Sunday, October 24, 2010
A New/Old Treatment for Opiate Addiction
Gov makes naltrexone legit for heroin.
Last week, the government officially sanctioned the use of naltrexone, trade name Vivitrol, for use in the treatment of heroin addiction. Approved years ago by the FDA for use in the treatment of alcoholism, naltrexone is a long-acting opiate receptor antagonist that has been widely used for heroin detoxification, withdrawal, and maintenance for some time. In that light, the official approval was a bit of an anticlimax, and of less scientific interest than naltrexone’s earlier approval for alcohol dependence.
While naltrexone has yet to become the huge treatment breakthrough for alcoholism that addiction researchers hoped for it, naltrexone did, in the end, prove to be the first anti-craving medication widely available for alcoholics. Using an opiate antagonist as an aid to the prevention of alcoholic relapse would have been unthinkable without the underpinnings of a neurophysiological model of addiction. Various investigators have also speculated that naltrexone, the drug used as an adjunct of heroin withdrawal therapy, may find use against symptoms of marijuana withdrawal in people prone to marijuana dependence
Naltrexone has something of a mixed reputation, however, in part due to its use in the highly controversial practice of “rapid detox.” Naltrexone, like methadone and buprenorphine, blocks the heroin high in a relatively neutral manner. It does so by knocking the opiate molecule off its receptors and replacing it with “dead weight,” so to speak. Naltrexone would seem to be the perfect drug for heroin addicts—but it is not. It does little to reduce cravings. Like acamprosate for alcohol, another blocking approach, its record of accomplishment is mixed, and the dropout rate is high. There is not even a mild drug-like effect to provide cross-tolerance and dampen the effects of withdrawal, as with methadone. Recently, naltrexone for heroin addiction has been offered as a form of rapid detoxification. The addict is anesthetized and placed on a respirator, then injected with naltrexone. The result: complete detoxification in a matter of hours, as the naltrexone molecules knock the opium molecules off their receptors. It can be lethal if not carefully controlled and supervised. The problem, as always, is that the detoxified addict is just as vulnerable to heroin addiction as before. Rapid detox does nothing to combat subsequent cravings, and relapse is frequent.
Naltrexone combined with buprenorphine is marketed as Subutex, and represents another treatment modality for opiate addiction. In addition, a University of Minnesota study of kleptomania—the compulsion to steal—showed that naltrexone drastically reduced stealing among a group of 25 shoplifters.
Naltrexone will be offered as a monthly injection, an approach that has not been widely tested on opiate addicts, but is potentially an advantage over frequent visits to methadone clinics or daily ingestion of other treatment drugs. Unfortunately, naltrexone is a potential problem for people with liver disease or hepatitis. At high doses, naltrexone has been implicated in liver damage. More common adverse effects include dizziness, lethargy, and headache.
Graphics Credit: http://www.cancercenter.ph/
Labels:
addiction shot,
heroin,
heroin addiction,
low-dose naltrexone,
Revia,
vivitrol
Thursday, October 21, 2010
Does Ketamine Cause Bladder Damage?
Special K and Cystitis.
Normally, Addiction Inbox steers clear of alarmist stories about drug use. A lifetime of wildly overstated verbiage about “false drugs,” as the Firesign Theatre comedy group once delightfully phrased it, has left me wary of drug scare stories. Even obvious cases, like Fetal Alcohol Spectrum Disorder and crack babies, are more nuanced problems than most coverage has alleged.
For years now, rumors about bladder problems in recreational users of ketamine have periodically surfaced. These stories go all the way back to the adventures of Dr. John Lilly, famous for dolphin research, as well as sensory deprivation experiments with LSD, ketamine, and other drugs (wildly overdramatized in the movie, “Altered States”). According to hipster lore, Lilly went through a long period of hourly ketamine ingestion in the 1970s, and ended his days in adult diapers, having lost control of his bladder due to ketamine damage.
