filled with marijuana--sometimes have substances such as crack cocaine, PCP, or embalming fluid added.

Marijuana can be addictive. Not everyone who uses marijuana becomes addicted, but some users do develop signs of dependence. In 1999, more than 220,000 people entered drug treatment programs to kick their marijuana habit.5



Know the law. It is illegal to buy or sell marijuana. In most States, holding even small amounts of marijuana can lead to fines or arrest.

Get the facts. Smoking any substance--tobacco, marijuana, or crack cocaine--increases your risk of developing pneumonia and other illnesses.6

Stay informed. It has not yet been proven that using marijuana leads to using other drugs. But very few people use other drugs without first using marijuana. Teens who smoke marijuana are more likely to try other drugs, in part because they have more contact with people who use and sell them.

Know the risks. Using marijuana or other drugs increases your risk of injury from car crashes, falls, burns, drowning, and other accidents.

Keep your edge. Marijuana affects your judgment, drains your motivation, and can make you feel anxious.

Look around you. Most teens aren't smoking marijuana. According to a 2002 study, about four out of five 12- to 17-year-old youths had never even tried marijuana.7



How can you tell if a friend is using marijuana? Sometimes it's tough to tell. But there are signs you can look for. If your friend has one or more of the following warning signs, he or she may be using marijuana:

Seeming dizzy and having trouble walking
Having red, bloodshot eyes and smelly hair and clothes
Having a hard time remembering things that just happened
Acting silly for no apparent reason
What can you do to help someone who is using marijuana or other drugs? Be a real friend. Encourage your friend to seek professional help. For information and referrals, call the National Clearinghouse for Alcohol and Drug Information at 800-729-6686.



Q. Isn't smoking marijuana less dangerous than smoking cigarettes?
A. No. It's even worse. One joint affects the lungs as much as four cigarettes.8

Q. Can people become addicted to marijuana?
A. Yes. Research confirms you can become hooked on marijuana.

Q. Can marijuana be used as a medicine?
A. While the active ingredient in marijuana, THC, can be manufactured in a pill available by prescription to treat nausea and vomiting associated with certain cancer treatments, scientists say that more research needs to be done on its side effects and other potential medical uses.9



To learn more about marijuana or obtain referrals to programs in your community, contact one of the following toll-free numbers:

SAMHSA’s National Clearinghouse for Alcohol and Drug Information
800-729-6686
TDD 800-487-4889
linea gratis en español
877-767-8432

Curious about the TV ads of the National Youth Anti-Drug Media Campaign? Check out the Web site at www.freevibe.com or visit the Office of National Drug Control Policy Web site at www.whitehousedrugpolicy.gov.

The bottom line: If you know someone who smokes marijuana, urge him or her to stop or get help. If you're smoking marijuana--stop! The longer you ignore the real facts, the more chances you take with your health and well-being.

It's never too late. Talk to your parents, a doctor, a counselor, a teacher, or another adult you trust.

Do it today!


--------------------------------------------------------------------------------

Footnotes

1 The DAWN Report. Major Drugs of Abuse in ED Visits, 2002 Update. Substance Abuse and Mental Health Services Administration (SAMHSA), May 2004.

2 Effects of Marijuana on the Lungs and Its Immune Defenses. University of California-Los Angeles School of Medicine Study, 1997.

3 Ibid.

4 Marijuana: Facts Parents Need to Know (Revised). National Institute on Drug Abuse (NIDA), 2002.

5 Ibid.

6 Mueller, M.D. NIDA Notes, Vol. 12, No. 1. NIDA, Jan/Feb 1997.

7 2002 National Survey on Drug Use and Health. SAMHSA, 2002.

8 Effects of Marijuana on the Lungs and Its Immune Defenses. University of California-Los Angeles School of Medicine Study, 1997.

9 Marijuana: Facts For Teens (Revised). National Institute on Drug Abuse (NIDA), 2003.

suggested link
http://www.whitehousedrugpolicy.gov/publications/marijuana_myths_facts/marijuana_myths_facts.pdf

WHO Project on Health Implications of Cannabis Use:

A Comparative Appraisal of the Health and Psychological Consequences of Alcohol, Cannabis, Nicotine and Opiate Use


II. THE PROBABLE HEALTH EFFECTS OF CANNABIS USE


Acute Psychological and Health Consequences

The acute toxicity of cannabis is very low. There are no confirmed cases of human deaths from cannabis poisoning in the world medical literature. Animal studies indicate that the dose of THC required to produce 50% mortality in rodents is extremely high by comparison with other commonly used pharmaceutical and recreational drugs. The lethal dose also increases as one moves up the phylogenetic tree, suggesting by extrapolation that the lethal increases as one moves up the phylogenetic tree, suggesting by extrapolation that the lethal dose in humans could not be very easily achieved by smoking or ingesting the drug (Grinspoon and Bakalar, 1993; Rosencrantz, 1983).

Dysphoric effects

The most common unpleasant acute psychological effects of cannabis use are anxiety, sometimes producing unpleasant depressive feelings (Tart, 1970; Weil, 1970). These effects are most often reported by naive users who are unfamiliar with the drug's effects, and by patients who have been given oral THC for therapeutic purposes. More experienced users may occasionally report these effects after receiving a much larger than intended dose of THC. These effects can usually be prevented by adequate preparation of users about the type of effects they may experience, or they can be managed by reassurance and support (Weil, 1970).

Motor vehicle accidents

The major potential health risks from the acute use of cannabis arise from its effects on cognitive and psychomotor performance. Intoxication produces dose-related impairments in a wide range of cognitive and behavioural functions that are relevant to a skilled performance like driving an automobile or operating machinery. These include: slowed reaction time and information processing, impaired perceptual-motor coordination and motor performance, impaired short term memory, signal detection, tracking behaviour and slowed time perception. (Chait and Pierri, 1992).

