Archive for the 'Drug Abuse Science' category

A Repost to mark the passing of Nancy Reagan

Mar 07 2016 Published by under Drug Abuse Science, Public Health

In terms of health and biomedical science, the Reagan Administration left a shameful legacy of refusing to respond to (or acknowledge, really) the HIV/AIDS crisis that blew up during their tenure in office.

As many of you recall, First Lady Nancy Reagan took up drug abuse and substance dependence as one of her signature issues and this is probably one of the other larger Reagan Administration legacies on health.

To mark her passing, I thought I would repost the following which first appeared on the blog 21 July 2008.

If you are a reader of my posts on drug abuse science you will have noticed that it rarely takes long for a commenter or three to opine some version of "The (US) War on Drugs is a complete and utter failure". Similarly, while Big Eddie mostly comments on the liberty aspects (rather than the effectiveness) of the WoD himself, a commenter to his posts will usually weigh in, commenting to a similar effect.

Now I'm open to all the arguments about personal liberty trade offs, economic costs, sentencing disparities, violations of other sovereign nations and the like. Nevertheless, I'm most interested in the fundamental question of whether the War on Drugs worked. That is, to reduce drug use in the US. For those who believe it has not worked, I have a few figures I would like explained to me.

I'm following up a story I started in a prior post by putting up the long term trends for cocaine use in the US. These data are from the 2006 Volume II monograph which focuses on the 18 yr old and older populations. As you will recall my hypothesis was / is that the Len Bias fatality had a dramatic effect on cocaine use. I still think this is the case and that this explains much of the timing of a reduction in cocaine prevalence observed consistently from the 18 yr old to 45+ age groups. However Len Bias's death was not an exclusive effect and must be considered in the context of changes in other drug use patterns. That context is something I want to delve into just a little bit.

As always, I depend on the data from the Monitoring the Future survey ( and I am pulling the figures from the 2006 Volume I monograph which focuses on the 8th, 10th and 12th grade populations in contrast to the older age cohorts outlined in the first graph.


2006-Fig5-4e-cocaine.jpgFirst up are the annual prevalence rates for powder cocaine, which I provide for reference to the previous graph for the older age ranges. I apologize for the blurry figures but my imaging skills are not up to any better- luckily, these reports are freely available on the MtF website. (I also encourage you to get the reports yourself because there are slight changes in the questions asked in some cases- if you see a discontinuity in the longitudinal data this is probably why.) The longest term trends are available for 12th graders, additional grades were added into the survey in the early 1990's. Prevalence of cocaine was reasonably steady in the 1979-1986 interval and it is stunningly apparent that cocaine became less popular with 12th graders after 1986 . It is also clear that it took about 5 additional years for prevalence to drop to the most recent nadir. So it wasn't all about Len Bias (he died of cocaine-related cardiac complications on June 19, 1986).
So, if it isn't all about Len Bias, perhaps we should see similar effects on population prevalence of other illicit drugs?

Marijuana and Amphetamine

2006-Fig5-4a-MJ-amp.jpgIt seems reasonable to turn our analysis to two perennial high-prevalence drugs for high school populations; marijuana (duh!) and the amphetamines. (In MtF parlance, the amphetamine class is for tablet or other prescription preparations after 1982.) In this case, the prevalences were at peak in the late 1970s and started to decline in the very early 1980s. Interestingly, there is no evidence of a change in the established trends from 1986-1987 as is observed for powder cocaine; I think this supports the Len Bias hypothesis. Nevertheless we can also see this as additional evidence for something else driving drug use downward.

This brings us to what are illicit drugs for most of these populations but, of course, licit drugs for individuals who have reached the legal age; 21 (alcohol) or 18 (cigarettes; this may be a substantial fraction of 12th graders). In theory, we might use these data to try to dissociate the anti-drug messaging from the drug interdiction / legal penalties side of the equation. Not perfect, but at least a hint.


The trends for annual prevalence of alcohol were very stable from 1978-1988 whereupon a decline was observed (questions were altered in 1993, making further comparison tricky). The trends for 5-drinks-in-a-row (currently the definition of a "binge") in the past two week interval were very stable from 1978-1983 and thereafter exhibited a slow decline until the early 1990s. Very reminiscent of the above mentioned drugs.


