The Cannabis-Psychosis Link

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The Cannabis-Psychosis Link

January 12, 2012 | Schizophrenia, Addiction, Alcohol Abuse, Psychotic Affective Disorders

By Marie-josee Lynch, MD, Rachel A. Rabin, MSc, and Tony P. George, MD, FRCPC

- See more at: http://www.psychiatrictimes.com/schizophrenia/cannabis-psychosis-link?cid=G+#sthash.f3kNav4B.dpuf

"Marijuana doesn’t count, does it?” Clinicians are familiar with this common reply when screening for drug use. Cannabis—the most common illicit substance—has managed to exempt itself from the hazardous reputation held by other illicit drugs.1 As mental health practitioners, it is our duty to educate our patients about the potential harms and consequences of cannabis use. This important task is complicated by the disagreement and uncertainty surrounding the nature of the interaction between cannabis and psychotic disorders.

While research suggests that cannabis use can induce an acute psychotic state, there is controversy about whether it may precipitate psychotic disorders, such as schizophrenia. In this article, we provide an update on the literature on this important issue, emphasize areas in need of research, and provide clinically useful recommendations.

More than 16 million Americans use cannabis on a regular basis, typically beginning in adolescence. Notably, it is estimated that approximately 4% of the population have a diagnosis of either cannabis abuse or dependence.1 A history of cannabis misuse is even more common in patients who are schizophrenic than in the general population; 25% of patients with schizophrenia have a comorbid cannabis use disorder. Cannabis use disorders are especially common in younger and first-episode patient samples and in samples with high proportions of males.2

Neurobiology

Marijuana contains more than 400 chemical compounds, including over 60 cannabinoids that contribute to its psychopharmacological effects. The primary psychoactive constituent of cannabis is delta-9-tetrahydrocannabinol (THC). Other plant cannabinoids include delta-8-tetrahydrocannabinol; cannabinol; and cannabidiol (CBD); CBD is the second major psychoactive constituent of cannabis.3 The ratios of these and other cannabinoids vary enormously in preparations of cannabis, and little information exists about the concentration of each of the particular cannabinoids in commonly used cannabis products. Concerns have been expressed regarding the large increase in the potency of cannabis and the surrounding health implications. In the 1960s, the THC content was thought to be in the range of 1% to 3%; today it can reach up to 20%.4

The endogenous cannabinoid system consists of 2 types of G-protein-coupled receptors: cannabinoid 1 (CB1) and cannabinoid 2 (CB2) receptors. CB1 receptors are the most abundant in the brain, while CB2 receptors predominate on immune cells. CB1 receptors are highly concentrated in brain regions implicated in the putative neural circuitry of psychosis and cognitive function. These include the hippocampus, prefrontal cortex, anterior cingulate, basal ganglia, cerebellum, and cortex, with lower levels present in the thalamus, hypothalamus, and amygdala. Activation of CB1 receptors mediates the behavioral and physiological effects of both endogenous and exogenous cannabinoids in the brain.4

An important role of the CB1 receptor is to modulate neurotransmitter release in a manner that maintains homeostasis by preventing excessive neuronal activity in the CNS.5 CB1 receptors are localized on presynaptic neuron terminals on both inhibitory and excitatory neurons, yet they predominate on γ-aminobutyric acid interneurons.6 It is the inhibitory neurons that are thought to mediate most of the effects of cannabinoids. In addition, the action of cannabinoids includes interactions, albeit indirectly, with the dopaminergic system.

THC is a partial agonist at the CB1 receptors, where it has modest affinity and low intrinsic activity. In contrast, CBD shows very little affinity for CB1 receptors. Moreover, the precise molecular mechanism of action of CBD remains unclear. The main endocannabinoids are anandamide and 2-arachidonylglycerol. In contrast to classic neurotransmitters, endocannabinoids can function as retrograde synaptic messengers—they are released from postsynaptic neurons and travel backward across synapses, activating CB1 on presynaptic axons and suppressing neurotransmitter release.