The negative effects of cannabis on the performance of psychomotor tasks is almost always related to dose (Chait and Pierri, 1992). The effects are generally larger, more consistent and persistent in different tasks which involve sustained attention. The acute effects of "recreational" doses of cannabis on driving performance in laboratory simulators and over standardised driving courses are similar to those of doses of alcohol that achieve BACs between 0.07% and 0.10% (Hansteen, Miller, Lonero, Reid and Jones, 1976; Peck et al, 1986; Smiley, 1986).

While cannabis impairs performance in laboratory and simulated driving settings, it is difficult to relate the magnitude of these impairments to an increased risk of being involved in motor vehicle accidents. Students of the effects of cannabis on on-road driving performance have found at most modest impairments (e.g. Sutton, 1983). Cannabis intoxicated persons drive more slowly perhaps because they are more aware of their level of psychomotor impairment than alcohol intoxicated drinkers who generally drive at faster speeds (Smiley, 1986).

No controlled epidemiological studies have established that cannabis users are at increased risk of motor vehicle accidents. A prospective Swedish study of mortality over 15 years among military conscripts found an increased risk of premature mortality among men who had smoked cannabis 50 or more times by age 18. Violent deaths were the major contributor to this excess, of which 26% were motor vehicle and 7% other accidents (e.g. drownings and falls). The increased risk disappeared, however, after multivariate statistical adjustment for confounding variables such as alcohol and other drug use (Andreasson and Allebeck, 1990).

Uncertainty about the role of cannabis in motor vehicle accidents is likely to remain since case-control studies are difficult to conduct and interpret (see chapter by Smiley this volume). Blood levels of cannabinoids do not indicate whether a driver or pedestrian was intoxicated with cannabis at the time of an accident, and many drivers with cannabinoids in their blood were also intoxicated with alcohol at the time of the accident (Smiley, 1986). Factors other than psychomotor performance also contribute to the danger of drug use when driving. Foremost among these is the user's preparedness to take risks when intoxicated, which the available evidence suggests is reduced by cannabis intoxication by contrast with alcohol intoxication which consistently increases risk-taking (Smiley, 1986)




http://www.druglibrary.org/schaffer/hemp/general/who-comparison.htm

same link

The Health Effects of Chronic Cannabis Use

The Immune System

There is reasonably consistent evidence that THC can produce cellular changes such as alterations in cell metabolism, and DNA synthesis, in vitro (Bloch, 1983). There is even stronger evidence that cannabis smoke is mutagenic in vitro, and in vitro, and hence, that it is potentially carcinogenic for the same reasons as tobacco smoke (Leuchtenberger, 1983).

There is reasonably consistent evidence that cannabinoids impair both the cell-mediated and humoral immune systems in rodents (Munson and Fehr, 1983). These changes have decreased resistance to infection by bacteria and viruses. There is also evidence that the noncannabinoid components of cannabis smoke impair the functioning of alveolar macrophages, the first line of the body's defence system in the lungs (Munson and Fehr, 1983). The relevance of these findings to human health is uncertain: the doses required to produce these effects are often very high, and the problem of extrapolating from the effects of these doses to those used by humans is complicated by the possibility that tolerance develops to the effects on the immune system (Hollister, 1992).

Moreover, the limited experimental and clinical evidence on immune effects in humans is mixed, with a small number of early studies that have suggested adverse effects not being replicated by later ones (Munson and Fehr, 1983; Hollister, 1992). At present, there is no conclusive evidence that consumption of cannabinoids predisposes humans to immune dysfunction, as measured by reduced numbers or impaired functioning of T-lymphocytes, B-lymphocytes or macrophages, or reduced immunoglobulin levels.

The clinical and biological significance of these possible immunological impairments in chronic cannabis uses is uncertain. To date there has been no epidemiological evidence of increased rates of disease among chronic heavy cannabis users. There is one large prospective study of HIV-positive homosexual men which indicates that continued cannabis use did not increase the risk of progression to AIDS (Kaslow et al, 1989). Given the duration of large scale cannabis use by young adults in Western societies, the absence of any epidemics of infectious disease makes it unlikely that cannabis smoking produces major impairments in the immune system.

It is more difficult to exclude the possibility that chronic heavy cannabis use produces minor impairments in immunity. Such effects would produce small increases in the rate of occurrence of common bacterial and viral illnesses among chronic users which would be of public health significance because of the increased expenditure on health services, and the increased loss of productivity that this would entail among the young adults who are the heaviest users of cannabis. A recent epidemiological study by Polen at al (1993) which compared health service utilisation by nonsmokers and daily cannabis only smokers has provided the first suggestive evidence of an increased rate of presentation for respiratory conditions among cannabis smokers. This remains suggestive, however, because infectious and noninfectious respiratory conditions were not distinguished.

The Cardiovascular System

The conclusion reached by the Institute of medicine in 1982 still stands: the smoking of marijuana "causes changes to the heart and circulation that are characteristics of stress ...[but] there is no evidence ... that it exerts a permanently deleterious effect on the normal cardiovascular system ..." (p 72). The cardiovascular effects of cannabis may be less benign in patients with hypertension, cerebrovascular disease and coronary atherosclerosis for whom marijuana poses a threat by increasing the work of the heart (Aronow and Cassidy, 1974, 1975).

The Respiratory System

Chronic heavy cannabis smoking impairs the functioning of the large airways, and probably causes symptoms of chronic bronchitis such as coughing, sputum, and wheezing (Bloom et al, 1987; Huber et al, 1988; Tashkin et al, 1988a, 1990). Given the documented adverse effects of tobacco smoke which is qualitatively very similar in composition to cannabis smoke (Tashkin, 1993; Wu et al, 1988). There is as yet little direct evidence that the latter occurs (Huber et al, 1988) although there is evidence that chronic cannabis smoking may produce histopathological changes in lung tissues of the kind that precede the development of lung cancer (Fligiel et al, 1988).

