Why Do Patients With Schizophrenia Smoke So Many Cigarettes?

For sound neurological reasons, that's why.

(Originally published May 2, 2012, by The Dana Foundation)

For mental health workers, it is well known that an overwhelming majority of psychiatric patients diagnosed with schizophrenia are heavy cigarette smokers. Surveys have shown that at least 60 percent of patients exhibiting symptoms of schizophrenia are smokers, compared with a national average that hovers just above 20 percent. Writing in the New England Journal of Medicine, researcher Judith J. Prochaska, associate professor of psychiatry at the University of California in San Francisco, found that “smokers with serious mental illnesses are dying 25 years sooner, on average, than Americans overall.” And tobacco is one of the reasons why.

Cigarettes, long familiar in institutional settings as a tool for reinforcing desired behavior, are slowly disappearing from state hospitals. “For state inpatient psychiatric facilities responding to surveys,” says Prochaska, “the best estimate is that about half have adopted smoke-free policies.” Increasingly, acute nicotine withdrawal is a strong part of the mix for the recently admitted smoker with schizophrenia.

An earlier study by Prochaska and colleagues, published in Psychiatric Services, found that while 42 percent of psychiatric patients at a smoke-free San Francisco hospital were smokers, averaging slightly more than a pack per day, none of the smokers received a diagnosis of dependence or withdrawal, and none were offered treatment planning for smoking cessation.

“Smokers who were not given a prescription for nicotine replacement therapy were more than twice as likely to be discharged from the hospital against medical advice as nonsmokers and smokers who were given a prescription for nicotine replacement therapy,” the study concludes. The authors believe that “nicotine withdrawal left unaddressed may compromise psychiatric care…. Given the complicated relationship between mental illness and smoking, integration of cessation efforts into psychiatric care is recommended.”

During the first few hours after patients with schizophrenia enter smoke-free psychiatric emergency settings, more than half become agitated, and 6 percent are physically restrained, according to a recent study by Dr. Michael H. Allen and coworkers at the University of Colorado School of Medicine. Published in the American Journal of Psychiatry, the double-blind study looked at 40 patients admitted to the psychiatric emergency service of the Hospital of the University of Geneva, and found that a relatively safe and simple addition to the emergency stabilization of patients with schizophrenia—a 21 mg nicotine patch—markedly reduced agitation in patients who smoked. The practice of “forced abstinence,” which is the consequence of recent trends toward smoke-free institutions, may not be in the patient’s best interest—especially since formal smoking cessation programs are not always a part of hospital routine.

Allen and colleagues gave out either the nicotine patch or a placebo patch to 40 smokers recently admitted to the hospital with symptoms of schizophrenia. While agitation diminished over time in both the intervention group and the placebo group, “the intervention group had a 33 percent greater reduction in agitation at 4 hours and a 23 percent greater reduction at 24 hours.” The authors say that the differences are similar to those observed in industry trials of common antipsychotics. According to Allen, “forced tobacco abstinence may have the effect of increasing aggressive behavior.” For patients with schizophrenia, smoking works.

The importance of nicotine to patients with schizophrenia should not be underestimated. There are rational biological reasons why schizophrenics smoke. A review of earlier studies published in Psychiatric Services suggests that smokers with schizophrenic symptoms may be self-medicating to improve the processing of auditory stimuli, and to reduce the side-effects caused by common antipsychotic medications. 

“Neurobiological factors provide the strongest explanation for the link between smoking and schizophrenia,” writes Edward R. Lyon, the study’s author, “because a direct neurochemical interaction can be demonstrated.” Flaws in sensory gating, the process by which the brain lowers its response to a repeated sound, are believed to be involved in the auditory hallucinations common to people with schizophrenia. And sensory gating improves for schizophrenics after they load up on nicotine.  Other research has shown a reduction in expression of nicotinic receptors in schizophrenia, suggesting that a susceptibility to smoking and schizophrenia may be related.

Prochaska sees smoking among patients in psychiatric settings as the consequence of several factors, including clinicians' failure to treat nicotine addiction, as well as the role nicotine plays as an antidote to drug side effects. Patients are familiar with the side effects of the drugs they take, “so they smoke and it reduces the blood levels of their medications,” she says. “They’re less sedated, and they can focus more.”