Cannabinoids produce an increase in the dopaminergic activity in the mesolimbic reward pathway, which plays a pivotal role in mediating the reinforcing effects of most drugs of abuse. The increased dopaminergic drive elicited by the cannabinoids could underlie the abusive property of the drug and increases in positive psychotic symptoms induced by THC.7 Recurrent cannabis use produces prolonged and excessive stimulation of the CB1 receptor, and this is thought to disrupt endocannabinoid system function.8 Several lines of evidence exist to suggest a role for cannabinoids and their receptors in the pathophysiology of schizophrenia. It has also been proposed that this CB1 receptor overstimulation may be a contributing factor in triggering THC-induced psychosis.9

The cannabis-psychosis link

Many studies have explored the link between cannabis and psychosis (Table). In a systematic review, Moore and colleagues10 surveyed the literature on this topic. They looked at population-based longitudinal studies as well as nested case-control studies that assessed the impact of cannabis use on the later development of psychosis. The “psychosis” outcomes required the diagnosis of a primary psychotic disorder or affective psychosis, or the occurrence of delusions, hallucinations, or thought disorder during the study period. Results from 7 cohort studies showed a 40% increased risk of psychosis in cannabis users compared with nonusers. The data also revealed a dose-response effect—the risk of psychotic symptoms was increased approximately 50% to 200% in those who used cannabis frequently compared with nonusers.

What is already known about the link between cannabis use and psychosis?

There is strong evidence to support the hypothesis that cannabis consumption is a risk factor for the development of psychotic symptoms and schizophrenia.

 

What new information does this article provide?

This article emphasizes the negative effects of cannabis use in young populations and in those who may confer a genetic risk. We further believe that even in the face of enhanced cognitive function among cannabis-using patients with established schizophrenia, this cannabis use worsens the clinical course and overall prognosis of the disorder.

 

What are the implications for psychiatric practice?

While scientists attempt to clarify the relationship between cannabis and psychosis, it is important that we take the link between cannabis and psychosis seriously by definitively assessing patients for cannabis use. Clinicians should be educating their clients about the potential dangers of using cannabis and the potential bene­fits of quitting.

Critics of this hypothesis believe that cohort studies have inherent limitations that prevent any clear conclusions from being drawn. McLaren and colleagues11 evaluated the methodological strength of the existing cohort studies. The definition of psychosis was a recurrent limitation in the studies. Many studies used psychotic symptoms, not diagnoses, as their outcome, which may not be of clinical significance. Moore and colleagues10 also noted this limitation and attempted to correct for it by separately analyzing the 2 studies that required the diagnosis of a primary psychotic disorder. Interestingly, they found an odds ratio of 2.6 for the development of psychotic disorders in those who had ever used cannabis compared with nonusers. Important confounding factors, such as noncannabis drug use, a family history of psychosis, and unmeasured vulnerability to psychosis, were not adequately controlled in these studies.11

Age at onset of psychosis and cannabis use

Certain risk factors have been reported to interact with cannabis use to increase vulnerability to developing psychosis. One suspected important variable is the age at which cannabis use is started. The age effect was first noted in a Swedish conscript cohort study that demonstrated that cannabis use by age 18 led to a 6-fold increase in the risk of schizophrenia later in life.12 It is unclear, however, whether the psychotic symptoms predated the cannabis use.

To clarify this issue, the Dunedin Multidisciplinary Health and Development Study conducted a prospective longitudinal study of adolescent cannabis use, taking into account psychotic symptoms that occurred before cannabis use.13 The data were compiled from a birth cohort that consisted of 1037 individuals born in Dunedin, New Zealand. Information about psychotic symptoms was obtained at age 11, and drug use was assessed by self-reports at ages 15 and 18 and by a standardized interview schedule at age 26. Two psychosis-related outcomes were measured—the presence of symptoms of schizophrenia and the diagnosis of schizophreniform disorder.