More recently, concern about respiratory cancers has been heightened by a series of case reports of cancers of the aerodigestive tract in young adults with a history of heavy cannabis use (e.g. Caplan and Brigham, 1989; Donald, 1991; Taylor, 1988). Although these reports fall short of providing convincing evidence because they were uncontrolled and many of the cases concurrently used alcohol and tobacco, they are clearly cause for concern since such cancers are rare in adults under the age of 60, even among those who smoke tobacco and drink alcohol (Tashkin, 1993). Smoking cannabis may also pose an acute risk to individuals with respiratory diseases such as asthma. Evidence linking tobacco smoke to asthma and asthmatic symptoms is increasing.

The potential adverse effects of cannabis on the respiratory system are specific to smoking as the route of administration, and could not result from oral ingestion.

Reproductive Effects

Chronic cannabis use probably disrupts the male and female reproductive systems in animals, reducing the secretion of testosterone, and sperm production, motility, and viability in males, and disrupting the ovulatory cycle in females (Bloch, 1983; Institute of Medicine, 1982). It is uncertain whether it is these effects in humans, given the inconsistency in the limited literature on human males (Mendelson and Mello, 1984), and the lack of research in the case of human females (Hollister, 1986). There is also uncertainty about the clinical significance of these effects in normal healthy young adults. They may be of greater concern among young adolescents, and among males whose fertility has been impaired for other reasons.

Cannabis smoking during pregnancy probably impairs foetal development Gibson et al, 1983; Hatch and Bracken, 1986; Tennes et al, 1985; Zuckerman et al, 1989, leading to a reduction in birthweight (Abel, 1985). This may be a consequence of a shorter gestation period, and probably occurs by the same mechanism as cigarette smoking, namely, foetal hypoxia. There is uncertainty about whether cannabis use during pregnancy produces a small increase in the risk of birth defects as a result of exposure of the foetus in utero. There is some animal evidence of such effects although these studies have usually involved very high doses by the oral route (Abel, 1985). The limited studies in humans have generally but not consistently produced null results (Gibson et al, 1983; Hatch and Bracken, 1986; Hingson et al, 1982; Zuckerman et al, 1989).

There is not a great deal of evidence that cannabis use can produce chromosomal or genetic abnormalities in either parent which could be transmitted to offspring. Such animal and in vitro evidence as exists suggests that the mutagenic capacities of cannabis smoke are greater than those of THC, and are probably of greater relevance to the risk of users developing cancer than to the transmission of genetic defects to children (Bloch, 1983; Hollister, 1986).

There is suggestive evidence that infants exposed in utero to cannabis may experience transient behavioural and developmental effects during the first few months after birth (e.g. Fried 1985, 1989). There are several case-control studies which suggest that there is an increased risk of certain childhood cancers (namely, astrocytomas and leukemia) among children born to women who reported that they had used cannabis during their pregnancies (Kuitjen et al, 1990; Robison et al, 1989).

Possible Health Effects of Contaminants in Cannabis

Because cannabis is an illegal drug its cultivation, harvesting and distribution are not subject to quality control mechanisms to ensure the reliability and safety of the product used by consumers. It is well recognised in developing countries, such as Kenya, that illicit alcohol production can result in the contamination with toxic by-products or adulterants that can kill or seriously affect the health of users. The same may be true of illicit drugs such as opiates, cocaine and amphetamine in developed societies. There is no evidence of comparable health effects for cannabis although there were concerns expressed about the possible health effects of the use of cannabis contaminated by herbicides (such as paraquat) that were used to control illicit cannabis cultivation in the US in the 1970s. These concerns proved unfounded (Hollister, 1986). There have also been concerns about the microbial contamination of cannabis leaf but there has been little evidence (other than a small number of case histories) that this has adversely affected the health of cannabis users (Hollister, 1986).

still same link

Psychological Effects of Chronic Cannabis Use

Adult Motivation

One of the major concerns about the psychological effects of chronic heavy cannabis use has been that it impairs adult motivation. The evidence for an "amotivational syndrome" among adults consists largely of case histories and observational reports (e.g. Kolansky and Moore, 1971; Millman and Sbriglio, 1986). The small number of controlled field and laboratory studies have not found compelling evidence for such a syndrome (Dornbush, 1974; Negrete, 1983; Hollister, 1986). The evidential value of the field studies is limited by their small sample sizes, and the limited sociodemographic characteristics of their samples, while the evidential value of the laboratory studies is limited by the short periods of drug use, the youthful good health of the volunteers, and minimal demands made on volunteers in the laboratory (Cohen, 1982). Some regular cannabis users report a loss of ambition and impaired school and occupational performance as adverse effects of their use (e.g. Hendin et al, 1987) and that some ex-cannabis users give impaired occupational performance as a reason for stopping (Jones, 1984). Nonetheless, it is doubtful that cannabis use produces a well defined amotivational syndrome. It may be more parsimonious to regard the symptoms of impaired motivation as symptoms of chronic cannabis intoxication rather than inventing a new psychiatric syndrome.

Adolescent Development

In the United States in the 1970s and 1980s, cannabis use appears to have increased the risk of discontinuing a high school education, and of experiencing job instability in young adulthood (Newcombe and Bentler, 1988). The apparent strength of these relationships in cross-sectional studies (e.g. Kandel, 1984) has been exaggerated because those adolescents who are most likely to use cannabis have lower academic aspirations and poorer high school performance prior to using cannabis than their peers who do not (Newcombe and Bentler, 1988). It remains possible that factors other than the marijuana use account for apparent causal relations. To the extent they may exist, these adverse effects of cannabis and other drug use upon development over and above the effect of pre-existing nonconformity may cascade throughout young adult life, affecting choice of occupation, level of income, choice of mate, and the quality of life of the user and his or her children.