To the best of my knowledge, this story has never been officially confirmed. But in the last two years, research has surfaced that tends to bolster the Lilly anecdote. What is disturbing is that today, unlike 40 years ago, ketamine has become a fairly common party drug among young users. The drug technically produces a state of “dissociative anesthesia.” Treated like a hallucinogen, ketamine was originally a tranquilizer used in veterinary medicine. In 1970, the FDA approved the use of ketamine for humans for the maintenance of anesthesia.
The journey from horse tranquilizer to party drug has eluded drug researchers until quite recently. However, in early 2008, researchers sat up and took notice of a report published in BJU International, a urology journal. “The destruction of the lower urinary tract by ketamine abuse: a new syndrome?”
The report details the discovery by physicians in Hong Kong of 59 ketamine abusers who had been admitted to urology units in local hospitals from 2000 to 2007. Interstitial cystitis, also known as painful bladder syndrome, can vary from mild to severe, and its cause is often not known. Symptoms include painful, frequent, or urgent urination. The researchers found that 71 % of the patients “showed various degrees of epithelial inflammation similar to that seen in chronic interstitial cystitis. All of 12 available bladder biopsies had histological features resembling those of interstitial cystitis.”
The authors conclude that “secondary renal damage can occur in severe cases, which might be irreversible, rendering patients dependent on dialysis.”
Scary stuff. If this were the only study available, it would be tempting to question the results. As it turns out, the Hong Kong study was neither the first nor the last. What is believed to be the first official report of the problem appeared in 2007 in Urology, documenting the case of nine Canadian ketamine users with bladder complications. The authors, affiliated with the University of Toronto, conclude: “As illicit ketamine becomes more easily available, ulcerative cystitis and potential long-term bladder sequelae related to its use may be a more prevalent problem confronting urologists.”
This year, similar reports from Bristol in the UK were published in Clinical Radiology. Researchers with the National Health Service and the Bristol Royal Infirmary discovered “a series of 23 patients, all with a history of ketamine abuse, who presented with severe lower urinary tract symptoms.” Various imaging techniques revealed smaller bladder volume, bladder wall thickening, inflammation, urethral strictures, and other bladder pathologies. The patients all reported symptoms similar to those reported by the earlier Hong Kong ketamine users.
The report concludes that “many users are well aware, but are often not forthcoming with this information.” They also maintain that “the key to the effective management of ketamine-induced bladder pathology is early diagnosis.”
Frequent recreational use of ketamine appears ill advised until more research can confirm the true scope of the problem.
Chu, P., Ma, W., Wong, S., Chu, R., Cheng, C., Wong, S., Tse, J., Lau, F., Yiu, M., & Man, C. (2008). The destruction of the lower urinary tract by ketamine abuse: a new syndrome? BJU International, 102 (11), 1616-1622 DOI: 10.1111/j.1464-410X.2008.07920.x
Mason K, Cottrell AM, Corrigan AG, Gillatt DA, & Mitchelmore AE (2010). Ketamine-associated lower urinary tract destruction: a new radiological challenge. Clinical radiology, 65 (10), 795-800 PMID: 20797465
Graphics Credit: http://theintelhub.com/
Labels:
bladder problems,
cystitis,
Ketamine,
ketamine and bladder,
party drug,
special K,
Vitamin K
Tuesday, October 19, 2010
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
Sunday, October 17, 2010
Codeine Blues: End of the Line for an Opiate with Issues
Canada, UK consider phasing out the drug.
Among the many memorable anecdotes that have been uttered at the opening of an AA or NA meeting, surely one of the great ones is this: “I’m an addict, and a heroin junky. I went to the dentist today, and he sent me home with a prescription for Tylenol 3. And I thought: Do I really want to endanger my sobriety over a shitty buzz like codeine?”
Canada and the United Kingdom are ready to phase it out entirely. The U.S. Food and Drug Administration (FDA) issued a warning about it for nursing mothers as far back as 2007. Codeine, widely popular for its low euphoriant effects, and subsequent (if theoretical) decreased potential for abuse, may not be as strong as morphine and dilaudid, but it is perhaps the most commonly prescribed opiate in the world—and it comes with a major flaw. Unlike other opiates, codeine is very unpredictable in its interactions with an enzyme called CYP2D6. This enzyme is a primary workhorse in the body’s process of breaking down and excreting many different drugs. Poor metabolizers produce less of this crucial enzyme, which means that drugs are broken down and excreted at a much slower pace (See my earlier post ).
