Abstract

Smoking cannabis daily doubles an individual’s risk of developing a psychotic disorder, yet indicators of specific vulnerability have proved largely elusive. Genetic variation is one potential risk modifier. Single-nucleotide polymorphisms in the AKT1 and catechol-O-methyltransferase (COMT) genes have been implicated in the interaction between cannabis, psychosis and cognition, but no studies have examined their impact on an individual’s acute response to smoked cannabis. A total 442 healthy young cannabis users were tested while intoxicated with their own cannabis—which was analysed for delta-9-tetrahydrocannbinol (THC) and cannabidiol content—and also ±7 days apart when drug-free. Psychotomimetic symptoms and working memory were assessed on both the sessions. Variation at the rs2494732 locus of the AKT1 gene predicted acute psychotic response to cannabis along with dependence on the drug and baseline schizotypal symptoms. Working memory following cannabis acutely was worse in females, with some suggestion of an impact of COMT polymorphism on working memory when drug-free. These findings are the first to demonstrate that AKT1 mediates the acute response to cannabis in otherwise healthy individuals and implicate the AKT1 pathway as a possible target for prevention and treatment of cannabis psychosis.

Discussion

To our knowledge, this study provides the first evidence that the acute psychotic effects of cannabis are predicted by variation at the rs2494732 locus of the AKT1 genotype. No evidence was found for an interaction of the COMT Val158Met genotypes with cannabis use, in producing psychotomimetic symptoms in this group of healthy cannabis users. Cannabis dependence predicted non-intoxicated schizotypal symptoms, but neither genotype had any impact on these. COMT Val158Met genotype had a marginal impact on performance on a working memory task when non-intoxicated and when memory load was low; however, at higher load, schizotypy was the only emerging predictor of performance. When intoxicated with cannabis, gender was the only predictor of working memory performance, with poorer performance in females at a high working memory load.

In the current study, which is the largest ever to be conducted on the acute response to cannabis, psychotomimetic symptoms while intoxicated were found to be predicted by variation at the rs2494732 locus of the AKT1 genotype in healthy young cannabis smokers, increasing with C allele dosage. These data are very important as acute psychotic response to cannabis is thought to be a marker of the risk of developing psychosis from smoking the drug.1 Two previous studies have implicated this polymorphism in the interaction with cannabis and psychosis,9, 18 but this work concentrated on individuals who were at familial risk of schizophrenia. This study is the first to demonstrate that the acute response to cannabis is modulated by AKT1 in otherwise healthy cannabis smokers. The mechanism for this modulation of acute effects may be through the interaction of AKT1 with dopamine.2, 9Our sensitivity analyses suggested that these effects may be confined to dependent cannabis smokers but further investigation of these data with larger samples is required.

AKT1 codes for a protein that is a serine/threonine kinase, which has a variety of functions, one of which is as a signalling molecule downstream of the dopamine D2 (DRD2) receptor. Decreased AKT1 functionality may result in enhanced responses to DRD2 receptor stimulation.19 THC has been found to acutely induce dopamine release in

rats20, 21 and in humans,22, 23 although not in all studies.24 Dopamine release is thought to occur via the blockade of cannabinoid 1 (CB1) receptors on GABAergic neurons that target pyramidal cells. These neurons normally exert an inhibitory effect on the firing of dopamine neurons that project back to the nucleus accumbens, so agonism of CB1 receptors by THC may produce increased dopamine release. This THC-mediated increase in dopamine release may be further exacerbated by decreased AKT1 functionality. Elevated levels of mesolimbic dopamine are known to have a role in the development of psychotic symptoms, potentially through disrupted salience attribution.25

In contrast to the role of variation at the rs2494732 locus of AKT1, this study found no support for the direct involvement of the functional polymorphism of the COMT gene in mediating acute psychotic response to cannabis. This is in contrast to one previous small-scale acute laboratory study giving acute THC to patients with schizophrenia,26 and other work that suggested that COMT may mediate the psychotomimetic risk of cannabis3 but in agreement with subsequent larger studies that failed to replicate these findings.4, 27 There was a marginal effect of COMT on working memory performance at a low load when not intoxicated. This polymorphism of COMT initially caused some excitement as several studies emerged demonstrating its association with working memory,28, 29 but this finding was not confirmed by meta-analyses,30 which suggested that this may be a case of publication bias.

Greater schizotypal symptoms predicted in poorer working memory performance on the more difficult section of the task among drug-free cannabis users. This echoes recent findings of poorer working memory in individuals high in schizotypy31 and indeed of the relationship between working memory performance and transition to psychosis.32 Working memory impairment is considered a central cognitive impairment in schizophrenia, and there is some evidence that such impairments are related to symptoms, particularly to negative symptoms.33, 34

Only gender predicted acute working memory impairment from cannabis, with greater impairment in females. Very few studies have examined gender differences in neurocognitive acute response to THC, with those that have using very small samples and in finding little evidence of gender differences.35 However, this study examined the acute effects of cannabis in over 400 cannabis smokers. There is an emerging preclinical literature that might explain this effect. CB1 density has been found to vary by gender, with animal studies reporting greater CB1 receptor density among males across several brain regions.36, 37 However, across their lifetime, adult female brains show increases in CB1 receptor density, with levels eventually surpassing those observed in males.38 Furthermore, greater CB1 de-sensitization after exposure to THC in the prefrontal cortex, hippocampus, striatum, amygdala and midbrain is seen in female adolescent rats.36, 37 Preclinical studies have also demonstrated that female rats preferentially metabolize THC to its most highly active metabolite, while male rats metabolize THC to multiple compounds.39 In combination, these findings may in part explain the finding of greater acute working memory impairment from cannabis in females. This also may partly be driven by gender differences in frequency of cannabis use. Users who smoked cannabis less frequently experienced stronger effects, and as there was a higher proportion of low frequency female cannabis users compared to males this may have contributed to the observed gender differences in working memory following the drug.

Strengths of this study include the large sample size for assessing acute cannabis effects. We also used independent verification of the cannabinoid content of the cannabis consumed and drug history. Further, the hypothesis-driven approach we took to genetic analysis was a strength, examining only loci implicated in previous studies and, therefore, circumventing some of the problems of type I error that have dogged earlier research. However, inevitably there are several limitations of the study. For the cannabis use data, while verifying past 3 months use with hair analysis, we inevitably relied on retrospective self-reports of drug use, which are particularly complicated as cannabis is known to acutely impair episodic memory. However, we opted to use years of cannabis use in this model as this was considered the most reliable to estimate. As we purposely recruited a young group of cannabis users, there was restricted variation in years used and future studies may investigate this further. We used a predominantly white Caucasian sample. However, it is unlikely that ethnic differences in allele frequency at rs2494732 biased the outcome of the study, as there was no difference between the frequency of rs2494732 alleles across the dichotomized ethnic groups. In addition, analyses with only Caucasian participants gave the same results to the analysis containing all ethnicities.

In summary, we found that the AKT1 rs2494732 C allele was associated with increased psychotomimetic symptoms after smoking cannabis. The other factor impacting on acute psychotomimetic response to cannabis was baseline schizotypy. Gender was the only factor to predict acute working memory impairment, with poorer performance in females. When drug free, cannabis dependence weakly predicted schizotypal symptoms and COMT genotype had a marginal impact on working memory, along with ethnicity. The findings of this study contribute to a recent and growing body of evidence suggesting that variation at the AKT1 locus confers details of the risk of cannabis smoking for schizophrenia. This is likely to be in the context of numerous other genetic variants, so the clinical utility at the moment is unclear. It is nonetheless encouraging that there is concordance between genetic influences on acute effects of cannabis and those mediating risk of psychosis. However, the fact that AKT1 is relevant to the biology of psychotic symptoms suggests that this might be a promising direction for novel therapeutics for cannabis-induced psychosis.

Source:  Citation: Translational Psychiatry (2016) 6, e738; doi:10.1038/tp.2015.219 Published online 16 February 2016 

For complete paper log on to: http://www.nature.com/tp/journal/v6/n2/full/tp2015219a.html

The letter below was written by a doctor in response to an article suggesting that  marijuana could be used to get people  off heroin.  Note that in Maine, before so-called medical marijuana was made legal it ranked 28th in teen use; seven years later, it was No. 1.

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The recent op-ed by a spokesperson for the marijuana industry saying that pot can be used for people trying to get off heroin, is both wrong and dangerous.

I’m a doctor who has spent 30 years treating drug addicts, starting in my residency at Maine Medical Center in Portland.

The aim in treating addicts is to get them off all addictive drugs, including alcohol and marijuana, not substitute one for another. And the reason is that addicts and alcoholics are happiest clean and sober. It is bad medical practice to prescribe marijuana or any other addictive drug to a recovering addict. Pope Francis probably said it best: “The problem of drug use is not solved with drugs!”

It’s actually bad practice to recommend marijuana for any medical condition. The American Academy of Child and Adolescent Psychiatry opposes medical marijuana laws because they make the drug widely available to teenagers. In 1999, shortly before Maine became one of the first states to legalize medical marijuana, it ranked 28th in teen use; seven years later, it was No. 1.

Yes, cannabinoids help with certain medical conditions, but the prescription cannabinoids Marinol and Cesamet work just as well as pot, have fewer side effects and are much longer-acting, so people don’t have to dose every few hours. No one needs to smoke pot, and we don’t need to make it so widely available that we create an epidemic of teenage use.

Medical marijuana laws are both unnecessary and bad for public health.

ABOUT THE AUTHOR  Ed Gogek, M.D., of Prescott, Ariz., is an addiction psychiatrist.

Source:  http://www.pressherald.com/2016/02/14/another-view-treatment-for-drug-addiction-should-never-include-marijuana/   Feb. 2016

Editor’s note: This commentary is by Patrick J. Kennedy, who is a former member of Congress from Rhode Island and an honorary adviser to SAM, Smart Approaches to Marijuana.