2006-Fig5-4k-cigarettes.jpg In this case, please note that we've shifted to 30-day prevalence rates (any, daily); obviously this is frustrating for direct comparison but this is what they provide in the monographs. Unfortunately the more recent monographs (it is currently on a reliable annual update schedule with available pdfs, the older ones are not available) seem to only start with the 1986 data in the Tables so one is left with their figures for the earlier part of the trends. With that caveat, we can see that cigarette prevalence in the high school population was reasonably stable during the interval in which the prevalence rates for the illicit-for-all drugs mentioned above were in decline.

So Did the War on Drugs Work or Not?

I do think the jury is still out on this one and the problem of shifting definitions about goals and successes is quite difficult. I feel confident the comments will stray afield a bit and explore some of these issues. However, as I intimated at the outset,
for those of you who insist vociferously that the War on Drugs (considered inclusively with the Just Say No, D.A.R.E, main-stream media reporting, and all that stuff that is frequently rolled into a whole by the legalization crowd) is an abject failure...

for those of you who insist vociferously that you cannot tell teenagers anything about the dangers of recreational drugs and expect them to listen to you...

I would like these data explained to me.
Update 7/23/08: Followup post from Scott Morgan at

14 responses so far

Vaping: Known Unknowns

Dec 21 2015 Published by under Drug Abuse Science, Nicotine

Unless you have been hiding under a rock, you know about e-cigarettes. These are devices which deliver a nicotine dose using a battery-heated element which vaporizes propylene glycol, polyethylene glycol, vegetable glycerin (mostly) and/or some other vehicles in which the nicotine has been dissolved.

These devices appeal to users as cessation aids to help quit smoking tobacco and as a safer alternative to cigarettes.

They also appeal to adolescents, apparently.

You will hear the occasional grand pronouncement hit the media circusit with more assertions than questions leaving people wondering.

Here is my general take on just about anything having to do with e-cigarettes: We don't really know and we need to do some more science to figure it out.

So here are the key questions all amenable to research, some of which is no doubt ongoing.

Do e-cigs help people quit smoking? The question is, in my view, do they do any better than cold turkey (accounting for subpopulations) and are they as effective or better than any other replacement therapy like the gum or patch.

Do e-cigs prolong nicotine use in individuals who would otherwise have quit smoking cigarettes? Very tricky question, this one. But if you have an individual who would have quit smoking but keeps using nicotine via e-cig, you've increased harm.

Do e-cigs cause novel harms? In other words, presumably the nicotine harm is the same (once individuals learn how to get their desired nicotine dose from these). But are there constituents of the vehicles, the flavorants or products created by the vaporization process that cause health risks? And no, just showing an ingredient is present is not evidence of harm. We need careful toxicology studies with relevant exposure doses and regimens.

Do e-cigs prevent well-established harms? The chronic smoking of tobacco, typically via the modern cigarette products, has very well established and very bad health consequences. Nicotine exposure is the cause of only a subset of the harms, even if it is the thing responsible for continued use. So getting combusted tobacco smoke exposure out of the situation cannot help but be a huge win. Huge. I don't see how this can really be argued until and unless we find some whopping big harms of the vapor exposure.

Do e-cigs addict new individuals to nicotine? One of the big fears of those concerned with e-cigs is that early data show that adolescents are more likely to try e-cigs than to try smoking cigarettes. There will be some work showing that daily nicotine users started off with e-cigs rather than tobacco cigarettes but as you know, it is impossible to establish causality with real human populations. The best we have, overwhelmingly likely causal relationships, has to wait on a whole lot of data. Which we won't have for many years.

Bonus Round:
Are e-cigs used without nicotine or other psychoactive? One parent I know has asserted that perhaps some adolescents are using e-cig devices with just the flavored vehicles and not to ingest nicotine or any other drug. Obviously this goes back to the above question about harms from the vehicle. But it also links to another concern...

Are e-cigs used to deliver other psychoactive drugs? The devices are very readily and broadly available. They are being used with crude marijuana extracts for certain sure. There have been media allegations that they are being used to ingest "flakka" (here, here, here). For a time, one assumes that by pretending to be smoking nicotine or the flavorant (see above) peope will be able to stroll about ingesting illegal substances in public view. Including adolescents, my friends. Yes, kids.