Specifically, as two physicians recently wrote in the Canadian Medical Association Journal (PDF),
“polymorphisms occur in the cytochrome P450 isoenzyme CYP2D6 that enhance codeine metabolism to morphine.” In 2007, following the death of an infant nursed by a codeine-using mother, the FDA “warned nursing mothers that if they took codeine after childbirth, their newborns might be at risk for a morphine overdose,” according to a New York Times report.
Alternatively, other metabolizers may have little or no reaction to codeine-based medications. Drugs of abuse severely complicate these enzymatic issues, since addicts and alcoholics are not known for volunteering information about their condition to medical or hospital personnel.
Testing for the enzyme is possible, but not likely to catch on with cash-strapped medical and dental centers. Dr. Noni MacDonald at the University of Halifax and Dr. Stuart MacLeod at the University of British Columbia argue in the CMAJ that these genetic variations “can have potentially serious clinical consequences. The wrong combination can result in toxic levels of morphine, even at conventional doses of codeine.” The younger the user, the more susceptible he or she will be to these effects, “possibly because of age-related maturation differences in the blood-brain barrier.” The authors warned that serious side effects “including life-threatening respiratory depression,” have also been reported in adults.
The ultrafast metabolizing variant of CYP2D6 is not evenly distributed throughout the world’s population. The number of people in danger of experiencing high morphine levels after codeine use range from 40% in North Africa to 3% in Europe, the authors say. Rates in the U.S. are 8%, meaning roughly one in ten Americans risk an adverse reaction when taking codeine.
Since the groups at highest risk are infants and children, nations have taken various steps to mitigate the risk. “Switzerland sets the minimum age for codeine-based treatment at 1- years, the Netherlands at 1 year, the United States at 3 years and Canada at 2 years.”
Despite these controls, the authors strongly argue for “a more direct approach,” calling for doctors to “stop using the prodrug codeine altogether and instead use its active metabolite, morphine. Not only is the metabolism of morphine more predictable that that of codeine, but also it’s cheaper.” So codeine is just not consistently good at what it does. Problem is, an opiate doesn’t have to be good to be great, as innumerable codeine addicts can attest.
The argument in Canada made sense to Britain’s watchdog agency for medicines, the Medicines and Healthcare products Regulatory Agency (MHRA). According to a report in The Independent by science editor Steve Connor, the MHRA “wrote to medical authorities in the UK warning that its experts have advised that all over-the-counter liquid cough medicines containing codeine should no longer be used in children under the age of 18,” and that “the risks of [over-the-counter] cough medicines for children containing codeine outweigh the possible benefits.”
Codeine is typically offered in paired form, with either acetaminophen or aspirin, as protection against opiate abuse. In theory, a drug abuser would be likely to trigger a Tylenol overdose before reaching an opiate overdose on codeine pills. However, it is perfectly possible to maintain an active opiate addiction on prescription Tylenol 3s, Fiorinal, or Phenergan cough syrup, among other drugs.
And finally, I would not be revealing any great secrets by suggesting that the extraction of codeine from a codeine-acetaminophen tablet through basic solubility and filtration procedures may not be something one needs to be a chemistry major to pull off.
The OTC medicine industry in the UK views all of this as a tired argument. A spokesperson for Britain’s Proprietary Association, which represents over-the-counter manufacturers, said: "There has already been a long-drawn-out discussion of codeine. If its value as a pain reliever had not outweighed the risks then it would have been withdrawn and the point is that codeine still has a value as a pain reliever.”
photo credit: http://www.buzzle.com/
Thursday, October 14, 2010
Who Controls Addiction Research?
The ongoing merger wars at the NIH.
As researchers await the National Institute of Health director’s decision on the matter of merging the nation’s two major addiction research agencies, interested parties to the dispute continued to wonder whether the alcoholic beverage industry will weigh in on the matter—with cash.