The epidemic of drug addiction and overdoses gripping Vermont, and our country at large, cries out for reform. We must change the perception that jail is an effective treatment for the disease of drug addiction, and give mental health issues the attention and funding they deserve, an opinion I know many Vermonters share.

But the legalization and commercialization of another addictive drug — marijuana — is precisely the wrong way to address this critical problem. Legalization has nothing to do with whether we lock up pot users, and everything to do with making money. Marijuana industry lobbyists that are pushing legalization to the Vermont Legislature disingenuously conflate the two issues, claiming that the only way to stop imprisoning marijuana users is to legalize the drug. They also make sweeping claims about how commercialization will control the black market and make the drug “safer.”

But both claims are demonstrably false. First of all, we can stop jailing marijuana users without letting big business sell marijuana at corner stores. Vermont has already decriminalized marijuana use for adults, and will not arrest or jail you if you possess an ounce or less of marijuana for personal use. And our Congress is already debating broader criminal justice reforms that may reduce the burden of arrests and imprisonment for drug offenses, especially on minority and low-income communities.

Second, and more broadly, we know from other states’ experiences that the billion-dollar marijuana industry — the folks behind the legalization effort — is more interested in profits than our health and safety. Legalization means inviting a powerful lobby into Vermont that pushes hard against regulations. Pot lobbyists in Colorado defeated restrictions on pot ads aimed at children. They have opposed restrictions on marijuana potency. And they are fighting laws keeping pot shops away from schools, parks, and day care centers in Oregon. Vermont legislators may think they have cracked the code on how to implement legalization “safely,” but it will not be long until industry forces expose and exploit any openings they see for the sake of profits.

Now, I put the call out to the Vermont Legislature: Please learn from the experiences of other states, and heed the warning signs — marijuana legalization does not reduce the toll drug addiction takes on our communities.

In other words, commercial marijuana behaves just like another large American industry peddling addiction — Big Tobacco. It may surprise Vermonters to know that the large tobacco companies have been studying the marijuana business since the 1960s, seeing it as a natural extension of their product line. And like tobacco, the marijuana business can only profit when it creates and cultivates heavy users. Just 20 percent of pot users consume 80 percent of all marijuana. Those heavy users, many of whom are addicts, are the target market for the pot industry, not the casual smoker.

This profit motive is why legalization and commercialization has yielded more pot use, not less, among children and adults. After legalizing pot, Colorado took the dubious honor of having the highest past-month marijuana use rates in the country in both age groups. A host of related problems have accompanied this dubious honor, including a surge in marijuana poisonings — up 148 percent overall, and up a shocking 153 percent

among children 0 to 5 years old — and a 32 percent spike in marijuana-related traffic fatalities. Even without legalization, Vermont already ranks No. 2 in past-month consumption. Commercialization will only push those numbers higher.

Moreover, legalization has not blunted Colorado’s black market. The state’s attorney general told the press last February that “The criminals are still selling on the black market. … We have plenty of cartel activity in Colorado. …” Colorado law enforcement officers have even indicated that black market activity may have increased, as people illegally export pot to other states.

Finally, like the tobacco companies, who once boasted that they targeted “the young, the poor, the black, and the stupid,” the marijuana industry has had an outsized impact on poor and minority communities in Colorado. A recent exposé showed that Denver’s pot business was highly skewed towards poor areas, with one neighborhood having one marijuana business for every 47 residents. A strategy of “profits before public health” is not the way to serve socioeconomic and racial justice.

Now, I put the call out to the Vermont Legislature: Please learn from the experiences of other states, and heed the warning signs — marijuana legalization does not reduce the toll drug addiction takes on our communities. It represents burning down the village in order to save it, by handing Vermont’s public health over to Wall Street and the marijuana lobby. Rather, I urge you to focus on solutions we know will work — sensible criminal justice reform and serious investments in drug prevention.

Source:   http://vtdigger.org/2016/02/03/patrick-kennedy-say-no-to-marijuana-legalization/

Law enforcement officials would love to have a clear way to tell when a driver is too drugged to drive. But the decades of experience the country has in setting limits for alcohol have turned out to be rather useless so far because the mind-altering compound in cannabis, THC, dissolves in fat, whereas alcohol dissolves in water.

And that changes everything. “It’s really difficult to document drugged driving in a relevant way,” says Margaret Haney, a neurobiologist at Columbia University, “[because of] the simple fact that THC is fat soluble. That makes it absorbed in a very different way and much more difficult to relate behavior to, say, [blood] levels of THC or develop a breathalyzer.”

When you drink, alcohol spreads through your saliva and breath. It evenly saturates your lungs and blood. Measuring the volume of alcohol in one part of your body can predictably tell you how much is in any other part of your body — like how much is affecting your brain at any given time.

That made it possible to do the science on alcohol and crash risk back in the mid-20th century. Eventually, decades of study helped formulate the 0.08 blood alcohol limit as too drunk to drive safely. “The 0.08 standard in alcohol is from decades of careful epidemiological research,” says Andrea Roth, a professor of law at the University of California, Berkeley.

But marijuana isn’t like that. The height of your intoxication isn’t at the moment when blood THC levels peak, and the high doesn’t rise and fall uniformly based on how much THC leaves and enters your bodily fluids, says Marilyn Huestis, who headed the chemistry and drug metabolism section at the National Institute on Drug Abuse.

Because THC is fat soluble, it moves readily from water environments, like blood, to fatty environments. Fatty tissues act like sponges for the THC, Huestis says. “And the brain is a very fatty tissue. It’s been proven you can still measure THC in the brain even if it’s no longer measurable in the blood.”

From her research, Huestis found that THC rapidly clears out of the blood in occasional users within a couple of hours. While they’re still high, a trickle of THC leaches out of their brains and other fatty tissues back into the blood until it’s all gone.

That means a lab test would only find a trace amount of THC in the blood of occasional smokers after a few hours. “You could have smoked a good amount, just waited two hours, still be pretty intoxicated and yet pass the drug test [for driving],” says Haney.

And if you eat the weed instead of smoking it, Haney says, your blood never carries that much THC. “With oral THC, it takes several hours for [blood THC] to peak, but it remains very low compared to the smoked route, even though they’re very high. It’s a hundredfold difference,” she says.

But daily users are different. Huestis says that heavy smokers build up so much THC in their body fat that it could continue leaching out for weeks after they last smoked. These chronic, frequent users will also experience a rapid loss of THC from their blood after smoking, but they will also have a constant, moderate level of blood THC even when they’re not high, Huestis says.

It gets trickier when you try to factor in the chronic effect of smoking weed, Huestis says. “We found [chronic, frequent smokers’] brains had changed and reduced the density of cannabinoid receptors,” she says. They were cognitively impaired for up to 28 days after their last use, and their driving might also still be impaired for that long. “It’s pretty scary,” she says.

The attitude difference between stoned drivers and alcohol drivers seems clear, Huestis

says. Pot smokers, she says, “tend to be more aware they’re impaired than alcohol users.” Drunk drivers are more aggressive, and high drivers are slower. But in her studies, she found that being blazed enough, as when a smoker’s blood THC level peaks at 13 nanograms per milliliter, could be just as a dangerous as driving drunk. The marijuana advocacy group NORML emphasizes that driving high can be dangerous, and  advises people to drive sober.

This all translates into a colossal headache for researchers and lawmakers alike. While scientists continue to bang their heads over how to draw up a biological measurement for marijuana intoxication, legislators want a way to quickly identify and penalize people who are too high to drive.

The instinct, Huestis says, is to come up with a law that parallels the 0.08 BAC standard for alcohol. “Everyone is looking for one number,” she says. “And it’s almost impossible to come up with one number. Occasional users can be very impaired at one microgram per liter, and chronic, frequent smokers will be over one microgram per liter maybe for weeks.”

The shaky science around relating blood THC to driving impairment is unfair for people living in marijuana-legal states that have absolute blood THC limits for driving, says Andrea Roth, a professor of law at the University of California, Berkeley.

In states like Washington, if a driver is found to have over 5 nanograms of THC per milliliter in their blood, they automatically get a DUI-cannabis. “If we are going to criminalize DUI marijuana, we need to take information from scientific studies and use it to decide if that risk is sufficiently high to be so morally blameworthy that we call it a crime. But we don’t, so picking 5 nanograms per milliliter is arbitrary,” Roth says.

The complicated biology of THC makes current DUI cases very tricky.

“Blood isn’t taken in the U.S. until 1.5 to four hours after the [traffic] incident,” Huestis says. By then, THC levels would have fallen significantly, and these people might have been impaired but passed the test. At the same time, a heavy user living in a state like Washington would get a DUI even if she or he hadn’t smoked in weeks.

As a result, it gets difficult to even understand how risky blazed driving is. Traffic studies that rely on blood THC measures could also be inaccurate if blood is drawn too late and THC has already left the system. And some state traffic databases, including Colorado’s, according to state traffic officials, link accidents to 11-nor-9-carboxy-THC, a byproduct of marijuana metabolism that marks only recent exposure and not intoxication. That might result in an overestimation of marijuana-related accidents.

In the meantime, Haney says, the challenge shouldn’t deter people from trying to find a marijuana DUI solution. People are working on breath tests, saliva, other blood markers and behavioral tests, just nothing that so far has stuck, she says. “We need something, because it’s an important public health issue. But how we’re going to get there? I just don’t know.”

Source:  http://www.npr.org/sections/health-shots/2016/02/09/466147956  Feb.2016

Everything you need to know about fake weed.

If you’re confused by synthetic marijuana, then a series of recent news stories about the drug probably didn’t clear things up. First, the Boston Globe reported that New England Patriots defensive end Chandler Jones “had a bad reaction to a substance he put into his body” and walked to a nearby police station to get help. That substance, the Globe later explained, was synthetic marijuana. Then last week, police in Washington state reported that another NFL player, Seattle Seahawks fullback Derrick Coleman, admitted to smoking synthetic weed in October before getting into a hit-and-run car accident. After the accident, witnesses described Coleman as acting “delirious and aggravated.”