A major finding of research into the adult consequences of adolescent cannabis use has been the strong evidence of a regular sequence of initiation into the use of illicit drugs among American adolescents in the 1970s in which cannabis use preceded involvement with "harder" drugs such as stimulants and opioids (Kandel et al, 1984; Donovan and Jessor, 1983; Yamaguchi and Kandel, 1984 a, b). The causal significance of this sequence of initiation into drug use remains controversial. The hypothesis that it represents a direct effect of cannabis use upon the use of the later drugs in the sequence is the least compelling. There is better support for two other hypotheses which are not mutually exclusive: that there is a selective recruitment into cannabis use of nonconforming adolescents who have a propensity to use other illicit drugs; and that once recruited to cannabis use, the social interaction with other drug using peers, and exposure to other drugs when purchasing cannabis on the black-market, increases the opportunity to use other illicit drugs (Baumrind, 1983; Goode, 1974; Kandel, 1988).

A Dependence Syndrome

A cannabis dependence syndrome as defined in DSM-IV (American Psychiatric Association, 1994) can occur in heavy, chronic users of cannabis. There is good experimental evidence that chronic heavy cannabis users can develop tolerance to its subjective and cardiovascular effects. There is also suggestive evidence that some users may experience a withdrawal syndrome on the abrupt cessation of cannabis use, although one that is much milder and less marked than that experienced when withdrawing from alcohol or opiates (Compton, Dewey and Martin, 1990; Jones and Benowitz, 1976). DSM-IV notes that "symptoms of possible cannabis withdrawal (e.g. irritable or anxious mood accompanied by physical changes such tremor, perspiration, nausea and sleep disturbances) have been described in association with the use of very high doses, but their clinical significance is uncertain." (American Psychiatric Association, 1994:215).

There is clinical and epidemiological evidence that some heavy cannabis users experience problems in controlling their cannabis use, and continue to use the drug despite experiencing adverse personal consequences of use (Jones, 1984; Roffman et al, 1988; Weller et al, 1984). There is limited clinical evidence for a cannabis dependence syndrome analogous to the alcohol dependence (Kosten et al, 1987). Epidemiological surveys of the prevalence of drug dependence in the general population (e.g. Anthony and Helzer, 1991) show that cannabis dependence, as defined in the diagnostic manuals, is among the most common forms of drug dependence in Western societies by virtue of its high prevalence of use. On the other hand, relatively few users seek treatment for cannabis dependence (American Psychiatric Association, 1994: 220-221).

Cognitive Effects

The weight of the available evidence suggests that even the long term heavy use of cannabis does not produce any severe or grossly debilitating impairment of cognitive function (Carter et al, 1980; Fehr and Kalant, 1983b, Rubin and Comitas, 1975; Wert and Raulin, 1986). If it did research to date should have detected it. There is some clinical and experimental evidence, however, that the long-term use of cannabis may produce more subtle cognitive impairment in the higher cognitive functions of memory, attention and organisation, and the integration of complex information (Page et al, 1988; Solowij et al, 1991, 1992, 1993 and see chapter by Solowij in this volume). While subtle, these impairments may affect everyday functioning, particularly among individuals in occupations that require high levels of cognitive capacity. The evidence suggests that the longer the period that cannabis has been used, the more pronounced is the cognitive impairment (Solowij et al, 1992, 1993). It remains to be seen whether the impairment can be reversed by an extended period of abstinence from cannabis.

Brain Damage

A suspicion that chronic heavy cannabis use may cause gross structural brain damage was provoked by a single poorly controlled study using an outmoded method of investigation which reported that cannabis users had enlarged cerebral ventricles (Campbell et al, 1971). This finding was widely and uncritically publicised. Since then a number of better controlled studies using more sophisticated methods of investigation have consistently failed to demonstrate evidence of structural change in the brains of heavy, long term cannabis users (e.g. Co et al, 1977; Kuehnle et al, 1977). These negative results are consistent with the evidence that any cognitive effects of chronic cannabis use are subtle, and hence unlikely to be manifest as gross structural changes in the brain.

Serious Psychiatric Disorder

There is suggestive evidence that large doses of THC can produce an acute psychosis in which confusion, amnesia, delusions, hallucinations, anxiety, agitation and hypomanic symptoms predominate. The evidence comes from laboratory studies of the effects of THC on normal volunteers and clinical observations of psychotic symptoms in heavy cannabis users which remit rapidly following abstinence (Bernardson and Gunne, 1972; Chopra and Smith, 1974; Edwards, 1976).

There is less support for the hypothesis that cannabis use can cause either an acute or a chronic functional psychosis (Thornicroft, 1990). Such possibilities are difficult to study because of the rarity of such psychoses, and the near impossibility of distinguishing them from schizophrenia and manic depressive psychoses occurring in individuals who also use cannabis (Ghodse, 1986).

There is strongly suggestive evidence from a prospective study that heavy cannabis use may precipitate schizophrenia in vulnerable individuals (Andreasson et al, 1987; Schneier and Siris, 1987; Thornicroft, 1990). This relationship is still only strongly suggestive because in the only prospective study conducted to date (Andreasson et al, 1987) the use of cannabis was not documented at the time of diagnosis, there was a possibility that cannabis use was confounded by amphetamine use, and there are doubts about whether the study could reliably distinguish between schizophrenia and acute cannabis, or other drug-induced, psychoses (Negrete, 1989; Thornicroft, 1990).

There is less support for the hypothesis that cannabis use can cause either an acute or a chronic functional psychosis (Thornicroft, 1990). Such possibilities are difficult to study because of the rarity of such psychoses, and the near impossibility of distinguishing them from schizophrenia and manic depressive psychoses occurring in individuals who also use cannabis (Ghodse, 1986). There is better evidence that cannabis use can adversely affect the course of schizophrenia in affected individuals who continue to use it (Cleghorn et al, 1991; Jablensky et al, 1991; Martinez-Arevalo et al, 1994).

same again

III. A QUALITATIVE COMPARISON OF THE HEALTH RISKS OF ALCOHOL, CANNABIS, NICOTINE AND OPIATE USE


A useful way of assessing the health risk posed by cannabis use is a comparative qualitative appraisal of its risks with those of other widely used recreational of its risks with those of other widely used recreational drugs such as alcohol and tobacco (ARF/WHO, 1981). The motive for such comparisons is to use a common standard when making societal decisions about the control and regulation of cannabis use. Like tobacco, cannabis is most commonly smoked, and like alcohol, cannabis is commonly used for its intoxicating and euphoriant effects in developed societies (although it may be used for more utilitarian reasons, such as, making heavy physical work tolerable, in some developing countries). The opiates provide a useful illicit drug class against which to calibrate the adverse effects of cannabis since this class of drugs has a fearsome although not always deserved reputation as a major risk to the health of young adults. Nonmedical use of opiates is initially primarily for euphoria or for relief of pain.