The National Institute on Drug Abuse (NIDA) and the National Institute on Alcohol Abuse and Alcoholism (NIAAA) exist within the large institutional framework of the National Institutes of Health (NIH), and operate under mandates that overlap enough to make them prime candidates for a cost-saving consolidation. Advocates of the merger, most of them advocates for NIDA, also suggest that the research itself will improve as a result of a decrease in “overlapping missions.” (See my earlier post.)
Recently, Nature News suggested the possibility of efforts against the merger from another interested party: “Although the alcohol industry is unlikely to relish its legal product being lumped in for study with street drugs such as cocaine and heroin, it has so far remained silent. US Trade groups including the Beer Institute, the Wine Institute, the American Beverage Institute and the Distilled Spirits Council of the United States all declined to comment for this article.”
DrugMonkey, an anonymous NIH-funded researcher, has noted on his blog: “I’m still betting [the beverage industry’s] entire strategy (if they actually care about this, which I suspect they do) is going to be by trying to get a pet Congress Critter or two to oppose the plan. Spirited opposition can probably block the whole plan.”
DrugMonkey even notes that by one common yardstick—recent success rates for grant applicants—NIAAA has actually put up better numbers than its larger cousin, NIDA, “something that NIAAA people have been quietly bragging about for the past several years.”
There have been other rumblings. Behind the scenes, some NIAAA proponents have criticized NIDA’s Nora Volkow for what they see as a heavy-handed attempt on her part to steamroll any opposition to the merger. The battle lines were clearly drawn earlier this year when Volkow testified before the Scientific Management Review Board. Quoted in the NIH Record, a National Institutes of Health publication, Volkow said that “all psychiatric disorders have similar roots involving combinations of genes and environment…. it is a serious problem, a devastating problem, whether you are talking about alcohol or drugs.” The NIDA director also said she was “impatient” with progress on the matter, arguing that the separation of resources had already resulted in missed research opportunities. “Why put roadblocks in the way of treatment and prevention?”
At the same meeting, acting NIAAA director Dr. Kenneth Warren offered up what has come to be seen as the basic counter-argument: “The best way forward is a structure that increases collaboration all across NIH… nothing is gained by structural merger.” Warren said he favored “a separate, but equal” pair of agencies. “Alcoholism is a much broader issue than simply addiction.”
Here is where it starts to get tricky. The assertion that alcoholism is not simply an addiction distills the disagreement down to its essence, which can be found not so much within the arena of science as within the arenas of morality, ethics, and the law. NIH Director Francis Collins told Science (sub. required): “Alcohol is after all a legal substance and 90% of us at some point in our lives are comfortable with taking it in while the drug abuse institute is largely focused on drugs that are not legal.”
As Maia Szalavitz wrote at TIME Healthland:
There's another, somewhat moralistic argument for keeping the institutes separate. As Dr. Deborah Hasin argued at a February national advisory meeting on the question, “[There is] a need for a public health message more nuanced for alcohol than for drugs, including nicotine. In contrast with drugs, light drinking is not “bad.'’ It was a curious statement from a scientist who is supposedly charged with studying the effects of psychoactive substances objectively.
Does the NIAAA really have any solid, science-based arguments against the creation of a combined research agency?
Just ask them. Officially, the NIAAA has a very long list of reasons why they are just saying no to the merger—which looks, from the NIAAA point of view, more like an acquisition, anyway. Here are some of acting director Warren’s arguments, taken from an appendix to the minutes of the February 3-4 meeting of the National Advisory Council to the NIAAA, over which Warren presided:
--Alcohol use disorders are different than drug addiction. "The genetics of alcoholism differs from the genetics of drug addiction. Prospective studies have shown that the sons of alcoholics are at greater risk for alcoholism than for drug dependence.”
--The existence of certain commonalities in the brain pathways that mediate the rewarding effects of alcohol and other drugs of abuse does not justify the merger of NIAAA and NIDA. "The fact that dopamine is an important neurotransmitter in signaling reward associated with motivational stimuli does not provide a strong rationale for merging institutes.”