Off the sports pages, you might have seen a story about a group of senior citizens in Pennsylvania who got arrested for running a synthetic marijuana trafficking ring worth more than $1.5 million. Or perhaps you saw the one about a pair of brothers in Milwaukee, ages 12 and 13, ending up in the hospital after smoking some fake pot and having a violent reaction that included foaming at the mouth, “throwing up white mucus,” “talking funny,” and shaking.

These are only the latest data points showing the rise of synthetic marijuana as a staple of recreational drug use in America. Against the backdrop of softening attitudes toward actual marijuana, synthetic weed has attracted a strange coalition of users, including athletes, curious teenagers, and desperate homeless people. Here’s a primer on the drug whose ambiguous legal status and unpredictable side effects have turned it into a bleak cultural phenomenon.

What is synthetic marijuana, and how is it different from normal weed?

The most important fact to understand about synthetic marijuana is that it isn’t just one thing. It’s more like a category of things, a family of man-made chemicals that have one major characteristic in common: They interact with the same cell receptors in the brain as THC, the active ingredient in natural cannabis. In theory, someone could ingest these chemicals in any number of ways, but manufacturers play up the association between their products and traditional marijuana by spraying their chemicals onto diced-up dry plant matter that can be sold in baggies and smoked.

When you buy one of these baggies, you’re basically getting a chemical—you never know which one—that’s been dressed up in a weed costume. But the similarities pretty much end there. In fact, most public health experts frown on the phrase “synthetic marijuana” because they think it overstates the extent to which the chemicals used to make it resemble THC. They prefer the term “synthetic cannabinoids.”

Where did synthetic cannabinoids come from, and how long have they been around?

Like ecstasy and LSD, SCs owe their existence to academic research. The chemist who developed the first SC compounds was a Clemson University professor named John W. Huffman, who was interested in the brain receptors that regulate “appetite, nausea, mood, pain and inflammation.” According to this Washington Post profile, Huffman synthesized a compound he called JHW-018 in 1993 and published a series of academic papers that contained the formula. Years later, that formula was used as a recipe by underground drugmakers, causing Huffman—now a reclusive 80-something who lives in the Smoky Mountains—great consternation. When he first heard that people were using the compounds he created to get high, Huffman told the Post, he thought it was kind of funny. “Then I started hearing about some of the bad results, and I thought, ‘Hmm, I guess someone opened Pandora’s box.’ ”

When did people start manufacturing synthetic marijuana as a recreational drug?

Products based on Huffman’s formula started popping up on a large scale in Europe and the United States in 2008 and 2009, according to the United Nations Office on Drugs and Crime (see p. 23-24).

I’ve heard of Spice and K2. Are those the same thing?

They refer to the same kind of thing, yes, though there’s a huge amount of variation when it comes to what’s actually in this stuff. Other names that have been used to market synthetic cannabinoids—and there are literally hundreds—include Bliss, Cowboy Kush, and Scooby Snax. They are almost universally embarrassing—and therefore, attractive to dumb young people—especially in conjunction with the doofy images of dragons, smiley faces, and cartoon animals that are used on the packaging.

How much does synthetic marijuana cost?

It’s cheap, which is a big part of the draw. You can find it in bulk online, where it costs in the neighborhood of $50 per ounce. In smoke shops and convenience stores, smaller packets are priced as low as $10.

How do synthetic cannabinoids make people feel?

It depends on the chemicals used to make them, plus how large a quantity of those chemicals gets sprayed on by the manufacturer. (According to a Time story from 2014, the “crude way in which producers spray the chemicals … can create hot spots where the concentration of the chemical is dangerously high.”) Side effects of smoking synthetic cannabinoids—or maybe just effects?—include catatonia, profound anxiety and paranoia, nausea and vomiting, elevated heartbeat and blood pressure, seizures, and hallucinations. They also seem to be addictive and, according to the Centers for Disease Control and Prevention, have been linked to acute kidney failure. Synthetic marijuana has also been linked to multiple deaths, including 15 in the first four months of 2015.

That sounds dangerous. Is the media just trying to scare me?

It’s definitely more dangerous than regular marijuana, which has mellowing properties that synthetic cannabinoids don’t have. While drugs like heroin and methamphetamine cause far more deaths in absolute terms, the number of emergency room visits involving synthetic cannabinoids does seem to be growing. According to the Substance Abuse and Mental Health Services Administration, there were approximately 28,531 emergency room visits involving synthetic cannabinoids in 2011, two and a half times more than in 2010. (More recent data are not available.) That’s a drop in the bucket compared with the nearly 2.5 million emergency room visits in 2011 that were linked to all drugs put together, but it’s not nothing. And the user base for SCs seems to be expanding: In 2010, SAMHSA’s data indicated that the number of emergency room visits linked to SC use among people older than 30 didn’t reach a measurable level, but in 2011 it did.

You make this drug sound terrible. What do people like about it?

Different people use it for different reasons, but one of the main sources of its appeal is that it’s hard for authorities to prove that using it or manufacturing it is illegal. The decreased risk of arrest and prosecution makes synthetic marijuana cheaper and more widely available than other drugs. This is because testing for a drug requires knowing exactly what you’re testing for, and the huge variety of chemical compounds used to manufacture synthetic marijuana makes this extremely difficult. The result is that synthetic cannabinoids have attracted an unusual coalition of users. That group includes the homeless, who gravitate to it because it’s cheap and long-lasting, as well as athletes (both college and pro), soldiers, and parolees, who like it because it

allows them to get high without having to worry about failing their mandatory drug tests.

Why is it harder for authorities to deal with synthetic cannabinoids than other drugs?

Because, again, it’s not just one drug! According to Barbara Carreno, a spokeswoman for the Drug Enforcement Administration, there are hundreds of cannabinoid compounds out there, and new ones are constantly being developed by entrepreneurial drugmakers who order the chemicals from China before packaging the drug here in the U.S. (Vice’s drug correspondent Hamilton Morris traveled to China and met some of the chemists responsible for filling the orders.) So even though state and federal governments have placed some varieties of SCs on their controlled substance schedules, manufacturers and distributors can avoid straightforward prosecution by tweaking their formulas and switching to varieties that are not, in the strictest sense, illegal. It’s a “whack-a-mole” problem—ban one form of the drug and another two will pop up instantly. Or, as SAMHSA researcher Donna Bush put it to me, “It’s a cat chasing a monster mouse.”

So is the drug-enforcement cat just totally powerless against this synthetic-marijuana mouse?

Not exactly. The single best weapon that law enforcement has for dealing with the whack-a-mole problem is the Federal Analogue Act, a section of the United States Controlled Substances Act that was passed in 1986. The Analogue Act gives prosecutors the power to pursue drugmakers and distributors who traffic in substances that are “substantially similar” in their chemical makeup and their pharmacological effect to Schedule I and II drugs.

So that makes not-quite-illegal substances de facto illegal by virtue of their similarity to substances that are illegal?

Yes, except there are a few catches. First, proving that two substances are “substantially similar” is hard, because the definition of “substantially similar” is on some level subjective. That makes the process expensive, because prosecutors have to enlist expert chemists to conduct tests and testify in court against experts hired by the defense. Prosecutors must also prove that their defendants knew that what they were selling was substantially similar to an illegal drug.

Is that why baggies containing synthetic cannabinoids are often marketed as “herbal incenses” or “potpourri,” or say that they’re “not intended for human consumption”?

Yes, although it’s not clear that helps get anyone off the hook. In fact, according to Carla Freedman, an assistant U.S. attorney who has prosecuted multiple synthetic cannabinoid cases, that kind of deceptive labelling can be seen as “evidence of a guilty mind,” as it was defined in a recent Supreme Court decision. “Usually you don’t have an issue showing that they didn’t really intend for the product to be used as incense or potpourri,” Freedman told me. “So then you have to ask, ‘If you knew it was going to be smoked and ingested, and you thought it was lawful, then why are you calling it something else?’ … If I’m selling Red Bull, I don’t call it window cleaner, I call it an energy drink. I don’t mislabel it.”

I’ve heard some people argue that legalizing marijuana—or just being more tolerant of it in contexts like sports—would result in fewer people using synthetic weed. Is that true?

No one really knows. It’s definitely true that some users say they use synthetic cannabinoids as a substitute for the real thing. In a big New York Times Magazinepiece from last summer, an addict was quoted saying it was a “miracle drug” because it didn’t show up on drug screens, but that nobody he knew would choose

it over real weed. Similarly, NFL stars like Chandler Jones likely wouldn’t turn to it if they didn’t have to worry about drug testing. But there seem to be lots of people who like SCs because they are cheap, powerful, and long-lasting, qualities that actual marijuana might not be able to match.

Source:http://www.slate.com/articles/news_and_politics/crime/2016/02/synthetic_marijuana

Seeking a safe haven in Colorado’s legal marijuana marketplace, illegal drug traffickers are growing weed among the state’s sanctioned pot warehouses and farms, then covertly shipping it elsewhere and pocketing millions of dollars from the sale, according to law enforcement officials and court records consulted by The Associated Press.

In one case, the owner of a skydiving business crammed hundreds of pounds of Colorado pot into his planes and flew the weed to Minnesota, where associates allegedly sold it for millions of dollars in cash. In another, a Denver man was charged with sending more than 100 pot-filled FedEx packages to Buffalo, New York, where drug dealers divvied up the shipment. Twenty other drug traffickers, many from Cuba, were accused of relocating to Colorado to grow marijuana that they sent to Florida, where it can fetch more than double the price in a legal Colorado shop.