The results showed that those who had used cannabis by ages 15 and 18 had more schizophrenia symptoms than controls, a finding that remained significant after controlling for the presence of psychotic symptoms at age 11. However, the increased likelihood of schizophreniform disorder at age 26 was no longer significant after controlling for psychotic symptoms at age 11. Taken together, this suggests that early cannabis use confers higher risk of psychosis.

These findings may be explained as follows: Adolescence represents a sensitive period of neurodevelopment, with the brain more vulnerable to the effects of cannabis. Alternatively, the heightened risk may simply be a consequence of greater cumulative cannabis use, since these subjects began using it at a younger age. These theories are not mutually exclusive, and the latter explanation is consistent with the previously mentioned dose-response relationship observed in many studies.

Genetic vulnerability

A subsequent study conducted with the Dunedin cohort investigated whether specific genes increase the risks associated with early cannabis use.14 The researchers examined the role of the catechol-O-methyltransferase (COMT) gene, whose link with psychosis has been the focus of many studies. The COMT gene encodes the enzyme responsible for the synaptic metabolism of dopamine. A functional polymorphism of this gene, Val158Met, has been shown to slow the breakdown of dopamine, which potentially increases the risk of psychosis.15,16 The results of the study showed that the presence of the valine polymorphism was not significant unless coupled with adolescent cannabis use.13

Persons with Val/Val or Val/Met genotypes and adolescent cannabis use were at increased risk for schizophreniform disorder (with respective odds ratios of 10.9 and 2.5), while individuals with Met/Met genotypes were not. These findings implicate genetic factors as important contributors to the cannabis-psychosis link, but they are in need of replication.

Impact of cannabis use on the course of schizophrenia

The extent to which cannabis use might alter the clinical course of schizophrenia remains a point of contention within the literature. Intuitively, one may expect cannabis to have a negative impact on the expression and course of schizophrenia. Findings suggest that patients with schizophrenia who use cannabis experience increased psychotic symptoms, are more likely to have relapses, have a greater likelihood of rehospital­ization, and experience poorer ther­apeutic response to antipsychotic medication than patients who are cannabis-naive.17,18 Furthermore, pre-onset cannabis use may trigger an earlier age of onset of psychosis, which is of critical importance given the negative prognostic features associated with earlieronset.19 These effects have been reported to be dose-dependent.

It is interesting to note that other studies have been unable to confirm these adverse findings after controlling for potential confounding factors, which include but are not limited to alcohol and drug use, premorbid functioning, and family history. Moreover, it has been suggested that patients with comorbid cannabis use constitute a clinically distinct subgroup of schizophrenia patients.

In this respect, cannabis use may trigger the onset of psychosis in vulnerable individuals in whom a psychotic disorder otherwise may not have developed. As a result, these patients have a better prognosis, exhibit fewer negative symptoms, have better social skills, and have an enhanced treatment response compared with nonusers. In addition, a recent meta-analysis demonstrated that patients with lifetime cannabis use disorders have superior cognitive function compared with nonuser counterparts.20

These conflicting findings may be due to the varying levels of THC/CBD found in street cannabis. The fact that these constituents have divergent properties may explain the manifestation of different psychological symptoms among users. In fact, CBD may actually attenuate some of the unwanted psychopharmacological effects of THC, because it may have anxiolytic and antipsychotic properties.21 Furthermore, CBD has been shown to have neutral or even procognitive effects.22

Conclusions

Despite all of the uncertainties surrounding the cannabis-psychosis link, we are left with the task of translating these results into clear recommendations for our patients. The evidence suggests that cannabis is associated with an increased risk of psychosis when it is used frequently. Whether cannabis can trigger a primary psychotic disorder that would not have otherwise occurred is unclear. However, in most individuals who use cannabis, psychosis does not develop, which suggests that the increased risk must be related to other vulnerability factors (genetics, frequency, or age of onset of cannabis misuse).