23 responses so far

Congress let the NIH drop the HIV/AIDS set-aside: Implications for NIDA?

Dec 15 2015 Published by under Drug Abuse Science, NIH, NIH Budgets and Economics

Jocelyn Kaiser reported in Science Insider:

the National Institutes of Health (NIH) today announced it will no longer support setting aside a fixed 10% of its budget—or $3 billion this year—to fund research on the disease. The agency also plans to reprogram $65 million of its AIDS research grant funding this year to focus more sharply on ending the epidemic.

Whoa. Big news. This is an old Congressional mandate so presumably it needs Congress to be on board. More from Kaiser:

The changes follow growing pressure in Congress and from some advocacy groups for NIH to reallocate its funding based on the public health burden a disease causes.... some patient groups and members of Congress have recently asked why AIDS receives disproportionately far more than diseases with higher death rates, such as heart disease and Alzheimer’s....Last year, Congress omitted instructions asking NIH to maintain the 10% AIDS set aside.

Emphasis added. An act by omission is good enough for gov'mint work, eh? Congress is on board.

@jocelynkaiser was kind enough to link to relevant NIH budgetary distributions:

As you can see, NIDA devotes about $300M to HIV/AIDS research. The annual NIDA budget allocation is about $1B so you can see that something on the order of 30% of the NIDA budget is (and has been) devoted to this Congressional Mandate.

Wait, whut? What about that 10% mandate above? Yep, the HIV/AIDS money has not been evenly distributed across the ICs.

Now, I don't know exactly when and how all of this shook down. It was FY 1987 when the NIAID budget went up by something like 47% when other similarly sized ICs didn't see such a large percentile increase. Clearly 1986 was when Congress got serious about HIV/AIDS research. We can't assess the meaning of

AIDS has received 10% of NIH’s overall budget since the early 1990s, when Congress and NIH informally agreed it should grow in step with NIH’s overall budget.
NIH must treat AIDS dollars as a distinct pot of money within its overall budget. That is because a 1993 law carved out a separate HIV/AIDS budget, Collins says. And undoing that law would take action by Congress.

from this article. It is a little frustrating, to be frank. But...on to the NIDA situation.

NIDA doesn't appear in the NIH tables until FY1993 because it didn't actually join the NIH until 1992. Nevertheless that history page on NIDA notes:

1986: The dual epidemics of drug abuse and HIV/AIDS are recognized by Congress and the Administration, resulting in a quadrupling of NIDA funding for research on both major diseases.

There are many ways of looking at this situation.

Some in the NIDA world who are not all that interested in HIV/AIDS matters complain bitterly about why "A third of our budget is reserved for HIV/AIDS". Our.

Another way of looking at this would be "If Congress mandated NIH devote 10% of its budget to HIV/AIDS but NIH did this by incorporating NIDA with its existing HIV/AIDS funding then the entire rest of NIH is shirking its response to the mandate on the back of NIDA".

And yet a final way of looking at this* would be "Dude, NIDA wouldn't even have this money if not for Congress' interest in funding HIV/AIDS research so it isn't 'our' funding being diverted to HIV/AIDS research."

Is this important? Yes and no.

The news is potentially huge for those who seek to get the HIV/AIDS funding via NIDA grants and for those who seek non-HIV/AIDS funding. It makes matters slightly better for the latter and worse for the former. Right? If there is no special set-aside, the latter folks now have at least a shot at that $300M that had been out of reach for them. This consequently increases the competition for those who have HIV/AIDS relevant proposals. Who are presumably sad right now.

But it all depends on what Collins plans to do with his newly won freedom. Back to Kaiser:

Francis Collins agrees: At a meeting of his Advisory Committee to the Director (ACD) today, he noted that no other disease receives a set proportion of the NIH budget and the argument that AIDS still deserves such a set-aside is “not a defensible one.”

The end of the set-aside has “free[d] us up” to refocus NIH’s AIDs portfolio, Collins says.

However the article only then talks about $65M being reprioritized. What about the rest of the 10% of the ~$30B / yr NIH budget? No idea.