These cases and others confirm a longstanding fear of marijuana opponents that the state’s much-watched experiment in legal pot would invite more illegal trafficking to other states where the drug is still strictly forbidden.

One source is Colorado residents or tourists who buy retail pot and take it out of state. But more concerning to authorities are larger-scale traffickers who move here specifically to grow the drug and ship to more lucrative markets.

The trend also bolsters the argument of neighboring Nebraska and Oklahoma, which filed a lawsuit in late 2014 seeking to declare Colorado’s pot legalization unconstitutional, arguing that the move sent a tide of illicit weed across their borders. The Obama administration last month urged the Supreme Court to reject the suit, saying that the leakage was not Colorado’s fault.

No one knows exactly how much pot leaves Colorado. When illegal shipments are seized, it’s often impossible to prove where the marijuana was grown. But court documents and interviews with law enforcement officials indicate well-organized traffickers are seeking refuge in Colorado’s flourishing pot industry.

“There’s no question there’s a lot more of this activity than there was two years ago,” said Colorado’s U.S. attorney, John Walsh.

Some in the legal industry say police have exaggerated the problem and put unfair scrutiny on people who legally grow pot on behalf of patients. Lawmakers last year limited unregulated pot growers to no more than 99 plants in an effort to crack down on those selling untaxed pot.

The federal government allowed Colorado’s experiment on the condition that state officials act to keep marijuana from migrating to places where it is still outlawed and out of the hands of criminal cartels. Federal authorities acknowledge that both things are happening but say that, because the state is trying to keep its industry tightly regulated, there’s no reason to end the legal pot trade.

(MY NOTE: This is an insane position to take. The feds are allowing large-scale manufacturing and distribution to take place in Colorado and elsewhere. All of it is in violation of numerous federal laws that bring mandatory minimum sentences to traffickers. This administration’s absolute failure to enforce federal law is catamount to aiding and abetting drug traffickers on a scale seldom seen in the drug trafficking world prior to legalization. DOJ’s initial claim was that federal resources would not be used to prosecute “patients”

who are in compliance with state “medi-pot” laws. In order words, it was supposed to be about leaving users alone. Nothing about the current situation is about “patients.” It is about commercialization and trafficking, with legalized states producing high-grade pot for the rest of the country.

The feds could immediately stop 90% of this nonsense for the cost of postage stamps — sending letters written on DOJ letterhead that provide notice of impending forfeiture of all property used in furtherance of large-scale trafficking and money laundering. This would include all drug proceeds (and arguably would include the seizure of drug proceeds disguised as “tax revenue.” I spent more than 20 years doing these cases in federal court, so I know what I am talking about. Back to the article.  Monte Stiles)

The pot industry also acknowledges the criminal activity and insists it is doing all it can to keep legally grown weed from crossing state lines. Among other safeguards, Colorado law requires growers to get a license and use a “seed-to-sale” tracking system that monitors marijuana plants at every stage.

Many of the illicit growers come from elsewhere, never obtain a growing license and “don’t even attempt to adhere to the law,” said Barbra M. Roach, special agent in charge of the Drug Enforcement Administration’s Denver field division.

“It’s like hiding in plain sight,” she said.  (EXACTLY WHAT WE HAVE BEEN SAYING ALL ALONG)

Authorities in Washington state, which also allows recreational marijuana, have noticed more marijuana leaving the state. But more reports are coming from Colorado, which has the nation’s most robust commercial market and an international reputation for producing premium, high-potency pot.

“It’s a brand name now,” Roach said.

Jason Warf, head of the Southern Colorado Cannabis Council, said people are “coming from out-of-state, buying products from licensed stores and being arrested on their way home.”

That “is really hard to curb,” he said. “We can’t essentially babysit adults and their behavior.”

The Colorado Department of Revenue’s marijuana-enforcement division cites shops if pot is unaccounted for but “after it’s sold, we have very little control what happens to the marijuana,” Director Lewis Koski said.

Police agencies seized nearly 2 tons of Colorado weed from drivers who had intended to take it to 36 other states in 2014, the year legal pot shops opened, according to the Rocky Mountain High Intensity Drug Trafficking Area, a federally funded drug task force. By comparison, they seized less than a ton in 2009.

U.S. postal inspectors seized about 470 pounds of Colorado pot from the mail in 2014, up from 57 pounds in 2010, according to the task force, whose findings are based on on voluntary submissions from law enforcement agencies and are largely anecdotal.

Some cases have comic overtones, like when a Wyoming patrolman discovered 7 ounces of high-grade weed in trick-or-treat bags the day after Halloween, or when police in northern Colorado seized stuffed animals full of marijuana destined for Florida.

Other operations are more sophisticated, like the one in which authorities say 32 people used skydiving planes and posed as licensed medical marijuana caregivers and small business owners to export tens of thousands of pounds of pot grown in Denver warehouses, usually to Minnesota. The organization made more than $12 million over four years, according to a state indictment.

When they busted illegal pot farms in southern Colorado in September, state and federal agents found 28 guns, more than 1,000 plants and $25,000 in cash.

A local UPS facility intercepts about 50 pounds of pot headed out of state each week, said Todd Reeves of the Colorado Drug Investigators Association. “We don’t have the resources,” he said, “to be able to go after every single one of these cases.”

Source:   SADIE GURMAN, ASSOCIATED PRESS DENVER — Jan 28, 2016, 2:11 AM ET  http://abcnews.go.com/US/wireStory/drug-traffickers-seek-safe-haven-amid-legal-marijuana-36564435

The overdose antidote is being offered for use in High Schools and is a sad indictment of the situation in the USA where lax drug policies have resulted in huge increases in drugs use – including heroin even amongst youth.

The opioid overdose antidote naloxone is being offered free to high schools around the country by the drugmaker Adapt Pharma, according to U.S. News & World Report.

Naloxone, sold under the brand name Narcan, quickly reverses overdoses from heroin and prescription painkillers. Naloxone will be offered in nasal spray form to high schools through state departments of education. The Clinton Foundation’s Health Matters Initiative is collaborating on the project.

Many states do not have rules that would permit high school staff to administer naloxone in an emergency without facing liability from parents or guardians, the article notes. There are significant variations in state and local rules about whether staff is allowed to administer medication to students. In some school districts, medication can only be administered by school nurses, who often work at more than one school.

The National Association of School Nurses (NASN) in June said that “incorporating use of naloxone into school emergency preparedness and response plans is a school nurse role.” In a statement, the group said “the safe and effective management of opioid pain reliever-related overdose in schools [should] be incorporated into the school emergency preparedness and response plan.” Last year, New York joined at least four other states in allowing public school nurses to add naloxone to their inventory. Other states with similar policies include Vermont, Massachusetts and Delaware.

Adapt Pharma is also providing a grant to NASN to support their education efforts concerning opioid overdose education materials. In a news release from the company, NASN President Beth Mattey said school nurses act as first responders in schools. “We educate our students, families, and school staff about prescription drug and substance abuse, and help families seek appropriate treatment and recovery options,” she said. “Having access to naloxone can save lives and is often the first step toward recovery. We are taking a proactive approach to address the possibility of a drug overdose in school.”

Source:  http://www.drugfree.org/join-together  26th Jan. 2016

After the Police Chief of Gloucester, Massachusetts announced the town will connect people with treatment when they come to the police station with illegal drugs and paraphernalia, instead of arresting them, 56 police departments in 17 states have started similar programs.

An additional 110 police departments are preparing to start programs that emphasize treatment over incarceration, The New York Timesreports. Two hundred treatment centers nationwide have agreed to be partners in these programs. In May 2015, Gloucester Police Chief Leonard Campanello posted on Facebook, “We will walk them through the system toward detox and recovery. We will assign them an ‘angel’ who will be their guide through the process. Not in hours or days, but on the spot.” Since then, Gloucester has developed a national network of centers that are willing to provide treatment beds and take referrals by police, whether or not a person has insurance.

Several local pharmacies have agreed to make the opioid overdose antidote naloxone available at a discount.

Most of the program’s costs are covered by the Police Assisted Addiction and Recovery Initiative, which Chief Campanello founded with Gloucester businessman John E. Rosenthal. The initiative has raised hundreds of thousands of dollars. It has also received millions of dollars in in-kind contributions, including placement in treatment centers.

The program has 55 volunteers in recovery or who are familiar with addiction, who listen and offer moral support. Local taxi companies provide free rides to treatment facilities or the airport, if the treatment facility is far away.

Since the program started, 391 people have turned themselves in at Gloucester’s police station. About 40 percent are from the local area. All have been placed in treatment, the article notes.

Source:  http://www.drugfree.org/join-together   26th Jan. 2016

Project Description/Goals

Marijuana legalization in Colorado has posed significant challenges for law enforcement resulting, stemming from the unanticipated consequences it has had on crime and public safety. Colorado law enforcement formed diverse partnerships to address the difficulties caused by conflicting state legislation and local ordinances, policies, and procedures. The situation was even more complex because marijuana remains a Schedule I controlled substance under federal law. The Police Foundation partnered with the Colorado Association of Chiefs of Police to produce a guidebook illustrating the challenges in policing legalized marijuana and the law enforcement practices that have been most successful in Colorado.

Study Design & Methods

Very little data was collected on how Colorado law enforcement was dealing with legalized marijuana before the beginning of 2015. Additionally, law enforcement agencies in the state have not conducted rigorous, evidence-based research to draw conclusions regarding the impact of legalized marijuana. This guide is based on interviews with 23 subject matter experts representing state and local government, state attorney’s office, city and local attorneys, and national police associations. Two focus groups were held with law enforcement executives, detectives, and officers selected based on their experience and knowledge of marijuana legalization and location in the state to get a diverse representation. Interviews were recorded whenever possible with the permission of the interviewee and then transcribed.