--Most people with AUDs (alcohol use disorders) do not abuse other drugs. “The large size of the population with AUDs who don’t abuse other drugs and the enormous public health burden of their illness justify NIAAA’s focused approach to research on AUDs, separate from drug dependence.”
--Alcohol differs from other drugs of abuse in the degree to which heavy use damages the brain and other organs. "Alcohol damages multiple organ systems through common mechanisms of toxicity, including oxidative stress, the disruption of critical cell signaling systems, and the generation of toxic metabolites, cytokines, and chemokines. The coordinated study of these multiple organ toxicities is best suited to a single alcohol Institute.”
--The systems approach is essential to the study of alcohol beneficial and adverse effects. "The merger of NIAAA with NIDA to form a new Institute focused on addiction would orphan and dissociate critical programs focused on alcohol and cardiovascular health, liver disease, pancreatitis, fetal alcohol spectrum disorders, immune disorders, myopathy, neuropathy, and brain disorders.”
Almost all of these contentions are open to debate. I believe some of them are just plain wrong. Nonetheless, the notion that a merger of two or more sprawling federal agencies will automatically streamline and strengthen government operations is equally open to question (See Department of Homeland Security).
But the greater weight of logic, it seems, continues to tip the argument in the direction of a merger. Legal or illegal should have very little to do with it. David Rosenbloom, director of Join Together, said in an excellent article by Bob Curley that a single NIH addiction institute could “yield important science and public health benefits.”
Rosenbloom added that “many individuals with addiction use alcohol and tobacco and drugs at the same time. A broad addiction institute may be better able to design and sponsor clinical, basic, and health services research that matches this real-world reality instead of focusing on just one substance at a time.”
Labels:
addiction research,
alcoholism,
government drugs,
NIAAA,
NIDA,
NIDA merger,
NIH
Monday, October 11, 2010
The New Cannabinoids
Army fears influx of synthetic marijuana
It’s a common rumor: Spice, as the new synthetic cannabis-like products are usually called, will get you high--but will allow you to pass a drug urinalysis. And for this reason, rumor has it, Spice is becoming very popular in exactly the places it might be least welcomed: Police stations, fire departments—and army bases.
What the hell is this stuff?
Little is known about spice and other synthetic twists on basic cannabinoid molecules. We do know that the near-cannabis compounds are hard to detect, and even harder to legislate against without closing down avenues of legitimate research. It appears evident that a number of cannabinoid compounds are in circulation, and the precise nature of any given dose is difficult to determine. Much like trying the brown acid, or the joint laced with PCP, the effects vary widely. There are numerous anecdotal reports that spice and its cousins are extremely dose dependent.
The best coverage of Spice, K2, and similar “legal highs” has been generated by science bloggers—especially David Kroll at Terra Sigillata, DrugMonkey at DrugMonkey blog, and Dr. Leigh at Neurodynamics. Readers are advised to consult these links for the most comprehensive coverage of this emerging drug issue.
David Kroll aptly summarized what we know about the "fake weed."
"Synthetic marijuana, marketed as K2 or spice, is an herbal substance sold as an incense or smoking material that remains legal in much of the United States but is being increasingly banned at the state and local levels. The products contain one or more synthetic compounds that behave similarly to the primary psychoactive constituent of marijuana, delta nine tetrahydrocannabinol or THC.”
Kroll writes that JWH–018 is "one of over 100 indoles, pyrroles, and indenes synthesized by the Huffman laboratory to develop cannabimimetics, drugs that mimic the effect of cannabinoids such as THC.”
Furthermore: “The compound most commonly found in these products is a chemical first synthesized by the well-known Clemson University organic chemist, Prof. John W Huffman: the eponymous JW H–018. Another compound, found in spice products sold in Germany, is an analog of CP-47, 497, a cannabinoid developed by Pfizer over 20 years ago."
The cannabimimetics are back.
Unfortunately, the chemical compositions vary, as do the effects, all of which is unpleasantly reminiscent of PCP problems in the past. To gain a better perspective on the matter, I spoke with Joe Gould, a staff writer for the Army Times who has been covering the issue of Spice use in the Armed Forces. Gould has written extensively on the case of Spc. Bryan Roudebush, who attacked his girlfriend in Hawaii while under the influence of Spice. Roudebush had been home from an Iraq deployment for a year when the incident occurred. Two earlier experiences with spice had produced marijuana-like effects. But for Roudebush, the third time was not the charm: He beat his girlfriend and tried to throw her out a window while experiencing what he described as a trance-like state.