This complicates the picture for psychiatric staff: Antipsychotic drugs are metabolized faster in smokers, leading to the need for higher doses of medication. Prochaska notes that tobacco smoke may inhibit the effect of commonly used drugs like haloperidol, and the inhibition “can be as high as an increase clearance of 40–98 percent for olanzapine, a costly medication.”

In an interview, Prochaska said that the heaviest smokers “may need to stay on cessation medications for an extended period, and that’s certainly better for them than smoking. Combination therapy also is recommended. In our studies, we combine the nicotine patch with gum or lozenge so they’re able to add to the patch to get sufficient coverage of withdrawal symptoms.”

Mental health professionals have traditionally argued that patients with schizophrenia do not want to quit smoking, but Prochaska’s work suggests otherwise. Patients in psychiatric settings are about as likely as the general population to want to quit smoking, her research shows. “There is growing evidence that smokers with mental illness are as ready to quit as other smokers and can do so without any threat to their mental health recovery,” she said.

By some estimates, people with psychiatric disorders make up almost half of the current U.S. market for tobacco products. As Prochaska has written, “nicotine dependence is the most prevalent substance use disorder among adult psychiatric patients, and it needs to be placed on the radar of psychiatric practice.”

It’s up to healthcare providers to get the ball rolling. “Many facilities are still struggling with it,” she says. “It’s not been in their purview traditionally, so changing the culture is a big piece of the solution. It’s very much a matter of trying to get tobacco treatment medicalized, having it be automatic, so that nicotine replacement is right there in the admitting orders. And ideally, working with patients while they are hospitalized to motivate smoking cessation, and supporting them when they leave.”

Photo Credit: http://www.ctri.wisc.edu/

A Chemical Peek at Modern Marijuana

Researchers ponder whether ditch weed is better for you than sinsemilla.

Australia has one of the highest rates of marijuana use in the world, but until recently, nobody could say for certain what, exactly, Australians were smoking. Researchers at the University of Sydney and the University of New South Wales recently analyzed hundreds of cannabis samples seized by Australian police, and put together comprehensive data on street-level marijuana potency across the country. They sampled police seizures and plants from crop eradication operations. The mean THC content of the samples was 14.88%, while absolute levels varied from less than 1% THC to almost 40%.  Writing in PLoS one, Wendy Swift and colleagues found that roughly ¾ of the samples contained at least 10% total THC. Half the samples contained levels of 15% or higher—“the level recommended by the Garretsen Commission as warranting classification of cannabis as a ‘hard’ drug in the Netherlands.”

In the U.S., recent studies have shown that THC levels in cannabis from 1993 averaged 3.4%, and then soared to THC levels in 2008 of almost 9%. THC loads more than doubled in 15 years, but that is still a far cry from news reports erroneously referring to organic THC increases of 10 times or more.

CBD, or cannabidiol, another constituent of cannabis, has garnered considerable attention in the research community as well as the medical marijuana constituency due to its anti-emetic properties. Like many other cannabinoids, CBD is non-psychoactive, and acts as a muscle relaxant as well. CBD levels in the U.S. have remained consistently low over the past 20 years, at 0.3-0.4%. In the Australian study, about 90% of cannabis samples contained less than 0.1% total CBD, based on chromatographic analysis, although some of the samples had levels as high as 6%.

The Australian samples also showed relatively high amounts of CBG, another common cannabinoid. CBG, known as cannabigerol, has been investigated for its pharmacological properties by biotech labs. It is non-psychoactive but useful for inducing sleep and lowering intra-ocular pressure in cases of glaucoma.

CBC, yet another cannabinoid, also acts as a sedative, and is reported to relieve pain, while also moderating the effects of THC. The Australian investigators believe that, as with CBD, “the trend for maximizing THC production may have led to marginalization of CBC as historically, CBC has sometimes been reported to be the second or third most abundant cannabinoid.”