Cannabis also seems to negatively alter the clinical course of schizophrenia. While meta-analyses suggest better cognitive function among cannabis-using patients, this may be a reflection of a higher-functioning subgroup of schizophrenia patients. Accordingly, cannabis-using patients who achieve abstinence may demonstrate improved symptoms and cognitive performance.

The first step in communicating this information to our patients consists of screening for cannabis use and obtaining a thorough substance use history. Psychoeducation and early interventions for young patients who may be vulnerable to psychosis should be used, and motivational interviewing and cognitive-behavioral therapy should be considered to encourage reduction and cessation of use.

There are no accepted pharmacological treatments for cannabis use disorders, yet several potential agents are under investigation. Future studies that control for both environmental and biological risk factors are needed to more clearly elucidate the mechanisms linking cannabis misuse to psychosis.

REFERENCES

References

1. United Nations Office on Drugs and Crime (UNODC). World Drug Report 2010. Vienna: United Nations; 2010.
2. Koskinen J, Löhönen J, Koponen H, et al. Rate of cannabis use disorders in clinical samples of patients with schizophrenia: a meta-analysis. Schizophr Bull. 2010;36:1115-1130.
3. Iversen LL. The Science of Marijuana. 2nd ed. New York: Oxford University Press; 2008.
4. Ameri A. The effects of cannabinoids on the brain. Prog Neurobiol. 1999;58:315-348.
5. Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153:199-215.
6. Eggan SM, Lewis DA. Immunocytochemical distribution of the cannabinoid CB1 receptor in the primate neocortex: a regional and laminar analysis. Cereb Cortex. 2007;17:175-191.
7. Szabo B, Siemes S, Wallmichrath I. Inhibition of GABAergic neurotransmission in the ventral tegmental area by cannabinoids. Eur J Neurosci. 2002;15:2057-2061.
8. Murray RM, Morrison PD, Henquet C, Di Forti M. Cannabis, the mind and society: the hash realities. Nat Rev Neurosci. 2007;8:885-895.
9. Morrison PD, Murray RM. From real-world events to psychosis: the emerging neuropharmacology of delusions. Schizophr Bull. 2009;35:668-674.
10. Moore TH, Zammit S, Lingford-Hughes A, et al. Cannabis use and risk of psychotic or affective mental health outcomes: a systematic review. Lancet. 2007;370:319-328.
11. McLaren JA, Silins E, Hutchinson D, et al. Assessing evidence for a causal link between cannabis and psychosis: a review of cohort studies. Int J Drug Policy. 2009;21:10-19.
12. Andréasson S, Allebeck P, Engström A, Rydberg U. Cannabis and schizophrenia. A longitudinal study of Swedish conscripts. Lancet. 1987;2:1483-1486.
13. Arseneault L, Cannon M, Poulton R, et al. Cannabis use in adolescence and risk for adult psychosis: longitudinal prospective study. BMJ. 2002;325:1212-1213.
14. Caspi A, Moffitt TE, Cannon M, et al. Moderation of the effect of adolescent-onset cannabis use on adult psychosis by a functional polymorphism in the catechol-O-methyltransferase gene: longitudinal evidence of a gene X environment interaction. Biol Psychiatry. 2005;57:1117-1127.
15. Lachman HM, Papolos DF, Saito T, et al. Human catechol-O-methyltransferase pharmacogenetics: description of a functional polymorphism and its potential application to neuropsychiatric disorders. Pharmacogenetics. 1996;6:243-250.
16. Bilder RM, Volavka J, Lachman HM, Grace AA. The catechol-O-methyltransferase polymorphism: relations to the tonic-phasic dopamine hypothesis and neuropsychiatric phenotypes. Neuropsychopharmacology. 2004;29:1943-1961.
17. Fergusson DM, Horwood LJ, Swain-Campbell NR. Cannabis dependence and psychotic symptoms in young people. Psychol Med. 2003;33:15-21.
18. Bowers MB Jr, Mazure CM, Nelson JC, Jatlow PI. Psychotogenic drug use and neuroleptic response. Schizophr Bull. 1990;16:81-85.
19. Linszen DH, Dingemans PM, Lenior ME. Cannabis abuse and the course of recent-onset schizophrenic disorders. Arch Gen Psychiatry. 1994;51:273-279.
20. Rabin RA, Zakzanis KK, George TP. The effects of cannabis use on neurocognition in schizophrenia: a meta-analysis. Schizophr Res. 2011;128:111-116.
21. Zuardi AW, Crippa JA, Hallak JE, et al. Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug. Braz J Med Biol Res. 2006;39:421-429.
22. Fadda P, Robinson L, Fratta W, et al. Differential effects of THC- or CBD-rich cannabis extracts on working memory in rats. Neuropharmacology. 2004;47:1170-1179.
23. Henquet C, Krabbendam L, Spauwen J, et al. Prospective cohort study of cannabis use, predisposition for psychosis, and psychotic symptoms in young people. BMJ. 2005;330:11.
24. Tien AY, Anthony JC. Epidemiological analysis of alcohol and drug use as risk factors for psychotic experiences. J Nerv Ment Dis. 1990;178:473-480.
25. van Os J, Bak M, Hanssen M, et al. Cannabis use and psychosis: a longitudinal population-based study. Am J Epidemiol. 2002;156:319-327.