 Results

The legalization of marijuana produced many unintended consequences, which led to a number of challenges and issues. Some of which have been addressed through ordinances,

policies, and procedures, while other issues are more complicated and have not found total resolution. The findings that make up the guidebook show:

* Data to determine the impact of legalized marijuana on crime and safety is limited and is a significant problem.

* Banking systems are unavailable to the marijuana industry because of federal laws, creating a dangerous level of cash that can lead to robberies.

* Difficulties in establishing what is a legal marijuana operation have created problems in conducting investigations, determining probable cause and search and seizure procedures.

* Marijuana illegal trading through the black and gray markets has not decreased, law enforcement agencies have found. Diversion across state boundaries has created issues for bordering states who do not have legalized marijuana laws.

* Public health and safety impacts concerns have occurred through the increased THC potency from marijuana hash oil extractions, which are used in making laced edibles and beverages. People have overdosed on the higher levels of THC leading to potential psychotic breaks and suicide attempts.

* Youth use and addiction rates have increased due to ease of accessibility.

* Detecting driving under the influence of marijuana is a significant challenge for law enforcement.

Funding and Collaboration

The Police Foundation funded this research and guide and partnered with the Colorado Association of Chiefs of Police in its production.

Implications for Policy & Practice

The findings from this exploratory research suggest that, in states where marijuana may become legalized, law enforcement should establish data collection systems, licensing and registration protocol. Guidelines should be established in advance for search and seizures in illegal home growing operations. Impacts to minors using illegal marijuana have significant health and potential crime problems for the community. The lessons, challenges, and successful measures applied by law enforcement and their partnerships need rigorous research in those states that have legalized marijuana. The dichotomy of state and federal laws compromise officers’ actions.

Source:  http://www.policefoundation.org/projects/colorados-legalization-of-marijuana-and-the-impact-on-public-policy

 

Consumption of illegal drugs begins at the age of 10

The National Council Against Addictions (Conadic) has estimated that over 2.38 million Mexican youths are in need of some kind of rehabilitation treatment for abuse of substances, mainly marijuana and alcohol.

This is but one of the staggering figures presented in the 2014 National Survey on Drug Use Among Students, conducted in public and private schools in the 32 states, which also indicated that children are beginning to consume illegal drugs at 10 years old, two years younger than had been thought.

The survey also established that addiction among youths in secondary and preparatory schools – nearly 80,000 young men and 50,000 young women – requires immediate intervention.

A broader number of the same spectrum of students, about 311,000 men and 260,000 women, were found to need brief support interventions, which could consist of counselling sessions or a short rehabilitation internment period.

The course of action to take in the case of younger, elementary school students is still being assessed.

Conadic chief Manuel Mondragón wants to know the how and where of treatment: “713,963 secondary and preparatory school students need to be treated for use of drugs, and 1.674 million for abuse of alcohol. The question is, where are we going to treat them, and who will provide the treatment? What are our infrastructural capabilities?”

Mondragón said nearly 1.8 million children and teenagers – from elementary to preparatory – have tried illegal drugs, 152,000 of which are fifth and sixth-grade students, and whose first experience was with marijuana, followed by inhalants and cocaine.  Of that 1.8 million, over 108,000 have used marijuana between one and five times.

The abuse of alcohol is no less worrisome: 1.5 million secondary and preparatory school students have abused it, consuming over five drinks at a time and becoming drunk. Over 110,000 elementary school students have done the same.

The states with the most substance abuse among children are Chihuahua, Jalisco, State of México, the Federal District and San Luis Potosí.

Nine out of every 10 children in Michoacán, Campeche and Quintana Roo are experimenting with and abusing harder substances like cocaine.

Mondragón stated that immediate measures to deal with the issue could consist of shutting down all establishments that sell alcohol to minors, as well as signing agreements in every state to strengthen the use of breathalyzers and control the sale of legal and illegal drugs.  Mondragón also said the federal government is open to raising the limit of recreational drugs an individual can carry, currently set at five grams. This would permit the reinsertion into society of non-violent, first-offender youths who are currently in jail for possession of illegal substances.

Meanwhile, in Congress, the first round of discussions around the use of marijuana and its derivatives is taking place with the participation of representatives from the United Nations and parents’ associations.  The discussion is focusing on the legalization of medicinal cannabinoid-based products.

Source: http://mexiconewsdaily.com/news/study-finds-2-million-students-need-rehab/#sthash.yh7m6JYS.dpuf   26th Jan. 2016

Nora D. Volkowa,b,1, Gene-Jack Wanga, Frank Telanga, Joanna S. Fowlerc,1, David Alexoffc, Jean Logand, Millard Jaynea, Christopher Wonga, and Dardo Tomasia

Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857; National Institute on Drug Abuse, Rockville, MD  20857; Biosciences Department, Brookhaven National Laboratory, Upton, NY 11973; and Department of Radiology, New York University Langone Medical Center, New York, NY 10016

Contributed by Joanna S. Fowler, June 20, 2014 (sent for review April 9, 2014; reviewed by Bertha Madras, Harvard University Medical School, and Karen Berman, National Institute of Mental Health)

Moves to legalize marijuana highlight the urgency to investigate effects of chronic marijuana in the human brain. Here, we challenged  48 participants (24 controls and 24 marijuana abusers) with methylphenidate (MP), a drug that elevates extracellular dopamine (DA) as a surrogate for probing the reactivity of the brain to DA stimulation. We compared the subjective, cardiovascular, and brain  DA responses (measured with PET and [11Craclopride) to MP between controls and marijuana abusers.

Although baseline (placebo) measures of striatal DA D2 receptor availability did not differ between groups, the marijuana abusers showed markedly blunted responses when challenged with MP. Specifically, compared with controls, marijuana abusers had significantly attenuated behavioural (“self-reports” for high, drug effects, anxiety, and restlessness), cardiovascular (pulse rate and diastolic blood pressure), and brain DA [reduced decreases in distribution volumes (DVs) of [11Craclopride, although normal reductions in striatal nondis placeable binding potential  (BPND)] responses to MP. In ventral striatum (key brain reward region),M P-induced reductions in DVs and BPND (reflecting DA increases) were inversely correlated with scores of negative emotionality, which were significantly higher for marijuana abusers than controls. In marijuana abusers, DA responses in ventral striatum were also inversely correlated with addiction severity and craving.

The attenuated responses to MP, including reduced decreases in striatal DVs, are consistent with decreased brain reactivity to the DA stimulation in marijuana abusers that might contribute to their negative emotionality (increased stress reactivity and irritability) and addictive behaviors.

Despite the high prevalence of marijuana consumption, the effects of marijuana abuse in the human brain are not well understood. Marijuana, like other drugs of abuse, stimulates brain dopamine (DA) signalling in the nucleus accumbens (1, 2), which is a mechanism believed to underlie the rewarding effects of drugs (3–5) and to trigger the neuroadaptations that result in addiction (reviewed in ref. 6). Indeed, in humans, imaging studies have shown that drugs of abuse increase DA release in striatum (including the nucleus accumbens), and these increases have been associated with the subjective experience of reward (7–9).

However, for marijuana, the results have been inconsistent: One study reported striatal DA increases during intoxication (10); two studies showed no effects (11, 12); and one study reported DA increases in individuals with a psychotic disorder and in their relatives, but not in controls (13). Imaging studies of the brain DA system in marijuana abusers have also shown different findings from those reported for other types of substance abusers. Specifically, substance abusers (cocaine, methamphetamine, alcohol, heroin, and nicotine), but not marijuana abusers (14–16), show reduced baseline availability of DA D2 receptors in striatum (reviewed ref. 6). Similarly, cocaine abusers (17, 18) and alcoholics (19, 20),but not marijuana abusers (16), show attenuated DA increases instriatum when challenged with a stimulant drug, although marijuana abusers with comorbid schizophrenia or risk for schizophrenia showed blunted DA increases to stimulants (21) and to stress (22). However, prior studies are limited by their small sample sizes (ranging from six to 16 subjects). Also, prior studies did not control for the potential confounds that the changes in cerebral vascular resistance associated with marijuana abuse (23– 25) could have on the delivery of the radiotracer to the brain when using a stimulant drug as pharmacological challenge, because stimulants decrease cerebral blood flow (26). Thus, the extent to which there are changes in brain DA signalling in marijuana abusers is still unclear. Here, we compared brain DA reactivity in healthy controls and marijuana abusers on a larger sample than that in prior studies and measured arterial concentration of non metabolized radiotracer to control for differences in radiotracer delivery to brain. We used PET and [11Craclopride (radioligand that binds to D2/D3 receptors not occupied by DA) to assess the effects of methylphenidate (MP) on the nondisplaceable binding potential [BPND; ratio of the distribution volume (DV) in striatum to that in cerebellum], which is the most frequent model parameter used to estimate DA changes (27), in 24 healthy controls and 24 marijuana abusers.We also quantified the DV,  which corresponds to the equilibrium measurement of the ratio of the concentration of the radiotracer in tissue to that in  arterial plasma, to control for potential changes in radiotracer delivery that could confound group comparisons of stimulant-induced changes in BPND. We used MP, which is a stimulant drug that blocks DA transporters, because it induces robust and reproducible DA increases in the human brain (28, 29). We predicted that MP’s behavioral effects in marijuana abusers would be attenuated, consistent with preclinical findings (30), and that decreased DA reactivity in ventral striatum would be associated with higher scores in negative emotionality (neuroticism), which mediates genetic risk for marijuana dependence (31), and with addiction severity.

Results

Participant Characteristics.

Tobacco smoking was more prevalent in marijuana abusers than controls; otherwise, there were no differences in demographics between groups (Table 1). However, the groups differed significantly in personality measures; marijuana abusers had significantly lower scores in positive emotionality (P = 0.05) and higher scores in negative emotionality (P = 0.002) than controls (Table 1).

Correlation analysis between scores in negative emotionality and history of marijuana abuse showed a negative correlation between age of I  the scores. The correlations with reported daily doses of marijuana and negative emotionality were not correlations with positive emotionality and history of marijuana abuse were not significant.