Is today’s potent, very high-THC marijuana a different drug entirely, compared to the marijuana consumed up until the 21st Century? And does super-grass have an adverse effect on the mental health of users? The most obvious answer is, probably not. Recent attempts to link strong pot to the emergence of psychosis have not been definitive, or even terribly convincing. (However, the evidence for adverse cognitive effects in smokers who start young is more convincing).

It’s not terribly difficult to track how ditch weed evolved into sinsemilla. It is the historical result of several trends: 1) Selective breeding of cannabis strains with high THC/low CBD profiles, 2) near-universal preference for female plants (sinsemilla), 3) the rise of controlled-environment indoor cultivation, and 4) global availability of high-end hybrid seeds for commercial growing operations. And in the Australian sample, much of the marijuana came from areas like Byron Bay, Lismore, and Tweed Heads, where the concentration of specialist cultivators is similar to that of Humboldt County, California.

The investigators admit that “there is little research systematically addressing the public health impacts of use of different strengths and types of cannabis,” such as increases in cannabis addiction and mental health problems. The strongest evidence consistent with lab research is that “CBD may prevent or inhibit the psychotogenic and memory-impairing effects of THC. While the evidence for the ameliorating effects of CBD is not universal, it is thought that consumption of high THC/low CBD cannabis may predispose users towards adverse psychiatric effects….”

The THC rates in Australia are in line with or slightly higher than average values in several other countries. Can an increase in THC potency and corresponding reduction in other key cannabinoids be the reason for a concomitant increase in users seeking treatment for marijuana dependency? Not necessarily, say the investigators. Drug courts, coupled with greater treatment opportunities, might account for the rise. And schizophrenia? “Modelling research does not indicate increases in levels of schizophrenia commensurate with increases in cannabis use.”

One significant problem with surveys of this nature is the matter of determining marijuana’s effective potency—the amount of THC actually ingested by smokers. This may vary considerably, depending upon such factors as “natural variations in the cannabinoid content of plants, the part of the plant consumed, route of administration, and user titration of dose to compensate for differing levels of THC in different smoked material.”

Wendy Swift and her coworkers call for more research on cannabis users’ preferences, “which might shed light on whether cannabis containing a more balanced mix of THC and CBD would have value in the market, as well as potentially conferring reduced risks to mental wellbeing.”

Swift W., Wong A., Li K.M., Arnold J.C. & McGregor I.S. (2013). Analysis of Cannabis Seizures in NSW, Australia: Cannabis Potency and Cannabinoid Profile., PloS one, PMID: 23894589

Graphics Credit: http://420tribune.com

“Spiceophrenia”

Synthetic cannabimimetics and psychosis.

Not long ago, public health officials were obsessing over the possibility that “skunk” marijuana—loosely defined as marijuana exhibiting THC concentrations above 12%, and little or no cannabidiol (CBD), the second crucial ingredient in marijuana—caused psychosis. In some cases, strong pot was blamed for the onset of schizophrenia.

The evidence was never very solid for that contention, but now the same questions have arisen with respect to synthetic cannabimimetics—drugs that have THC-like effects, but no THC. They are sold as spice, incense, K2, Aroma, Krypton, Bonzai, and dozens of other product monikers, and have been called “probationer’s weed” for their ability to elude standard marijuana drug testing. Now a group of researchers drawn primarily from the University of Trieste Medical School in Italy analyzed a total of 223 relevant studies, and boiled them down to the 41 best investigations for systematic review,  to see what evidence exists for connecting spice drugs with clinical psychoses.

Average age of users was 23, and the most common compounds identified using biological specimen analysis were the now-familiar Huffman compounds, based on work at Clemson University by John W. Huffman, professor emeritus of organic chemistry: JWH-018, JWH-073, JWH-122, JWH-250. (The investigators also found CP-47,497, a cannabinoid receptor agonist developed in the 80s by Pfizer and used in scientific research.) The JWH family consists of very powerful drugs that are full agonists at CB-1 and CB-2 receptors, where, according to the study, “they are more powerful than THC itself.” What prompted the investigation was the continued arrival of users in hospitals and emergency rooms, presenting with symptoms of agitation, anxiety, panic, confusion, combativeness, paranoia, and suicidal ideation. Physical effects can includes elevated blood pressure and heart rate, nausea, hallucinations, and seizures.