“What we were told by the folks at the Army Criminal Investigation Lab is that it started showing up on bases,” said Gould, “and the investigators on the bases were baffled, and the crime lab wasn’t sure what it was at first.”
What investigators discovered was “all that really defines a synthetic cannabinoid is that it activates cannabinoid receptors. We know what THC does. But the chemical composition is not THC. There are all these different strains. Some of the state laws we’ve been seeing, they’re targeting specific varieties of this stuff, but there are other varieties that the law doesn’t know about yet. So I think what the Army has done, intentionally or not, it has sort of skirted this whole question by just calling it all Spice.”
As for the Roudebush case, Gould said: “The first two times he tried it, it was very much like pot. And then the third time, by his and his girlfriend’s description, he goes into a violent trance. They think it was just a different variety. It’s kind of a mystery. What was in that batch? Why did it affect him the way it did? It just goes to how little is known about the drug. You don’t know from one batch to another.”
The U.S. Army currently has no specific testing program in place for Spice. Can you pass a drug test on Spice? “That’s what we heard,” Gould told me. “A researcher from NIH told us exactly that—they believe that the reason it’s popular, the reason they’ve seen officials using it, is because it can’t be tested for.” Despite this, Gould said he knew of “at least nine Commands that have individually passed regulations to target Spice.”
Gould downplayed any talk of an epidemic of usage, and made clear that his research shows that Spice usage is not rampant. “It’s not entirely clear how many soldiers are using Spice. The Army’s not really tracking the use of Spice. Each of these commands passed these regulations either because they saw a problem, or because they were trying to get out in front of what could potentially be a problem.”
Too far out in front for Phillip Cave, a Virginia attorney who has represented military personnel in cases involving Spice. Gould quotes Cave calling the whole thing a “witch hunt,” noting that alcohol is freely available on base, and that researchers do not yet knew whether Spice and its analogs are unsafe or addictive—and they are illegal in only a handful of states at present. Cave also objects to the fact that most cases have been resolved by an Article 15 discharge from service.
“The European Union study says there is the potential for abuse,” said Gould. “How bad it gets, we won’t know until we see more studies.”
Hand-in-hand with restrictions on Spice have come crackdowns on the use of Salvia, a plant responsible for brief but intense bouts of hallucinogenic effects. “The state laws have tended to tackle the two at once,” according to Gould. “Like the state legislatures, the Army has a patchwork of bans they’re putting out there, and there also hitting Salvia. But what I was told by the folks at the lab was that they’re not seeing it in the same kinds of numbers. It’s been sporadic at best.”
Labels:
cannabinoids,
k2,
marijuana,
spice,
Spice Gold,
synthetic marijuana
Sunday, October 3, 2010
Marijuana and Memory
Do certain strains make you more forgetful?
Cannabis snobs have been known to argue endlessly about the quality of the highs produced by their favorite varietals: Northern Lights, Hawaiian Haze, White Widow, etc. Among dedicated potheads, debates about the effects of specific cannabis strains are often overheated, and, ultimately, kind of boring. It's a bit like listening to a discussion of whether the wine in question evinces a woody aftertaste or is, instead, redolent of elderberries. For most people, the true essence of wine drinking is pretty straightforward: a drug buzz, produced by a 12 to 15 % concentration of ethyl alcohol derived from grapes, which can be had in a spectrum of varietal flavors.
However, there is no doubting that, unlike the case of wine, different strains of marijuana can have markedly different psychoactive effects. With weed, it's not just a matter of taste.
Over the past couple of years, the cannabis debate has taken a nasty turn, after British scientists published several controversial studies suggesting that high-THC "skunk" cannabis was responsible for increased mental problems among young people--including an increased risk of developing the symptoms of schizophrenia. British drug policy makers have continued to lead the charge on this, with mixed results. See my earlier post.