Plasma Concentrations of MP and Behavioral and Cardiovascular Effects. 

MP concentrations in plasma (nanograms per milliliter) did not differ between groups at 10 min (controls, 195 ± 51; abusers, 194 ± 45), 25 min (controls, 125 ± 24; abusers, 121 ± 19), or 40 min (controls, 102 ± 25; abusers, 94 ± 15). MP had significant behavioral effects, and these effects were attenuated in marijuana abusers compared with controls (Fig. 1A). Specifically, MP significantly increased scores on self-reports (averaged measures), and the effects differed between groups, with controls reporting a more robust “high” (drug effect: F = 92, P = 0.0001; interaction: F = 6.2, P = 0.02), “restlessness” (F = 35, P = 0.0001; interaction: F = 5.8, P = 0.02), “anxiety” (F = 7, P = 0.01; interaction: F = 5.8, P = 0.02), and “drug effects” (F = 100, P = 0.0001; interaction F = 4, P = 0.05) than marijuana abusers.

Also, comparisons of “peak” behavioral effects to MP were significantly stronger for controls for high (P = 0.01), restlessness (P = 0.003), anxiety (P=0.03),and drug effects

(P=0.02), than for the marijuana abusers. The potency of MP was also reported to be stronger by the controls than by the marijuana abusers (8.3 ± 2 vs. 5.8 ± 3; t = 3.4, P = 0.002). In marijuana abusers, MP increased self-reports of marijuana craving (Placebo: 4.0 ± 3–MP: 6.3 ± 3; P = 0.006) and tobacco craving (Placebo: 2.4 ± 2–MP: 3.8 ± 4; P = 0.05).

PLUS

MP increased heart rate

(F = 98, P = 0.0001) and systolic (F = 153, P = 0.0001) and diastolic (F = 65, P = 0.0001) blood pressure in both groups, and MP’s effects differed between groups for heart rate (interaction effect; F = 4.6, P = 0.04) and diastolic blood pressure (interaction effect: F = 4.0, P = 0.05), but not for systolic blood pressure (Fig. 1B). Post hoc t tests revealed that MP-induced increases in heart rate and diastolic pressure were significantly stronger (P < 0.05) in controls than in marijuana abusers.

Effects of MP on the DVs of [11Craclopride.

The SPM analysis showed no group differences in baseline measures of DV. It also showed that MP significantly decreased DV in brain and that the effects were significantly larger in controls than in marijuana abusers (Fig. 2). Individual plotting of MP-induced changes in DV showed that MP-induced changes in cerebellum were decreased in controls but not in marijuana abusers and that there were larger decreases of MP-induced changes in striatum in controls than in marijuana abusers (Fig. 2). The ROI analysis corroborated that MP decreased the DV in cerebellum and striatum and that the effects were larger for controls than abusers.

For cerebellum, the drug (F = 15, P = 0.0004) and drug × group interaction (F = 8.2, P = 0.007) were significant; post hoc t tests showed larger decreases in controls (13 ± 11%) than abusers (1.4 ± 16%) (P = 0.01). For caudate, the drug (F = 41, P = 0.0001) and interaction (F = 4.8, P = 0.04) were significant; post hoc t tests revealed larger decreases in controls (22 ± 18%) than abusers (9 ± 22%) (P = 0.05).

For putamen, drug (F = 93, P = 0.0001) and interaction (F = 6.9, P = 0.02) were significant; post hoc t tests showed larger decreases in controls (30 ± 16) than abusers (16 ± 21%) (P = 0.02). For ventral striatum, drug (F = 56, P = 0.0001) and interaction (F = 7.3, P = 0.01) were significant; post hoc t tests showed greater decreases in controls (25 ± 18%) than abusers (11 ± 25%) (P = 0.02). A group (controls vs. abusers) by region (delta DV in caudate, putamen, ventral striatum, and cerebellum) comparison revealed that group differences differed between regions (F = 3.5, P = 0.02); post hoc analysis showed that group differences in cerebellum were larger than in putamen (P = 0.02) and ventral striatum (P = 0.02), and showed a trend in caudate (P = 0.07).

This finding is significant; it confounds group comparisons of BPND because the latter measure is normalized to the DV in cerebellum. Note that attenuated decreases in cerebellar DV with MP in the marijuana abusers could result in an overestimation of their DA increases, reflecting an apparent lower striatal-DV/cerebellar-DV ratio (BPND) with MP (see below).

Correlations Between MP-Induced Changes in DV and Clinical Measures.

Correlation analysis revealed that MP-induced decreases in DV in ventral striatum were negatively associated with scores in negative emotionality (r = 0.51, P = 0004), and weaker correlations were observed in putamen (r = 0.37, P = 0.02) and caudate

(r = 0.35, P = 0.02) such that the larger the DV decreases, the lower were the scores of negative emotionality. Correlation with positive emotionality and constraint were not significant. MP-induced craving for marijuana in the marijuana abusers was negatively associated with DV decreases in putamen (r = 0.46, P = 0.03) and ventral striatum (r = 0.51, P = 0.01) such that participants with the smallest decreases had the most intense craving.

Baseline Measures of D2/D3 Receptor Availability (BPND).

For the baseline (placebo) measures, the SPM analysis revealed no group differences in BPND (D2/D3 receptor availability). When we decreased the threshold of significance to uncorrected P < 0.05, SPM showed lower values in marijuana abusers than in controls in ventral striatum (0, −2, −8; statistical t values = 2.59, P uncorrected = 0.007). The ROI analysis also showed a nonsignificant trend toward lower baseline BPND in marijuana abusers than in controls in ventral striatum (controls, 3.20 ± 0.3; abusers, 2.97 ± 0.59; P = 0.11) and no differences in caudate (controls, 2.80 ± 0.36; abusers 2.76 ± 0.57) or putamen (controls, 3.42 ± 0.41; abusers, 3.35 ± 0.57).

Effects of MP on BPND. 

The SPM analysis revealed significant decreases in BPND with MP compared with placebo (interpreted as reflecting DA increases) in striatum in both controls and marijuana abusers (Fig. 3 and Table 2). The SPM analysis revealed no group differences in MP-induced decreases in BPND in striatum but unexpectedly revealed larger BPND decreases in marijuana abusers than in controls in midbrain (region centered in susbtantia nigra that also encompassed sub thalamic nucleus; center of cluster left: 12, −14, −10, and 132 voxels, t = 3.1; center of cluster right: 14, −18, −8, and 27 voxels; t = 2.9; PFWE < 0.05; SVC = 10 voxels) (Fig. 3 and Table 2). The ROI analysis corroborated a significant group × drug interaction in midbrain (F = 14, P = 0.0006), and post hoc t test analyses showed that whereas in marijuana abusers, MP decreased BPND in midbrain (−3.5 ± 8%; F = 5.4, P = 0.03), MP increased BPND in controls (4 ± 6%; F = 9.2, P = 0.006).

Correlations Between MP-Induced Changes on BPND and Clinical Measures.

Voxel-wise correlation analysis revealed that MP-induced decreases in BPND in ventral striatum were inversely associated with scores in negative emotionality (Fig. 3 B and C) such that the larger the BPND decreases, the lower the scores. The striatal correlations with positive emotionality and constraint were not significant. Because the SPM revealed a significant group difference in MP-induced changes in midbrain BPND, we also performed correlations with this brain region and showed a significant correlation with positive emotionality (r = 0.42, P = 0.003) such that the greater the BPND decreases, the lower the scores. In the marijuana abusers, MP-induced decreases in BPND in midbrain were correlated with increases in marijuana (r = 0.40, P = 0.05) and tobacco (r = 0.45, P = 0.03) craving, as well as with the dependency scores (r = 0.43, P = 0.04), such that the greater the decreases in BPND, the higher was the craving triggered by MP and the higher were the dependency scores.

Discussion

Here, we show that marijuana abusers had attenuated behavioural and cardiovascular responses and blunted reductions in striatal DV (although normal reductions in BPND) when challenged with MP compared with controls, which is consistent with decreased brain reactivity to DA stimulation. We also corroborate prior findings (14–16) of no significant differences in baseline striatal D2/D3 receptor availability between controls and marijuana abusers and provide preliminary evidence of abnormal midbrain

DA reactivity in marijuana abusers. DA D2/D3 Receptor Availability in Striatum.

Only four brain imaging studies (totalling 42 marijuana abusers) have measured DA D2/ D3 receptors (14–16, 42). These studies showed no differences in striatal D2/D3 receptors between marijuana abusers and controls, but their generalizability is limited by the small sample sizes (samples ranged from n = 6 to n = 16). Thus, our results showing no differences in D2/D3 receptor availability (except for a trend in ventral striatum), using a larger sample (24 marijuana abusers) than that used for studies that identified reductions in striatal D2/D3 receptors in alcoholics and cocaine abusers, indicate that marijuana abusers, different from other drug abusers, do not show significant striatal D2/D3 receptor reductions. This difference could reflect marijuana’s agonist properties at cannabinoid 1 (CB1) receptors, which heteromerize with D2 receptors, antagonizing their effects (43). Both CB1 and D2 receptors couple to Gi-o proteins and inhibit adenylyl-cyclase, whereas their co-stimulation results in Gs protein-dependent activation of adenylylcyclase (44, 45).

Moreover, CB1 receptor agonists and antagonists counteract and potentiate, respectively, D2 receptor agonist effects (46–49), although D2 and CB1 receptor interactions might differ between rodents and primates (50, 51). It is therefore possible that in marijuana abusers, chronic CB1 receptor stimulation prevented the striatal D2/D3 receptor down-regulation observed < 0.005) and group comparisons for the effects of MP (ΔBPND) (P < 0.01, cluster size of 10 voxels). The contrast MA > HC indicates that MP induced with repeated drug use (reviewed in ref. 6). However, it should be noted that the marijuana abusers studied in the present and prior studies have been at least 10 y younger than the cocaine abusers and alcoholics studied by prior PET studies, which is relevant because striatal D2/D3 receptors decrease with age (52), and it is hypothesized that drugs accelerate the effects of brain aging (53). Thus, studies in older marijuana abusers are needed to clarify this.