One of the many problems for researchers and health officials is the lack of a widely available set of reference samples for precise identification of the welter of cannabis-like drugs now available. In addition, the synthetic cannabimimetics (SCs) are frequently mixed together, or mixed with other psychoactive compounds, making identification even more difficult. Add in the presence of masking agents, along with various herbal substances, and it becomes very difficult to find out which of the new drugs—none of which were intended for human use—are bad bets.

Availing themselves of toxicology tests, lab studies, and various surveys, the researchers, writing in Human Psychopharmacology’s Special Issue on Novel Psychoactive Substances, crunched the data related to a range of psychopathological issues reported with SCs—and the results were less than definitive. They found that many of the psychotic symptoms occurred in people who had been previously diagnosed with an existing form of mental disturbance, such as depression, ADHD, or PTSD. But they were able to determine that psychopathological syndromes were far less common with marijuana than with SCs. And those who experienced psychotic episodes on Spice-type drugs presented with “higher/more frequent levels of agitation and behavioral dyscontrol in comparison with those psychotic episodes described in marijuana misusers.”

In the end, the researchers can do no better than to conclude that “the exact risk of developing a psychosis following SC misuse cannot be calculated.” What would the researchers need to demonstrate solid causality between designer cannabis products and psychosis? More product consistency, for one thing, because “the polysubstance intake pattern typically described in SC misusers may act as a significant confounder” when it comes to developing toxicological screening tools. Perhaps most disheartening is “the large structural heterogeneity between the different SC compounds,” which limited the researchers’ ability to interpret the data.

This stuff matters, because the use of Spice-type drugs is reported to be increasing in the U.S. and Europe. Online suppliers are proliferating as well. And the drugs are particularly popular with teens and young adults. Young people are more likely to be drug-naïve or have limited exposure to strong drugs, and there is some evidence that children and adolescents are adversely affected by major exposure to drugs that interact with cannabinoid receptors in the brain. 

Graphics credit: http://scientopia.org/blogs/drugmonkey/

Marijuana Can Make You Vomit, and Other Stories

Short subjects, various.

First, a recap of an earlier story, and a very strange story at that. Cannabinoid hyperemesis, as it's known, was not documented in the medical literature until 2004, and was first brought to wider attention earlier this year by the biomedical researcher who blogs as Drugmonkey. Episodes of serial vomiting appear to be a very rare side effect of regular marijuana use. Posting on his eponymous blog, Drugmonkey documented cases of hyperemesis that had been reported in Australia and New Zealand, as well as Omaha and Boston in the U.S.

As Drugmonkey reported, “patients had discovered on their own that taking a hot bath or shower alleviated their symptoms. So afflicted individuals were taking multiple hot showers or baths per day to obtain symptom relief.”

A year ago, I published a post on this topic, titled "Marijuana, Vomiting, and Hot Baths." Sure enough, a number of people left comments about their own experiences with this unusual and unpleasant effect. Recently, one of my commenters caught drugmonkey’s eye, and he noted it in his new blog post on the phenomenon:

“Dirk Hanson's post on cannabis hyperemesis garnered another pertinent user:

Anonymous said...
My son suffers from this cannabinoid hyperemesis. At this moment he is here at my home on the couch suffering. I have been up with him for 3 days with the vomiting and hot baths. He says this time its over for good. This is our third bout. The first two time we went to ER, they put him on a drip to hydrate him, and gave him some pain medicine and nausea medicine. After a few hours he went home and recovered. This time we went to Urgent Care, put him on a drip, pain med, Benadryl, and Zofran….