Another cause of California's drought: Pot farms

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Another cause of California's drought: Pot farms

These farms in the wilderness soak up a tremendous amount of water, especially at the peak of summer.

By: John Platt

Mon, Apr 07, 2014 at 10:52 AM

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Photo: Don DeBold/Flickr

California's ongoing drought has been blamed on a lot of different factors, ranging from climate change to over consumption to the agricultural industry. But here's one more factor that may be draining California dry: marijuana farms. These farms – some legal, most not – soak up a tremendous amount of water in the wilderness. At summer's peak, each plant can soak up about six gallons of water a day, according to a recent report from McClatchy DC. It's so bad in some regions, particularly California's North Coast, that important fish populations are suffering.

Illegal pot farms in Northern California have already been linked to extensive wildlife deaths, as the farms are often protected with rat bait. This has even affected federally protected endangered species. (California banned the sale of rat poison last month to help protect wildlife.)

All of these problems are compounded by the fact that many pot farms are situated, illegally, on public land. "Those are lands that you and I own," Congressman Mike Thompson told McClatchy. "And when people are growing dope there and guarding their operations with guns and the likes, and sometimes with booby traps, we can't use the land that we own. It happens all over."

Other pot farms are apparently being set up in secret on land belonging to traditional farmers. "[Pot] grows hidden in trees on someone else's farm have become more and more common over the past two years," an undercover drug agent told KCRA in February. The National Guard reported that these illegal growers put pumps, dams and irrigation tubing on the sites, diverting water from the farmers' canals. These illegal sites also use pesticides, which end up in the water, sometimes in wells intended for drinking.

None of this is new, of course. Marijuana plots were blamed for diverting hundreds of millions of gallons of water during California's 2009 drought.

The marijuana industry, perhaps not surprisingly, says it is being scapegoated. "It's really easy to point fingers at a very large cash crop that's completely unregulated," Emerald Growers Association founding Chairwoman Kristen Nevedal told McClatchy. "It's one of the main cash crops of the state." Marijuana sales are projected to reach nearly $1 billion in California in 2014.

That number could actually be hard to predict: the California drought is predicted to tighten marijuana supplies and drive up pot prices around the country.

Veteran journalist Dan Rather recently looked into the problem of pot farming in California. You can see the first part of his report in the video below:

24 Mind-Blowing Facts About Marijuana Production in America

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ENVIRONMENT

→ Economy, Energy, Food and Ag

24 Mind-Blowing Facts About Marijuana Production in America

The only thing green about that bud is its chlorophyll.