MP-Induced Changes in DV.

In controls but not in marijuana abusers, MP reduced cerebellar DV. To ensure that the DV responses in the controls were consistent with prior findings, we performed a secondary analysis on the effects of MP on the cerebellar DV in an independent cohort of controls, which showed a 12% reduction, and in a sample of adults with attention deficit hyperactivity disorder (ADHD), which also showed an 11% reduction (for controls of the current cohort, the cerebellar DV decrease was 13 ± 11%). The mechanism underlying the lack of an effect of MP in cerebellar DV in abusers is unclear but could reflect the effects of chronic marijuana on cerebrovascular reactivity (increased cerebral vascular resistance) (23–25), which might have prevented MP-induced vasoconstriction and associated reductions in radiotracer delivery to the brain.

The attenuated decreases in DV with MP in the marijuana abusers were observed throughout the brain but were most accentuated in cerebellum. The higher sensitivity of the cerebellum to what we interpret to reflect changes in vascular reactivity with marijuana abuse is consistent with clinical findings that report strokes associated with marijuana abuse are more frequently localized in the posterior circulation and ischemia is most frequently observed in cerebellum (25, 54–56). Cerebellar arteries express CB1 receptors in the smooth muscle layer (57), but because comparisons with arteries in other brain regions have not been done, it is not possible to determine if higher levels of CB1 receptors in cerebellar arteries underlie their higher sensitivity to vascular effects from marijuana.

However, CB1 receptors in cerebellum are also expressed in neurons and glia (58), and the cerebellum is a region that is affected in marijuana abusers (59–61); thus, we cannot rule out the possibility that other factors contribute to the lack of an effect of MP on the cerebellar DV in the marijuana abusers. MP also decreased the DV in striatum to a greater extent in controls than in abusers (Fig. 2). In ventral striatum, these decreases were associated with negative emotionality and with marijuana craving such that the lower the response, the higher the negative emotionality and the craving. This would suggest that these attenuated responses might reflect reduced striatal DA reactivity in marijuana abusers compared with controls even though there were no group differences in MP-induced decreases in BPND (see below). This is consistent with findings from an imaging study with [18F]-dopa that reported lower than normal DA synthesis capacity in the striatum of marijuana abusers (62).

MP-Induced Changes in BPND.

We showed no group differences in MP-induced changes in BPND in striatum, which is the standard measure for assessing DA changes. Similarly, a prior study reported no differences in amphetamine-induced decreases in BPND between marijuana abusers and controls (16). However, the significant group differences in MP’s effects on the DV in cerebellum confound the findings because BPND uses the cerebellum as a reference region to normalize for nonspecific binding. Because the DV in cerebellum was not decreased by MP in marijuana abusers but was decreased in controls, this would result in an overestimation of the decrease in BPND with MP (cerebellar denominator would have a relatively larger value) and an overestimation of DA increases in marijuana abusers compared with controls.

Interestingly, an imaging study comparing DA increases using BPND and 4-propyl-9-hydroxynaphthoxazine ([11C]PHNO)

(radiotracer with >20-fold higher affinity for D3 over D2 receptors, and presumably more sensitive to competition with endogenous DA) (63, 64) in response to a stressor in individuals at high risk for schizophrenia showed that those who abused marijuana had a blunted response, consistent with decreased DA signalling (22). Because the study used cognitive stress as a challenge, it was not confounded by potential group differences in stimulant-induced changes in cerebellar radiotracer delivery.  Unexpectedly, SPM revealed that MP decreased BPND in midbrain (centered in substantia nigra) in marijuana abusers but not in controls. Although the mechanism(s) underlying this group difference is unclear, we speculate that because the midbrain has a high concentration of D3 receptors (65), which are more sensitive to endogenous DA than D2 receptors (66), it could reflect up-regulation of D3 receptors in marijuana abusers.

Indeed, in rodents, chronic Δ (9)-tetrahydrocannabinol (THC; the main psychoactive ingredient of marijuana) increased D3 receptors in midbrain (30). In the marijuana abusers, an MP-induced decrease in midbrain BPND correlated with craving and with dependency scores. A similar finding was reported in methamphetamine abusers, in whom up-regulation of D3 receptors in midbrain (assessed with [11C]PHNO) correlated with amphetamine-induced craving (30, 67). This, along with preclinical studies showing that D3 receptor antagonists interfere with drug seeking and cue- and receptor signalling in midbrain might contribute to drug craving and to decreased sensitivity to reward in marijuana abusers (see below).

However, because the midbrain finding was unexpected, we report it as a preliminary finding in need of replication.

Blunted Behavioral and Cardiovascular Responses to MP in Marijuana Abusers.

Behavioral and cardiovascular effects of MP have been associated with MP-induced DA increases in striatum (9, 69), so the blunted responses in the marijuana abusers are also consistent with decreased striatal reactivity to DA signaling. Although, to our  knowledge, this is the first clinical report of an attenuation of the effects of MP in marijuana abusers, a preclinical study had reported that rats treated chronically with THC exhibited attenuated locomotor responses to amphetamine (2.5 mg/kg

administered i.p.) (30). Such blunted responses to MP could reflect neuroadaptations from repeated marijuana abuse, such as downregulation of DA transporters (70). The attenuation of MP’s effects could also reflect abnormal D2 receptor function, as was previously suggested to explain findings in marijuana-abusing schizophrenic patients, who, despite displaying low DA release, showed increases in psychotic symptoms when challenged with amphetamine (21). Finally, it is also possible that the attenuated responses reflect blunting of MP’s noradrenergic effects because MP blocks both DA and norepinephrine transporters. Our findings of blunted responses to MP in marijuana abusers have clinical implications because they suggest that individuals with ADHD who abuse marijuana might be less responsive to the therapeutic benefits derived from stimulant medications.

Reduced Positive Emotionality and Increased Negative Emotionality in Marijuana Abusers.

Marijuana abusers showed lower scores on positive emotionality and higher scores on negative emotionality than controls, consistent, on the one hand, with lower reward sensitivity and motivation and, on the other hand, with increased stress reactivity and irritability. These characteristics overlap with the amotivational syndrome (71) and with the enhanced sensitivity to stress associated with marijuana abuse and other addictions (72, 73). Positive emotionality was inversely associated with MP induced increases in midbrain DA, which could reflect the fact that in midbrain, D2 and D3 are autoreceptors; therefore, their stimulation would result in decreased DA release in striatum (including accumbens) (74), leading to decreased sensitivity to reward and amotivation (75). In contrast, MP-induced DA increases in ventral striatum were negatively associated with scores on negative emotionality, which is consistent with the protective role of DA signalling in negative emotions (76). The association between negative emotionality and age of initiation of marijuana abuse is consistent with prior findings of worse outcomes with earlier initiation of marijuana abuse (77).

Study Limitations.

The main limitation of this study was the inadequacy of BPND for comparing the DA increases between controls and marijuana abusers due to the group differences on  the effects of MP on cerebellar DV. Also, [11Craclopride cannot distinguish between D2 and D3 receptors, so studies with D3 receptor ligands are needed to determine if the increased midbrain DA response in marijuana abusers reflects D3 receptor upregulation. The relatively poor spatial resolution of PET limits accuracy in the quantification of small brain regions, such as midbrain. Our study cannot ascertain if group differences reflect chronic use of marijuana rather than premorbid differences, and whether marijuana abusers will recover with detoxification. Although attenuation of the effects of MP could reflect interference from CB1 receptor stimulation by marijuana, this is unlikely because marijuana abusers reported that their last use of marijuana was 1–7 d before the study when cannabinoids in plasma are still detectable but at concentrations unlikely to have pharmacological effects (78). However, future studies done after longer periods of withdrawal are needed to control for potential confounds from THC and its metabolites in plasma and to determine if the blunted responses recover.

We did not obtain MRI scans on the participants. However, this is unlikely to have affected the results because measures of [11Craclopride binding are equivalent when using a region extracted from an MRI scan or from the [11Craclopride scan

(79), and there is no evidence that marijuana abusers have striatal or cerebellar atrophy (reviewed in ref. 80). Finally, the groups differed in smoking status, but this is unlikely to account for the group differences because CO levels were used as a covariate in the analysis and there were no differences in the effects of MP between marijuana abusers who smoked cigarettes and those who did not.

Conclusions

The significantly attenuated behavioral and striatal DV response to MP in marijuana abusers compared with controls, indicates reduced brain reactivity to DA stimulation that in the ventral striatum might contribute to negative emotionality and drug craving.

Source:  http://www.pnas.org/content/111/30/E3149

Study Highlights:

* Secondhand marijuana smoke may have similar cardiovascular effects as tobacco smoke.

* Lab rats exposed to secondhand marijuana smoke had a 70 percent drop in blood vessel function.