Drugmonkey writes: “I reviewed several case reports back in 2010.... and there was considerable skepticism that the case report data was convincing. So I thought I'd do a PubMed search for cannabis hyperemesis and see if any additional case reports have been published…. One in particular struck my eye. Simonetto and colleagues (2012) performed a records review at the Mayo Clinic. They found 98 cases of unexplained, cyclic vomiting which appeared to match the cannabis hyperemesis profile out of 1571 patients with unexplained vomiting and at least some record of prior cannabis use… this is typical of relatively rare and inexplicable health phenomena. The Case Reports originally trickle out... this makes the medical establishment more aware and so they may reconsider their prior stance vis a vis so-called "psychogenic" causes. A few more doctors may obtain a much better cannabis use history then they otherwise would have done. More cases turn up. More Case Reports are published. etc. It's a recursive process. “
------------------------------

In a story I think of as vaguely related, in the sense that it is a rare drug phenomenon unrecognized by the public, I recently wrote an article  for The Dana Foundation on the subject of “Smoking’s Ties to Schizophrenia.” In addition, check out a story about plans by the Air Force to make their hospitals and clinics smoke-free HERE. In brief: Smoke-free clinics pose major problems for heavy smokers with mental health disorders.
------------------------------

Speaking of hospitals, Michelle Andrews reports in Kaiser Health News that about half of the patients undergoing treatment in hospital emergency rooms are under the influence of booze. Alcohol screening and counseling can be effective in this context—but there’s a catch. “Regardless of state law, self-insured companies that pay their employee’s health care costs directly can refuse to cover employees for alcohol-related claims.”

Even though the National association of Insurance Commissioners does not recommend it, dozens of states have passed laws allowing health insurers to deny payment for a patient’s injuries if they were incurred while he or she was under the influence of alcohol. About as many states have passed laws prohibiting such exclusions due to alcohol. The result is one big mess, and confusion reigns. As a professor of health law put it: “There’s no reason to think that insurers, eager to hold down costs, wouldn’t continue” to deny payment for alcohol-related injuries.
-------------------------------

And finally, some news about Chantix (varenicline), the drug both patients and doctors love to hate. It often works very well as an anti-craving medication for smoking cessation. But it can also, in some cases, present patients with a bewildering array of psychological side effects, including rare cases of suicidal ideation. A new study  by researchers at the Ernest Gallo Clinic and Research Center at the University of California, San Francisco, suggests that Chantix may have application in the treatment of alcoholism as well. Participants in the study reduced the average number of drinker per week on Chantix, compared to placebo. The study was funded by the National Institutes of Health and the State of California. Pfizer, the company that markets Chantix, did not fund or participate in the study.

Graphics Credit: http://teesdiary.files.wordpress.com/

Medical Cigarettes

Is it “Inhumane” to Take Cigarettes Away from Schizophrenics?

In an article for Brain Blogger a couple of years ago, I looked into the astonishing fact that, as a typical study of in-patient smoking among schizophrenics in Britain revealed, about 80-90% of the patients diagnosed with schizophrenia were cigarette smokers. Given that the running rate in the general population hovers around 20-25% on average, this is really quite amazing. It seems clear that nicotine is doing something for a schizophrenic that makes cigarettes into a form of self-medication that almost all schizophrenics apparently discover at one time or another.

A review of relevant studies through 1999, undertaken by Lyon and published in Psychiatric Services, shows unequivocally that schizophrenic smokers are self-medicating to improve processing of auditory stimuli and to reduce many of the cognitive symptoms of the disease. “Neurobiological factors provide the strongest explanation for the link between smoking and schizophrenia,” Lyons writes, “because a direct neurochemical interaction can be demonstrated.” According to Lyon, “Several studies have reported that smokers require higher levels of antipsychotics than nonsmokers. Smoking can lower the blood levels of some antipsychotics by as much as 50%…. For example, Ziedonis and associates found that the average antipsychotic dosage for smokers in their sample was 590 mg in chlorpromazine equivalents compared with 375 mg for nonsmokers.”

In particular, smoking seems to help quell auditory and visual hallucinations. The process known as “sensory gating” refers to lower response levels to repeated auditory stimuli. A schizophrenic’s response to a second stimulus is greater than a normal person’s, and this is also impacted by cigarettes. Sensory gating may be involved in the auditory hallucinations common to schizophrenics. Receptors for nicotine are involved in sensory gating, and several studies have shown that sensory gating among schizophrenics is markedly improved after smoking.