In undertaking this qualitative comparison we have avoided the necessity to comprehensively review the vast literatures on the health effects of alcohol and tobacco by using the following authorities as the warrant for our assertions about their health risks: Anderson et al (1993); Holman et al's (1988) compendium of the health effects of alcohol and tobacco; the Institute of Medicine (1987); the International Agency for Research into Cancer (1990); Roselle et al (1993); and the Royal College of Physicians (1987).

In the absence of an authoritative current review of the health effects of the opioids as a class of drugs, it was necessary to look to several sources to identify the health effects of opioids. General pharmacological texts, and other reviews, were used to describe the pharmacological effects of the opioids (e.g., Belkin and Gold, 1991; Jacobs and Fehr, 1987; Duggan and North, 1983). In addition, information on the chronic health effects and social consequences of illicit opiates (injectable and non-injectable) and of methadone was taken from reports of several longitudinal studies of opioid users (e.g. Vaillant, 1973; O'Donnell, 1969; Maddux and Desmond, 1981; Simpson, Joe, Lehman and Sells, 1986; Joe and Simpson, 1987; 1990). These cohort studies typically involve populations in contact with drug treatment services rather than representative samples of users.

Acute Effects

Alcohol

The major risks of acute cannabis use show some parallels with the acute risks of alcohol intoxication. First, both drugs produce psychomotor and cognitive impairment, especially of memory and planning. The impairment produced by alcohol increases risks of various kinds of accident. It may also increase the likelihood of engaging in risky behaviour such as dangerous driving, and unsafe sexual practices. While cannabis intoxication increases the risks of casualties in hazardous situations, it remains to be determined to what extent it increases the likelihood of engaging in risky behaviour.

Alcohol and cannabis intoxication appear to differ in their relation to intentional rather than accidental casualties. Alcohol intoxication is strongly associated with aggressive and violent behaviour. The relationship is complex, and the nature and extent of drinking's causal effect remains controversial at the level of the individual drinker (Pernanen, 1991; Martin, 1993; Pohorecky, Brick and Milgram, 1993). But there is good causal evidence that changes in the level of alcohol consumption affect the incidence of violent crime, at least in some populations (Room, 1983; Lenke, 1990; Cook and Moore, 1993). There is also increasing evidence to indicate that alcohol may play a role in suicide (Edwards et al., forthcoming). There is little to suggest that causal relationship of cannabis use to aggression or violence, at least in present-day developed societies.

Second, there is good evidence that substantial doses of alcohol taken during pregnancy can produce a foetal alcohol syndrome. There is suggestive but far from conclusive evidence that cannabis can also adversely affect the development of the foetus when used during pregnancy. A clear equivalent for cannabis of the foetal alcohol syndrome has not been established.

Third, there is a major health risk of acute alcohol use that is not shared with cannabis. In large doses alcohol can cause death by asphyxiation, alcohol poisoning, cardiomyopathy and cardiac infarct. There are no recorded cases of overdose fatalities attributed to cannabis, and the estimated lethal dose for humans extrapolated from animal studies is so high that it cannot be achieved by recreational users.

Tobacco

The major acute health risks that cannabis shares with tobacco are the irritant effects of smoke upon the respiratory system, and the stimulating effects of both THC and nicotine on the cardiovascular system, both of which can be detrimental to persons with cardiovascular and respiratory diseases. For both drugs, the respiratory effects do not apply to ingestion that is not by inhalation.

Opioids

Some of the opioids share with alcohol and cannabis an acute intoxicating effect, although the sedative effect is more pronounced. Acute administration of heroin causes euphoria in many users, although other opioids such as methadone do not have this effect in tolerant individuals. The extent of euphoria is also affected by route of administration. As is found with cannabis, some naive users report unpleasant feelings with opiate use, specifically nausea and dysphoria. All opioids are CNS depressants and as such can reduce level of consciousness and cause sleep.

The literature on the effects of opiates on driving and other exacting skills is not well developed. A maintenance dose in a tolerant user may produce little psychomotor or cognitive impairment. A heroin user who has reached a stage of "nodding" is in no condition to drive a car, but will probably have little inclination to do so. As with cannabis, there is little direct epidemiological evidence of opiate-induced casualties. One study showed that the driving-related skills of persons maintained on stable doses of methadone were not impaired when assessed on a laboratory task that is sensitive to the effects of alcohol (Chesher, Lemon, Gomal and Murphy, 1989).

While there is no risk of overdose associated with cannabis, use of illicit opioids carries a real risk of overdose. High doses of most opioids can lead to suppression of breathing rate and blood pressure and cause respiratory arrest. The risk of overdose is worsened by use in combination with alcohol or other drugs, and is thought to be worsened by variations in the potency of opiates obtained illegally.

Opioids, like cannabis, cause some suppression of hormone levels. These decreased hormonal levels, however, do not necessarily result in infertility in men or women using opioids\do for extended periods (Belkin and Gold, 1991; Duggan and North, 1983; Martin and Martin, 1980). Like alcohol, tobacco and cannabis, the opiates have been associated with miscarriage, foetal death and low birth-weight. There is no clear relationship with an identifiable syndrome of foetal defects from opioids that parallels foetal alcohol syndrome. Although poor nutrition and pre-natal care clearly contribute to the risk of adverse outcomes in pregnant women addicted to street drugs, even methadone maintenance has been found to result in higher rates of pregnancy problems. Methadone and other orally administered opioids have been shown to cause foetal death and low birthweight in laboratory animals (Martin and Martin, 1980; Caviston, 1987; Woody and O'Brien, 1991).