*  Breathing secondhand marijuana smoke could damage your heart and blood vessels as much as secondhand cigarette smoke, according to preliminary research presented at the American Heart Association’s Scientific Sessions 2014.  In the study, blood vessel function in lab rats dropped 70 percent after 30 minutes of exposure to secondhand marijuana smoke. Even when the marijuana contained no tetrahydrocannabinol (THC) — a compound in marijuana that produces intoxication — blood vessel function was still impaired.  Reduced blood vessel function may raise the chances of developing atherosclerosis and could lead to a heart attack. Atherosclerosis is the disease process that causes plaque build-up in the arteries which narrows them and restricts blood flow.  “Most people know secondhand cigarette smoke is bad for you, but many don’t realize that secondhand marijuana smoke may also be harmful,” said Matthew Springer, Ph.D., senior author of the study and cardiovascular researcher and associate professor of Medicine at the University of California, San Francisco’s Cardiology Division.  Marijuana and tobacco smoke are chemically and physically alike, aside from their active ingredients.  The drop in blood vessel function from THC-free marijuana suggests that the compound isn’t responsible for the effect. Similarly, this study confirms that nicotine is not required for smoke to interfere with blood vessel function.  In the study, researchers used a modified cigarette smoking machine to expose rats to marijuana smoke. A high-resolution ultrasound machine measured how well the main leg artery functioned. Researchers recorded blood vessel dilation before smoke exposure and 10 minutes and 40 minutes after smoke exposure.  They also conducted separate tests with THC-free marijuana and plain air. There was no difference in blood vessel function when the rats were exposed to plain air.  In previous tobacco studies, blood vessel function tended to go back to normal within 30 minutes of exposure. However, in the marijuana study, blood vessel function didn’t return to normal when measured 40 minutes after exposure.  Now that marijuana is becoming increasingly legalized in the United States, its effect on others is a growing public health concern, Springer said.  “If you’re hanging out in a room where people are smoking a lot of marijuana, you may be harming your blood vessels,” he said. “There’s no reason to think marijuana smoke is better than tobacco smoke. Avoid them both.”  Secondhand tobacco smoke causes about 34,000 premature deaths from heart disease each year in the United States among non-smokers according to the U.S. Surgeon General’s 2014 report on the consequences of smoking.  More research is needed to determine if secondhand marijuana smoke has other

similar effects to secondhand cigarette smoke in humans.  The National Institute on Drug Abuse and the Elfenworks Foundation funded the study.  Here is the abstract:

* Brief Exposure to Marijuana Secondhand Smoke Impairs Vascular Endothelial Function

Xiaoyin Wang, Ronak Derakhshandeh, Shilpa Narayan, Emmy Luu, Stephenie Le, Olivia M. Danforth, Hilda J. Rodriguez, Richard E. Sievers, Suzaynn F. Schick, Stanton A. Glantz, Matthew L. Springer, Univ of California, San Francisco, San Francisco, CA Objectives: Despite general public awareness that tobacco secondhand smoke (SHS) is harmful, much of the public still regards marijuana SHS as benign. Because marijuana smoke and tobacco smoke are chemically and physically similar (other than nicotine and tetrahydrocannabinol (THC)), we tested this assumption by asking whether short exposure to marijuana SHS causes acute vascular endothelial dysfunction similar to that caused by tobacco SHS. Exposure to tobacco SHS impairs arterial flow-mediated dilation (FMD) in humans and rats.

Methods: We used a rat model to test the effects of secondhand marijuana smoke on FMD. We exposed anesthetized rats to marijuana SHS using a modified cigarette smoking machine, and measured FMD three times: before 30-min exposure (“pre”), 10 min after end of exposure (“post10”), and 40 min after end of exposure (“post40”). FMD was measured by micro-ultrasound measurements of femoral artery diameter before and after transient (5 min) surgical ligation of the common iliac artery. Concentrations of respirable suspended particles <2.5 μm (RSP) fell during exposure; exposure conditions are denoted by starting concentrations.

Results: Marijuana SHS starting at 667±62 μg/m3 RSP (n=8) caused FMD to fall from 7.5±0.94% (SEM) pre to 2.3±0.50% at post10 and 2.2±0.80 at post40 (P<0.01 for both post10 and post40 vs. pre, adjusted for multiple comparisons). SHS from placebo marijuana lacking THC starting at 671±49 μg/m3 RSP (n=7) similarly impaired FMD (9.9±1.4% pre, 4.3±0.64% post10 (p<0.01), 5.5±1.3% post40 (P<0.05)), confirming that impairment did not depend on the THC. In contrast, air in the exposure chamber (1.8±0.7 μg/m3RSP; n=8) did not alter FMD (11.0±0.64% pre, 11.4±0.72% post10, 11.7±0.86% post40, P>0.70).

Conclusions: Marijuana and tobacco SHS impair endothelial function similarly under comparable exposure conditions. Public exposure to SHS should be avoided whether the source is tobacco or marijuana.

Source:  https://tobacco.ucsf.edu/secondhand-marijuana-smoke-may-damage-blood-vessels-much-tobacco-smoke  2014-11-16

As Colorado “celebrates” its third year of marijuana legalization, reporters and marijuana enthusiasts gloat of the state’s sweeping success. “Live and let live,” they naively remark, with all the wisdom of a 1970s hippie fresh out of Woodstock. But perhaps the cannabis devotees should pause and ask themselves by what metric success ought be measured.

Most accounts of Colorado’s triumph extol the vast revenue accrued via legalization and subsequent taxation (see here, here, and here). These heralds, however, neglect to tell you the rest of the story.

Just off 15th and Little Raven Streets in Denver, Colorado is a place called “Stoner Hill.” At Stoner Hill, Colorado’s homeless youth, who are ever-growing in number, congregate and smoke in what a Denver news site, Westword, describes as “a perpetual party, a misdemeanor micro-economy and a meeting ground for Denver’s youngest homeless and assorted travelers.” Westword reports, “The grassy hilltop is where a housing crisis meets legal cannabis, and it just happens to have a panoramic view of booming downtown Denver.”

Stoner Hill is emblematic of the growing crisis Colorado and other legalization states like Washington, Oregon, and Alaska face. Coincidentally – or perhaps not so coincidentally – both Colorado and Washington, the first two states to legalize, were among the top three states with the largest increases in youth homelessness from 2013 to 2014. In each state, the youth homelessness rate grew by 27 and 13.3 percent respectively in just one year.

The youth-related marijuana numbers are no less concerning and should be alarming to anyone concerned with the betterment of America’s youth. Just this month, the U.S. Department of Health and Human Services released a survey showing that Colorado now ranks number one for regular marijuana use among youth. This proud achievement only came incrementally, though; Colorado once ranked a distant 14th in the country for youth usage. Once again, this jump in the rankings coincided with Colorado’s 2012 passage of Amendment 64, which legalized marijuana for recreational use.

These numbers are unsurprising, though, since Colorado’s “edibles” often intentionally resemble candy or cookies. Much like the big tobacco advertising campaigns geared toward young people, big marijuana is marketing its drug as an innocuous or appealing snack, sure to garner youth attention. Stanford Law Professors Rob MacCoun and Michelle Mello have dubbed it an “attractive nuisance.”

The distrusting naysayer would retort that Colorado is just one state and should not be a bellwether for the nation. Colorado, however, is not alone in its marijuana accolades. When you consider “average past month use of marijuana by those 12 to 17 years old” – the main metric for youth usage – the cynic has a lot of explaining to do. Average youth use among teens in recreational/medical marijuana states rests at 10.5 percent compared to 8.9 percent in states where it is only legal for medicinal purposes and 6.1 percent in states were the drug is banned altogether. In other words, there is a direct correlation between availability of marijuana and teen usage.

Teenage use numbers alone do not fully capture the impending crisis Colorado and other states face. According to Arapahoe House Treatment network in Colorado, teenage admissions for marijuana addiction in Colorado increased by 66 percent between 2011 and 2014, again correlating with the 2012 passage of Amendment 64. This phenomenon is entirely predictable by science. Dr. Christian Thurstone of the University of Colorado explains the epidemic this way:

I’m interested in this subject because 95 percent of the teenagers treated for substance abuse and addiction in my adolescent substance-abuse treatment clinic at Denver Health are there because of their marijuana use,

and because nationwide, 67 percent of teens are referred to substance treatment because of their marijuana use. Marijuana is the No. 1 reason why adolescents seek substance-abuse treatment in the United States.

Citing a study by Wayne Hall and Louisa Degenhardt, Dr. Thurstone points out that two-thirds of new marijuana users annually are under the age of 18, and one in six of those new users will go on to use regularly or become dependent on the substance. For Colorado, this is a troubling finding.

Marijuana usage is not only detrimental for its addictive characteristics but also for its long-term effects on the adolescent brain. Marijuana has “acute (meaning up to six hours), subacute (6 hours to 20 days) and long-term (more than 20 days) effects.” Where the subacute effects of alcohol can be the annoyance of a brief hangover, marijuana can have substantial lingering effects, especially for young people. Charles Stimson of the Heritage Foundation reports that, while alcohol is broken down quickly, THC – the main active chemical in marijuana – is stored in the body, where it can remain for days or weeks and impair cognitive ability for enduring periods of time. Consequently, using the drug is associated with “lower test scores and lower educational attainment.”

The long-term effects are most worrisome. A comprehensive New Zealand study of 1,000 individuals over many years found that participants who used cannabis heavily in their teens had an astonishing average loss of eight IQ points. Accordingly, Dr. Michelle Cretella, President of the American College of Pediatricians, notes that “[m]arijuana’s impact on the teen brain leads to an increased risk of motor vehicle accidents, sexual victimization, academic failure, permanent loss of IQ, psychopathology, addiction, and psychosocial and occupational impairment.”

Sadly, youth usage is not the only devastating impact legalization has had. In Colorado, “pot-positive traffic fatalities” have increased 100 percent, emergency room visits related to marijuana have increased 57 percent, and infant exposure has increased 268 percent since legalization.

But the adverse impact on America’s youth should be enough by itself to trigger scrutiny and reform. Former Drug Czar William Bennett remarked: “We know we have a problem, and we have not managed to keep those

things from kids. Colorado was supposed to eliminate the marijuana black market, but it did not.”

While supporters applaud America’s new cash cow – marijuana – perhaps we should ask ourselves whether this newfound flow of revenue should be hoarded at the expense of America’s youth – the marijuana martyrs.

Source:  http://abovethelaw.com/2015/12/americas-youth-the-marijuana-martyrs/