—By Josh Harkinson, Brett Brownell, and Julia Lurie

| March/April 2014 Issue

2001

You thought your pot came from environmentally conscious hippies? Think again. The way marijuana is grown in America, it turns out, is anything but sustainable and organic. Check out these mind-blowing stats, and while you're at it, read Josh Harkinson's feature story, "The Landscape-Scarring, Energy-Sucking, Wildlife-Killing Reality of Pot Farming."

Sources: Jon Gettman (2006), US Forest Service (California outdoor grow stats include small portions of Oregon and Nevada), Office of National Drug Control Policy, SF Public Utilities Commission, Evan Mills (2012).

UPDATE: Beau Kilmer of the RAND Drug Policy Research Center argues that the government estimates of domestic marijuana production used in this piece and many others are in fact too high. Kilmer's research,published last week, suggests that total US marijuana consumption in 2010 (including pot from Mexico) was somewhere between 9.2 and 18.5 million pounds.

Even Casual Marijuana Use Causes Brain Abnormalities

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Even Casual Marijuana Use Causes Brain Abnormalities

Written by

Jason Koebler

@jason_koebler jasontpkoebler@gmail.com

April 15, 2014 // 06:15 PM EST

Image: Shutterstock

Even casually smoking marijuana can cause abnormalities in the developing brain, according to the results of a new study funded by the National Institutes of Health.

High-resolution MRI scans of the brains of adults between the ages of 18-25 who reported smoking weed at least once a week were structurally different than a control group: They showed greater grey matter density in the left amygdala, an area of the brain associated with addiction and showed alterations in the hypothalamus and subcallosal cortex. The study also notes that marijuana use “may be associated with a disruption of neural organization.” The more weed a person reported smoking, the more altered their brain appeared, according to the Northwestern University and Harvard Medical School study, which was published in the Journal of Neuroscience.

The finding already has the study’s authors calling for states to reconsider legalizing the drug. Hans Breiter, the lead author, said he’s “developed a severe worry about whether we should be allowing anybody under age 30 to use pot unless they have a terminal illness and need it for pain.”

Previous marijuana studies have shown brain abnormalities in chronic users and in teens, but the researchers say this is the first time that there are structural differences between recreational users and those who don’t smoke weed. The study says that the parts of the brain altered have been associated with schizophrenia, Parkinson’s disease, obsessive-compulsive disorders, and Tourette’s syndrome. 

The study suggests that “pending confirmation in other cohorts of marijuana users, the present findings suggest that further study of marijuana effects are needed to help inform discussion about the legalization of marijuana.”

The veracity of the study’s findings comes down to how you define “recreational.” Though none of the users were “addicted” to weed (the researchers’ words, not mine, so take up your “weed is not addictive" battle with them), most of them smoked pot fairly regularly. On average, those studied smoked weed about 4 days a week, smoked 11 joints a week, had regularly smoked weed for about six years, and had started when they were about 16. 

It's the first study that has found these brain abnormalities in casual users (previous mice studies have had similar results), but it's just another study in the proverbial garden of them. It further muddles what legalization is getting at: Is weed good or bad (or, beyond that—should adults be able to decide if they want to do it anyway)?

Take, for instance, the news that NIH director Francis Collins said there is now a scientific basis for the fact that weed often eases anxiety. So, weed is good. Then, later in his blog post, he suggested that “frequent or heavy marijuana use among adolescents should be a cause of major concern.” So, weed is bad.

The fact that Colorado is raking in far more tax money from legal weed than it originally expected (good!) and hasn’t seen any disastrous things happen (good!) has certainly piqued the interest of other states looking to cash in on the crop. Now there's this study (bad!). Whether it has any impact on legalization efforts around the country remains to be seen, but it certainly doesn’t help the cause. 