Chronic Effects

Alcohol

There are a number of risks of heavy chronic alcohol use some of which may be shared by chronic cannabis use. First, heavy use of either drug increases the risk of developing a dependence syndrome in which users experience difficulty in stopping or controlling their use. There is strong evidence of such a syndrome in the case of alcohol and reasonable evidence in the case of cannabis. A major difference between the two is that withdrawal symptoms are either absent or mild after dependent cannabis users abruptly stop their cannabis use, whereas the abrupt cessation of alcohol use in severely dependent drinkers produces a well defined withdrawal syndrome which can be potentially fatal.

Second, there is reasonable clinical evidence that the chronic heavy use of alcohol can produce psychotic symptoms and psychoses in some individuals, either during acute intoxication or during the process of withdrawal in dependent drinkers. There is some clinical evidence that chronic heavy cannabis use may produce a toxic psychosis. One prospective epidemiological study suggests that heavy cannabis use may precipitate schizophrenia in predisposed individuals,. that is, those with a personal or a family history of psychiatric disorder. There is better evidence that continued cannabis use may worsen the course of schizophrenia.

Third, there is good evidence that chronic heavy alcohol use can indirectly cause brain injury - the Wernicke-Korsakov syndrome - with symptoms of severe memory defect and an impaired ability to plan and organise. With continued heavy drinking, and in the absence of vitamin supplementation, this injury may produce severe irreversible cognitive impairment. There is good reason for concluding that chronic cannabis use does not produce cognitive impairment of comparable severity. There is suggestive evidence that chronic cannabis use may produce subtle defects in cognitive functioning, that may or may not be reversible after abstinence.

Fourth, there is reasonable evidence that in the absence of countervailing cultural beliefs chronic heavy alcohol use generally impairs occupational performance in adults and educational achievements in adolescents. There is suggestive evidence that chronic heavy cannabis use produces similar, albeit more subtle impairments in occupational and educational performance of adults.

Fifth, there is good evidence that chronic, heavy alcohol use increases the risk of premature mortality from accidents, suicide and violence. There is no comparable evidence for chronic cannabis use, although it is likely that dependent cannabis users who frequently drive while intoxicated with cannabis would increase their risk of accidental injury or death.

Sixth, alcohol use has been accepted as a contributory cause of cancer of the oropharangeal organs in men and women. There is suggestive clinical evidence that chronic cannabis smoking may also be a contributory cause of cancers of the aerodigestive tract. There is also some epidemiological evidence that alcohol use moderately increases the risk of cancer of the breast in women and of the colon in both sexes.

Seventh, alcohol use is a major cause of liver cirrhosis, accounting for upward of 80% of cases in non-tropical countries with substantial alcohol consumption levels. Heavy drinking is also implicated in gastritis, high blood pressure, stroke, cardiac arrhythmias, cardiomyopathy, pancreatitis, and polyneuropathy. On the other hand, regular drinking of small amounts of alcohol appears to reduce the risk of coronary heart disease, particularly in older individuals with positive risk factors such as tobacco smoking or a fatty diet. No equivalent protective effects have been found for cannabis although there is some evidence for the therapeutic usefulness of some cannabinoids (Hall et al, 1994).

Tobacco

The major adverse health effects shared by chronic cannabis and tobacco smokers are chronic respiratory diseases, such as chronic bronchitis, and probably, cancers of the aerodigestive tract (i.e. the mouth, tongue, throat, oesophagus, lungs). The increased risk of cancer in the aerodigestive tract is a consequence of the shared route of administration by smoking. It is possible that chronic cannabis smoking also shares the cardiotoxic properties of tobacco smoking, although this possibility remains to be investigated. These respiratory risks could be avoided by a change to the oral route of administration which would also reduce but not eliminate the cardiovascular risk since THC affects the cardiovascular system when taken orally.

Tobacco smoking is associated with a wide variety of other chronic health conditions for which cannabis smoking has not so far been implicated. These include cancer of the cervix, stomach, bladder and kidney, coronary heart disease, peripheral vascular disease, and stroke, as well as cataracts and osteoporosis.

Opioids

The specific health effects of opioid use largely depend on the route of administration. The use of injectable opiates carries risks not common to alcohol, tobacco or cannabis, especially when associated with illegally obtained injectables and shared needles. Injecting heroin or morphine can lead to trauma, inflammation and infection at the site of administration. Liver damage in opiate addicts may be caused by viral hepatitis contracted through needle sharing or from chronic alcohol abuse. Serious infection such as endocarditis is also possible. Local tissue and organ damage may also result from the adulterants in injection drugs obtained on the street (Belkin and Gold, 1991). Intravenous drug use is a major concern for the transmission of communicable diseases such as viral hepatitis and AIDS.

Chronic use of non-injected opioids appears to carry little risk of adverse health effects other than a modest effect on endocrine activity, some suppression of the immune system which has similar implications to the immune suppression associated with cannabis use, and chronic constipation.

While it is unclear that a withdrawal syndrome exists for cannabis, physical dependence on opiates has been recognised for centuries. Opiate withdrawal is associated with considerable discomfort but is rarely life-threatening. The withdrawal syndrome is generally less dangerous than rapid withdrawal from sedatives-hypnotics or from alcohol, although it may be life-threatening in neonates. Despite the low risk, avoidance of withdrawal appears to be a powerful motive for continued use of opiates among very heavy users.

Chronic opioid users may experience instability of mood, anorexia, lethargy and depression which are related to acute drug effects. Opioids have not been linked to chronic psychiatric disorders, but street addicts have a shortened life expectancy and more frequently experience social and emotional problems. This is in part due to their exposure to infection, violence and poor living conditions rather than their drug use.