Recently, a study published in the British Journal Of Psychiatry concluded that marijuana
high in THC--including so-called "skunk" cannabis--caused markedly more memory impairment than varieties of marijuana containing less THC.
high in THC--including so-called "skunk" cannabis--caused markedly more memory impairment than varieties of marijuana containing less THC.
In an article at Nature News, Arran Frood spelled out the details of the study:
"Curran and her colleagues traveled to the homes of 134 volunteers, where the subjects got high on their own supply before completing a battery of psychological tests designed to measure anxiety, memory recall and other factors such as verbal fluency when both sober and stoned. The researchers then took a portion of the stash back to the laboratory to test how much THC and cannabidiol it contained.... Analysis showed that participants who had smoked cannabis low in cannabidiol were significantly worse at recalling text than they were when not intoxicated. Those who smoked cannabis high in cannabidiol showed no such impairment."
The two main ingredients in cannabis are THC and cannabidiol (CBD). CBD shows less affinity for the two main types of cannabis receptors, CB1 and CB2, meaning that it attaches to receptors more weakly, and activates them less robustly, than THC. The euphoric effects of marijuana are generally attributed to THC content, not CBD content. In fact, there appears to be an inverse ratio at work. According to a paper in Neuropsychopharmacology, "Delta-9-THC and CBD can have opposite effects on regional brain function, which may underlie their different symptomatic and behavioral effects, and CBD's ability to block the psychotogenic effects of delta-9-THC."
So, CBD specifically does not produce the usual marijuana high with accompanying euphoria and forgetfulness and munchies. What the researchers found was that pot smokers suffering memory impairment and those showing normal memory "did not differ in the THC content of the cannabis they smoked. Unlike the marked impairment in prose recall of individuals who smoked cannabis low in cannabidiol, participants smoking cannabis high in cannabidiol showed no memory impairment."
As far as memory goes, THC content didn't seem to matter. It was the percentage of CBD that controlled the degree of memory impairment, the authors concluded. "The antagonistic effects of cannabidiol at the CB1 receptor are probably responsible for its profile in smoked cannabis, attenuating the memory-impairing effects of THC. In terms of harm reduction, users should be made aware of the higher risk of memory impairment associated with smoking low-cannabidiol strains of cannabis like 'skunk' and encouraged to use strains containing higher levels of cannabidiol."
The idea that cannabidiol may protect against THC-induced memory loss is still quite speculative. Other research has suggested that a paucity of CB1 receptors may be protective against memory impairment. Marijuana growers select for high-THC strains, not high-CBD strains, and thus there is little data available about the CBD levels of most marijuana.
An earlier study in Behavioural Pharmacology by Aaron Ilan and others at the San Francisco Brain Research Institute did not find any connection between memory and CBD content. However, Ilan speculated in the Nature News article that the difference might have been due to methodology: In Britain, the subjects were studied using marijuana of their own choosing. In the U.S., National Institute of Health research policy has decreed that marijuana for official research must be supplied by the National Institute on Drug Abuse (NIDA). And if there is one thing many researchers seem to agree on, it is that NIDA weed "is notorious for being low in THC and poor quality."
But CBD still does something, and that something just might be pain relief. Lester Grinspoon, a long-time marijuana researcher at Harvard Medical School, thinks that if the study proves out, it could have an important impact on the medical use of marijuana. Also quoted in Nature News, Grinspoon said: "Cannabis with high cannabidiol levels will make a more appealing option for anti-pain, anti-anxiety and anti-spasm treatments, because they can be delivered without causing disconcerting euphoria."
Morgan, C., Schafer, G., Freeman, T., & Curran, H. (2010). Impact of cannabidiol on the acute memory and psychotomimetic effects of smoked cannabis: naturalistic study The British Journal of Psychiatry, 197 (4), 285-290 DOI: 10.1192/bjp.bp.110.077503
Graphics Credit: http://sites.google.com
Labels:
cannabis,
CB1,
CBD,
marijuana,
marijuana and memory,
memory impairment,
THC
Subscribe to:
Posts (Atom)