Topics: Study Says, marijuana, weed, drugs, nih, discoveries

Popular New Marijuana Product Called 'Wax' Is Now the Target of Govt. Drug Panic Propaganda

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AlterNet / By Helen Redmond

Popular New Marijuana Product Called 'Wax' Is Now the Target of Govt. Drug Panic Propaganda

 

 

The DEA is whipping up fears in California over butane hash oil.

Cannabis wax in a small plastic container with uncovered butane vapor pipe alongside.
Photo Credit: a katz/ Shutterstock.com

March 2, 2014  |  

 

A concentrated form of marijuana known as wax or butane hash oil (BHO) is becoming more popular and its production and use increasingly controversial in states across the country.

While Colorado's pot shops are embracing wax as a popular, potent form of newly legal cannabis, the Drug Enforcement Administration is whipping up a drug panic in California. In a Yahoo News article, Gary Hill, assistant special agent in charge at the DEA's San Diego office warned, “We have seen people have an onset of psychosis and even brain damage from that exposure to that high concentration of THC. Our concern is that this is going to spread before we get it under control.”

Agent Hill offered no studies or data to back up these claims.

But the DEA, once again, is too late. BHO has been around for at least a decade and now it is more available than ever—and the wax is here to stay.

In order to be consumed, wax is vaporized, which makes it a popular alternative for cancer patients, the elderlyand others who don't want to smoke.

In Colorado where cannabis is legal for both recreational and medical use, wax is available in marijuana dispensaries. Daniel de Sailles, a partner at Top Shelf Extracts in Denver, explained to High Times:

“I’m a 100 percent proponent of BHO, because I’ve seen it make people’s pain just evaporate. As medicine, it helps with both harm reduction—it practically cures withdrawal symptoms in people who are alcoholics or addicted to speed or pharmaceuticals—and pain management. It works every single time, and it’s easier to regulate your dosage. You take a fraction of a percent of a gram, and you’re fully medicated and exactly where you want to be."

Wax is also sold in the newly opened marijuana shops in Colorado to customers who want a quicker, more intense buzz from pot. Because it is a concentrated form of the oils in marijuana, it delivers a potent dose of the active psychoactive ingredient, THC, to the user. Think of wax like 100 proof vodka vs. 50 proof.
BHO is just another form of cannabis, despite the panic over the wax on the part of drug warriors. The only potential danger, according to experts, is in the manufacturing process. Butane, which is used to make wax, is highly flammable and sparks can set off an explosion. There have been numerous reports of explosions while attempting butane extractions, most likely by do-it-yourself novice chemists.

Some have posed a concern about the health risks of ingesting butane into the lungs, but according to Bob Melamede, associate professor of biology at the University of Colorado and the president/CEO of Cannabis Science Inc., butane is not a significant concern.

“The biggest concern is the quality of the marijuana—who’s been growing it and what they used," he said. "If you have contaminants (i.e., pesticides, herbicides, fungi) on your plant, that’s going to come off into the extract."

Cannabis activists in Los Angeles have a measure on the ballot that calls for the testing and regulation of wax and a ban on production of any marijuana product that uses flammable products like butane.

William Breathes, a cannabis critic for Denver’s Westword newsweekly, samples and reviews a wide array of pot products and said wax is “the same as weed" only stronger.

"There are people using it recreationally, and that’s wonderful, but we’re looking at it as a new way of medicating," he said. "For somebody who’s really sick—battling nausea, for example—maybe choking down a whole joint isn’t for them. Vaping one little hit of oil or solventless wax is so potent all at once, it’s great medicine. We need to talk about that—that’s how we bring it to the public and stop people from being scared of it.” 

Helen Redmond is a freelance journalist and a drug and health policy analyst.