Marijuana Research
Current restrictions on marijuana research are absurd
By The Editors

The human brain naturally produces and processes compounds closely related to those found in Cannabis sativa, better known as marijuana [see "The Brain's Own Marijuana," by Roger A. Nicoll and Bradley E. Alger. These compounds are called endogenous cannabinoids or endocannabinoids. As the journal Nature Medicine put it in 2003, "the endocannabinoid system has an important role in nearly every paradigm of pain, in memory, in neurodegeneration and in inflammation." The journal goes on to note that cannabinoids' "clinical potential is enormous." That potential may include treatments for pain, nerve injury, the nausea associated with chemotherapy, the wasting related to AIDS and more.

Yet outdated regulations and attitudes thwart legitimate research with marijuana. Indeed, American biomedical researchers can more easily acquire and investigate cocaine. Marijuana is classified as a so-called Schedule 1 drug, alongside LSD and heroin. As such, it is defined as being potentially addictive and having no medical use, which under the circumstances becomes a self-fulfilling prophecy.

Any researcher attempting to study marijuana must obtain it through the National Institute on Drug Abuse (NIDA). The U.S. research crop, grown at a single facility, is regarded as less potent--and therefore less medicinally interesting--than the marijuana often easily available on the street. Thus, the legal supply is a poor vehicle for studying the approximately 60 cannabinoids that might have medical applications.

This system has unintended, almost comic, consequences. For example, it has created a market for research marijuana, with "buyers" trading journal co-authorships to "sellers" who already have a marijuana stockpile or license. The government may also have a stake in a certain kind of result. One scientist tells of a research grant application to study marijuana's potential medical benefits. NIDA turned it down. That scientist rewrote the grant to emphasize finding marijuana's negative effects. The study was funded.

Some may argue that researchers do not need to study the drug--after all, there is Marinol, a synthetic version of marijuana's major active compound, tetrahydrocannabinol, or THC; it relieves nausea and stimulates appetite. But patients are often disappointed with Marinol as compared with marijuana. A 1997 editorial in the New England Journal of Medicine noted that "it is difficult to titrate the therapeutic dose of this drug, and it is not widely prescribed. By contrast, smoking marijuana produces a rapid increase in the blood level of the active ingredients and is thus more likely to be therapeutic."

The reasonable course is to make it easier for American researchers to at least examine marijuana for possible medical benefits. Great Britain, no slacker in the war on drugs, takes this approach: the government has authorized a pharmaceutical firm to grow different strains of marijuana for clinical trials.

This call for marijuana research is not a closet campaign for drug legalization--easing research barriers would not require that marijuana be reclassified, nor would it have any bearing on individual states' decisions to approve limited use of medical marijuana. As a 1995 editorial in the Journal of the American Medical Association said, "We are not asking readers for immediate agreement with our affirmation that marijuana is medically useful, but we hope they will do more to encourage open and legal exploration of its potential." After almost a decade of little progress, we reiterate that sentiment.
http://www.sciam.com/article.cfm?id=marijuana-research

Good stuff fella. Now, after all that reading, I could right go a spliff!

This one seems to support the 'rape and murder your daughter' argument

The Reader's Digest - February 1938
Marijuana --- Assassin of Youth (Condensed from The American magazine) H.F.Anslinger U.S. commissioner of Narcotics with Courtney Ryley cooper

Not long ago the body of a young girl lay crushed on the sidewalk after a plunge from a Chicago apartment window. Everyone called it suicide, but actually it was murder. The killer was a narcotic known to America as marijuana, and to history as hashish. Used in the form of cigarettes, it is comparatively new to the United States and as a coiled rattlesnake.

How many murders, suicides, robberies and maniacal deeds it causes each year, especially among the young, can only be conjectured. In numerous communities it thrives almost unmolested, largely because of official ignorance of its effects.

Marijuana is the unknown quantity among narcotics. No one knows, when he smokes it, whether he will become a philosopher, a joyous reveler, a mad insensate, or a murderer.

The young girl's story is typical. She had heard the whisper which has gone the rounds of American youth about a new thrill, a cigarette with a "real kick" which gave wonderful reactions and no harmful aftereffects. With some friends she experimented at an evening smoking party.

The results were weird. Some of the party went into paroxysms of laughter; others of mediocre musical ability became almost expert; the piano dinned constantly. Still others found themselves discussing weighty problems with remarkable clarity. The girl danced without fatigue throughout a night of inexplicable exhilaration.

Other parties followed. Finally there came a gathering at a time when the girl was behind in her studies and greatly worried. Suddenly, as she was smoking, she thought of a solution to her school problems. Without hesitancy she walked to a window and leaped to her death. Thus madly can marijuana "solve" one's difficulties. It gives few warnings of what it intends to do to the human brain.

Last year a young marijuana addict was hanged in Baltimore for criminal assault on a ten-year old girl. In Chicago, two marijuana-smoking boys murdered a policeman. In Florida, police found a youth - staggering about in a human slaughterhouse. With an ax he had killed his father, mother, two brothers, and a sister. He had no recollection of having committed this multiple crime. Ordinarily a sane, rather quiet young man, he had become crazed from smoking marijuana. In at least two dozen comparatively recent cases of murder or degenerate sex attacks, marijuana proved to be a contributing cause.

In Ohio a gang of seven addicts, all less than 20, were caught after a series of 38 holdups. The boys' story was typical of conditions in many cities. One of them said they had first learned about "reefers" in high school, buying the cigarettes at hamburger stands, and from peddlers who hung around the school. He told of "booth joints" where you could get a cigarette and a sandwich for a quarter, and of the shabby apartments of women who provided the cigarettes and rooms where boys and girls might smoke them.

His recollection of the crimes he had committed was hazy. "When you get to 'floating,' it's hard to keep track of things. If I had killed somebody on one of those jobs, I'd never have known it. Sometimes it was over before I realized that I'd even been out of my room."