There is an additional reason why smoking is an issue of importance for health professionals. Dr. Bill Yates at Brain Posts recently examined a small study by Michael Allen and colleagues in the American Journal of Psychiatry in which 40 schizophrenic patients were admitted to a psychiatric emergency service, where they were given standard antipsychotic therapy. In addition, the researchers randomly assigned either a 21mg nicotine patch or a placebo patch to the subjects upon admission. As Dr. Yates summarized the results:

--Nicotine patches reduced agitation by 33% in the first four hours and 23% at 24 hours. And the reduction was greater than with either the antipsychotic alone, or in conjunction with the placebo patch.

--Subjects with lower nicotine dependence scores tended to show the most response compared to placebo.

--The effect of nicotine replacement on agitation reduction approached the level seen with standard antipsychotic therapy.

As Yates notes, this finding is “pretty dramatic.” It seems to show that acute nicotine withdrawal only makes the situation worse in a clinical setting. The study authors also argue that stronger patches combined with nicotine gum might quell agitation more quickly and effectively. “Encouraging patients with psychotic disorders and mood disorders to quit smoking is an important general health strategy,” Dr. Yates writes. “However, this study suggests that attempting this during an acute psychotic break is probably counter productive and may be inhumane.”

Photo Credit:http://drugabuse.gov/

Strong Pot: What Do Schizophrenics Think?

Small study asks patients for their opinions.

The theory, fiercely debated in the research community, that strong cannabis can actually cause schizophrenia—or is associated with relapse in schizophrenics who smoke it—is the subject of a small study from Switzerland on outpatient schizophrenics, some of whom were pot smokers.

 A study of this kind, with only 10 subjects, verges on the anecdotal. Nonetheless, it is worth a look, just to see if any verification of the theory lurks therein.

In their paper for the open access Harm Reduction Journal—“Do patients think cannabis causes schizophrenia? A qualitative study on the causal beliefs of cannabis using patients with schizophrenia”—psychiatric workers with the Research Group on Substance Use Disorders interviewed patients who attended an outpatient clinic at the Psychiatric University Hospital in Zurich. The researchers did it because, as the paper states, “patients’ beliefs on the role of cannabis in the pathogenesis of schizophrenia have—to our knowledge—not been studied so far…”

“None of the patients described a causal link between the use of cannabis and their schizophrenia,” the researchers determined. However, several of the schizophrenics did have their own version of a disease model to account for their illness. Five of the patients attributed their schizophrenia to “upbringing under difficult circumstances,” and three placed the blame on “substances other than cannabis (e.g. hallucinogens).” The remaining two patients gave “other reasons.”

Interestingly, four of the patients “considered cannabis a therapeutic aid and reported that positive effects (reduction of anxiety and tension) prevailed over its possible disadvantages (exacerbation of positive symptoms).” The authors conclude that excluding schizophrenic patients from treatment settings because of marijuana use “may cause additional harm to this already heavily burdened patient group.”

Graphics Credit: http://www.salem-news.com

Media Suffers Attack of Cannabis Psychosis

Bad Science Makes for Bad Science Journalism

According to the London Daily Mail, smoking a single joint of marijuana increases your risk of developing schizophrenia by 41 per cent. The Mail quoted Professor Robin Murray of the Institute of Psychiatry in London, who dutifully warned that the risk was perhaps even higher than that, due to the increasing use of what the newspaper termed “powerful skunk cannabis.” The skunk effect, said Murray, meant that the study’s estimate that “14 per cent of cases of schizophrenia in the UK are due to cannabis is now probably an understatement.”

Marjorie Wallace of the mental health charity SANE told BBC News: “The headlines are not scaremongering, but reflect a daily, and preventable, tragedy.”

Wow. As Gertrude Stein once put it, “Interesting if true.”

But it’s not true at all, of course. Or, to put it more accurately: If it were true, there is no way in hell the meta study under question could be used to prove it.

Speaking as a science journalist, this is the sort of thing than can really ruin your day.