Philip Seymour Hoffman's Cause Of Death A Toxic Mix Of Heroin And Other Drugs

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Philip Seymour Hoffman's Cause Of Death A Toxic Mix Of Heroin And Other Drugs

 

 | by  JAKE PEARSON 

 

Posted: 02/28/2014 4:16 pm EST Updated: 03/01/2014 4:59 am EST 

 

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NEW YORK (AP) — Philip Seymour Hoffman died from taking a combination of heroin, cocaine and other drugs, the New York City medical examiner ruled Friday, a toxic mix that addiction specialists say is not uncommon in the tens of thousands of overdose deaths in the U.S. each year.

Hoffman, 46, who was found Feb. 2 with a needle in his arm on the floor of his Manhattan apartment, also had taken amphetamines and benzodiazepines, which are drugs such as Xanax and Valium that are widely prescribed for anxiety, trouble sleeping and other problems, said a spokeswoman for the medical examiner. The death was ruled accidental.

The medical examiner didn't provide the names of the drugs or the amounts found in the actor's system, making it impossible to determine which drug was the major factor, said Dr. Charles McKay, a medical toxicologist for Hartford Hospital in Connecticut and a spokesman for the American College of Medical Toxicology.

"There's a difference between a stimulant death, which would be cocaine and the amphetamines, and a narcotic death, like heroin," he said.

The first two can cause heart rhythm problems, a stroke or heart attack, whereas heroin, especially with sedatives such as benzodiazepines, can depress breathing.

In any case, McKay said, the combination of drugs "suggests someone who has been using drugs repetitively."

Police had been investigating Hoffman's death as a suspected drug overdose. Tests found heroin in samples from at least 50 packets in his Manhattan apartment. Authorities also found unused syringes, a charred spoon and various prescription medications, including a drug used to treat heroin addiction, a blood-pressure medication and a muscle relaxant.

More than half of overdose deaths in the U.S. involve a mix of drugs, said Dr. Len Paulozzi, a medical epidemiologist with the Centers for Disease Control and Prevention. At least a fifth also involve alcohol, he said. There were more than 38,000 drug overdose deaths nationwide in 2010, according to the most recent CDC figures.

If multiple drugs are listed on a death certificate, often "it means the coroner or medical examiner thought all of these contributed to the death," said Paulozzi, who researches overdose death trends.

"The drug of that combination that is most associated with overdose death is heroin," said Cindy Kuhn, a pharmacology professor at Duke University. "People just stop breathing. It's especially dangerous in combination with other sedatives like the benzodiazepines."

Hoffman, who won an Oscar for "Capote" and starred in numerous other movies as well as New York stage productions, had been frank about struggling with substance abuse. He told CBS' "60 Minutes" in 2006 that had he used "anything I could get my hands on" before getting clean at age 22. But in interviews last year, he said he'd relapsed, had developed a heroin problem and had gone to rehab for a time.

Heroin addicts often mix heroin with a stimulant like cocaine — a practice known as speedballing — to break the effect of the opiate, said addiction specialist Dr. Louis Baxter, a former president of the American Society of Addiction Medicine.

"They're doing self-medication or self-regulation," said Baxter. "It's just a part and parcel of what happens with long-term abuse of substances: People will go from just their drug of choice to experimentation and 'self-regulation' of other drugs."

A Hoffman family spokesperson didn't immediately return messages seeking comment. In his will, Hoffman bequeathed his estate to his longtime partner, Mimi O'Donnell, with a trust fund for their 11-year-old son. They also have two other children.

Investigators have been probing how Hoffman may have obtained the heroin. Tests found it was not cut with a dangerous additive such as fentanyl, a synthetic form of morphine used to intensify the high that has been linked to deaths in other states.

A musician, veteran jazz player Robert Vineberg, was charged amid the investigation into Hoffman's death with keeping a heroin stash in a lower Manhattan apartment. Vineberg, who has said he was a friend of the Tony Award-nominated Hoffman, hasn't been charged in Hoffman's death and has said he didn't sell him the heroin found in his apartment.
___

AP Chief Medical Writer Marilynn Marchione in Milwaukee and Medical Writer Mike Stobbe in Atlanta contributed.