It is the useless destruction of youth which is so heartbreaking to all of us who labor in the field of narcotic suppression. The drug acts as an almost overpowering stimulant upon the immature brain. There are numerous cases on record like that of an Atlanta boy who robbed his father's safe of thousands of dollars in jewelry and cash. Of high school age, this boy apparently had been headed for an honest career. Gradually, however, his father noticed in him spells of shakiness, succeeded by periods when the boy would assume a grandiose manner and engage in excessive laughter and extravagant conversation. When these actions finally were climaxed by robbery the father went at his son's problem in earnest - and found the cause of it in a marijuana peddler who catered to school children.

In Los Angeles a boy of 17 killed a policeman who had been his great friend. A girl of 15 ran away from home and was picked up with five young men in a marijuana den in Detroit. A Chicago mother, watching her daughter die as an indirect result of marijuana addiction, told officers that at least 50 of the girl's friends were slaves of the narcotic. The same sort of report comes in from cities all over the country. In New Orleans, of 437 persons of varying ages arrested for a wide range of crimes, 125 were addicts. Of 37 murderers, 17 used marijuana.

The weed was known to the ancient Greeks. Homer wrote that it made men forget their homes and turned them into swine. In Persia in 1090 was founded the military and religious order of the Assassins, whose history is one of cruelty and murder. Its members are confirmed users of hashish, taking their name from the Arabic "basbsbasbin." It is hashish which causes Moros and Malays to "run amok" and engage in violent and bloody deeds.

Although an ancient drug, the menace of marijuana is comparatively new to the United States. It came in from Mexico, and swept across the country with incredible speed. In 1931, the marijuana file of the United states narcotic Bureau was less than two inches thick. The traffic's most rapid growth came in 1935 and 1936, and today our reports crowd many large cabinets. They indicate that high school students particularly are the prey of the reefer peddlers.

Among those who first spread its use were musicians. They brought the habit northward with the surge of "hot" music demanding players of exceptional ability, especially in improvisation. Along the Mexican border and in southern seaport cities it had long been known that the drug has a strangely exhilarating effect upon the musical sensibilities. The musician who uses it finds that the musical beat seemingly comes to him quite slowly, thus allowing him to interpolate improvised notes with comparative ease. He does not realize that he is tapping the keys with a furious speed impossible for one in a normal state.

Soon a song was written about the drug. Perhaps you remember:

Have you seen That funny reefer man? He says he swam to China; Any time he takes a notion. He can walk across the ocean.

It sounded funny. Dancing girls and boys pondered about "reefers" and learned that these cigarettes could make one accomplish the impossible. Sadly enough, they can - in the imagination. The girl who decided suddenly to elope with a boy she did not even know a few hours before, does so with the confident belief that this is a thoroughly logical action without the slightest possibility of disastrous consequences. Command a person "high" on "mu" or "muggles" to crawl on the floor and bark like a dog, and he will do it without a thought of the idiocy of the action. Everything, no matter how insane, becomes plausible.

Reports from various sections indicate that the sale of marijuana has not yet passed into the hands of gangster syndicates. The supply is so vast that gangsters have found it difficult to dominate the source. It is to be hoped that the menace can be wiped out before they are able to do so.

A big hardy weed, of the Indian hemp family, with serrated sword like leaves topped by bunchy small blooms, it grows wild in the West, and is cultivated in practically every state, in fields, gardens, vacant lots. In New York State alone, 200 tons of the growing weed were destroyed in 1936. A raid near La Fitte, Louisiana, resulted in the destruction of 500,000 plants. Similar raids have been conducted in Texas, New Jersey, Mississippi, Michigan and elsewhere.

Every state except one has laws to cope with the traffic, but unfortunately there is no federal law dealing with it. Hence there is need for unceasing watchfulness by every local police department and by every civic organization. There should be campaigns of education in every school, so that children will not be deceived by the wiles of peddlers, but will know of the insanity, the disgrace, the horror which marijuana can bring to its victim. There must be constant enforcement and constant education against this enemy, which has a record of murder and terror running through the centuries.

Copywrite 1937, The Crowell Pub. Co., 250 Park Ave., N.Y.C. (The American Magazine, July, 37)

Excellent posts and very informative. thank you.

Does cannabis use affect treatment outcome in bipolar disorder? A longitudinal analysis.van Rossum I, Boomsma M, Tenback D, Reed C, van Os J; EMBLEM Advisory Board.
Collaborators (18)

Sabbe B, Larsen JK, Koponen H, Gasquet I, Azorin JM, Grunze H, Cassano GB, Nolen W, van Os J, Aarre T, Arriaga F, Pinto AG, Haro JM, Vieta E, Angst J, Cookson J, Knapp M, Tohen M.

Medical Department, Eli Lilly Nederland, Houten, The Netherlands. van_rossum_inge@lilly.com

Research suggests that cannabis use affects negatively on onset and outcome of schizophrenia, but less is known about possible effects in mood disorders. Bipolar in- and outpatients (N = 3459) were enrolled in an observational study. The influence of cannabis exposure on clinical and social treatment outcome measures was examined over the course of 1 year, as well as the effects on these associations of third mediating variables. Over 12 months of treatment, cannabis users exhibited less compliance and higher levels of overall illness severity, mania, and psychosis compared with nonusers. Additionally, cannabis users experienced less satisfaction with life and had a lower probability of having a relationship compared with nonusers. There was little evidence that cannabis-outcome associations were mediated by third variables. An independent impact of cannabis use on psychopathologic outcomes in patients with bipolar disorder was apparent, whereas the impact on social outcomes was modest.

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=AbstractPlus&list_uids=19155808&tool=MedlinePlus

The real danger of cannabis?

A dry spell.

Cartoon Head wrote:The real danger of cannabis?

A dry spell.

Yep. I hear it doesn't do to well out in the sahara at all.