As always, it helps to start with the original published article, a meta-analysis published in the British medical journal Lancet under the title, “Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review.” 2007 370: 319-28. Mark Hoofnagle, a MD/PhD Candidate in the Department of Molecular Physiology and Biological Physics at the University of Virginia, discussed the paper in depth on his Denialism Blog:

“First of all, the statement that ‘just one joint’ increases risk by 41% is absurd. The study here is of those who have tried marijuana once or more, not of people who have only tried it once. So already, the Daily Mail and every other news organization is way off. Second, I think we're ultimately seeing a post-hoc ergo propter hoc argument, and a dose-response that's more characteristic of the population studied than a real pharmacologic effect.”

Here’s why:

--People who suffer from a mental illness do more drugs than “normal” people. They are a high-risk population when it comes to addiction. There are people who have a propensity for addiction, and people who do not. Many of those who do will get hooked, but this does not mean that everything which follows is a result of the drugs.

--Latent schizophrenics often suffer their first break while under the influence of psychoactive drugs. Pot, along with LSD, physical trauma, the death of a loved one, and other intense emotional events can all trigger a schizophrenic break in late adolescence. So naturally there would be a correlation.

--The assumption that pot causes susceptibility to mental illness, rather than the other way around, can’t be proven. Hoofnagle uses the example of cigarette smoking. Anyone who has researched schizophrenia, or been around schizophrenics, knows that almost all schizophrenics smoke. (It helps quell hallucinations). Most of them began to smoke before the onset of their illness. Using the assumptions of the current study, we could say that cigarette smoking is almost certain to cause schizophrenia. Correlation, as Hoofnagle reminds us, is not causation.

--Daily pot smokers confound such a study. Are some of them exhibiting symptoms of schizophrenia, or are they exhibiting the symptoms of chronic marijuana intoxication? If they quit smoking so much, would they stop acting so crazy?

--Comorbidity is exceedingly common in drug addicts and users. There is a well-documented causal connection between depression and the use of psychoactive drugs. People suffering from depression often resort to cannabis and other drugs as a form of self-medication. Again, the mental condition leads to the drug use, and not the other way around.

--Finally, where is the epidemic of schizophrenia caused by millions of people smoking marijuana for years? What field evidence can be drawn upon to support this remarkable conclusion?

To be fair to the authors, bets are hedged. In their conclusion, Moore, et.al. state: “The possibility that this association results from confounding factors or bias cannot be ruled out, and these uncertainties are unlikely to be resolved in the near future.”

Nevertheless, the authors go on to conclude that “We believe that there is now enough evidence to inform people that using cannabis could increase their risk of developing a psychotic illness later in life.”

At www.badscience.net, Ben Goldacre wryly notes that “You know when cannabis hits the news you’re in for a bit of fun…” Of 175 studies identified as potentially relevant, Goldacre maintains that only 11 papers, describing 7 discrete data sets, actually turned to be relevant for purposes of the study. If every assumption in the paper is taken to be correct, and causality is accepted, Goldacre calculated, about 800 cases of schizophrenia per year could be attributed to marijuana in the U.K. “But what’s really important,” Goldacre writes, “is what you do with this data. Firstly you can misrepresent it….not least of all with the ridiculous ‘modern cannabis is 25 times stronger’ fabrication so beloved by the media and politicians.”

As it happens, all of this comes at a time in Britain when efforts to reclassify cannabis are being hotly debated in the government. As propaganda, the report is useful, but as a means of clarifying the debate, it will only produce confusion and demagoguery.

Sources:

--Moore, Theresa H.M., et. Al. “Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review.” Lancet. 2007 370: 319-28 http://www.thelancet.com/

--MacCrae, Fiona and Andrews, Emily. “Smoking just one cannabis joint raises danger of mental illness by 40%.” London Daily Mail. 26/07/07

--“Cannabis ‘raises psychosis risk.’” BBC News. 2007/07/27 http://news.bbc.co.uk/2/hi/health/6917003.stm

--Cressey, Daniel. “Medical opinion comes full circle on cannabis dangers.” Nature. 27 July 2007.

--Hoofnagle, Mark. “Does Smoking Cannabis Cause Schizophrenia?” Denialism Blog. July 30, 2007. http://scienceblogs.com/denialism/2007/07/does_smoking_cannabis_cause_sc.php

medical marijuana