So I want to know a few things. Is the $300M in the NIDA budget that goes to HIV/AIDS part of this 10% overall NIH mandate? If so, will Collins try to claw that back for some other agenda?

If a miracle occurs and it stays within NIDA, will Nora Volkow use this new-found freedom to ease the pressure on the non-HIV/AIDS researchers by letting them (ok, "us") get a shot at that previously-sequestered pool?

Or will Volkow use it to pay for the latest boondoggle initiatives of ABCD and BRAINI?

The way I hear it, this latter is likely to happen because up to this point all other NIDA initiatives are being squeezed** to make ABCD and BRAINI happen.

Obviously I would prefer to see Volkow choose to use this new freedom a little more democratically by spreading the love across all of the portfolio.

*this has been my view for some time now.

**this manifests, IME, as profound pessimism on the part of POs that anything in the grey zone (which is robust reality at no-public-payline-NIDA) will be picked up because all spare change is going to the two aforementioned boondoggles.

27 responses so far

Light matters

Dec 11 2015 Published by under Drug Abuse Science, Drug Fatality

A recent exchange on the Twitter reminded me of an old paper from 1968.

The paper in question is

Scheving LE, Vedral DF, Pauly JE. Daily circadian rhythm in rats to D-amphetamine sulphate: effect of blinding and continuous illumination on the rhythm. Nature. 1968 Aug 10;219(5154):621-2. [PubMed]

Scheving68F1The key takeaway message for me is captured in the first figure (click to embiggen), which represents the percentage of rats that died within 24 h of being injected with either 26 mg/kg (darker line) or 30 mg/kg (dotted line) of amphetamine. The X axis depicts the time of day at which the groups were injected and the bar that forms the X axis indicates when the lights were on (6 am to 6 pm) and off.

As you are aware, rats are a nocturnal species and the wiggle trace just above the X-axis confirms this with activity patterns based on noise recording of the colony.

So, back to the point. The only difference across points within a single amphetamine dose is the time of day at which the drug was administered. Mortality rates change from 20% to nearly 80% with the lowest observed during the inactive part of the rats' day.

Light cycle and circadian phase matter. A lot.

This brings me to a second example, which is from one of the papers in a series of investigations by Dave Roberts at Wake Forest. In

Roberts DC1, Brebner K, Vincler M, Lynch WJ. Patterns of cocaine self-administration in rats produced by various access conditions under a discrete trials procedure. Drug Alcohol Depend. 2002 Aug 1;67(3):291-9. [PubMed]

the authors use a procedure in which rats are allowed to self-administer cocaine 24 h per day. The one major difference from the usual 1-2 h per day type of model is that the number of opportunities for cocaine were limited. These "discrete trial" opportunities ranged from 2-5 per hour and each time the animal was permitted 10 min to make a response once the lever was extended. Each response terminated the discrete trial so animals could only take 2-5 infusion per hour.

Roberts02-coc-circadianThe figure that continues the point most effectively is from a set of manipulations in which the discrete trial was set to 3 per hour and the per-infusion dose was varied. The data represent the total cocaine intake per hour so look at the 1.0 and 2.0 mg/kg/infusion doses if you want to figure out how many responses out of the 3 opportunities per hour were being made.

The point is again obvious, namely that circadian factors and light cycle matter a lot to the outcome. Imagine the more typical 1 h or 2 h operant self-administration session for cocaine being placed at various points across the rat's light cycle. On average, you might expect different mean intakes.

This is going to contribute to replication and reliability issues, particularly if you expect a given mean amount of drug intake.

It gets even tricker if you want to start exploring the effect of different interventions on cocaine self-administration. Who knows if they themselves have circadian-dependent effects or if the interaction with cocaine taking does? Who knows which direction it takes? We don't know until someone does the study.

And we can all see how much exacting work with light cycles there will be to satisfy ourselves that we know what the influence is. Work that, should it turn out negative, will be nigh on unpublishable.

And to be clear, there are hard practicalities of research that make us ignore these factors at times. Mostly across studies, but sometimes within them. Take the big issue of running behavior in the light or dark cycle of a rat (or mouse). This depends on University Facilities level decision making. Can the rooms be reverse-cycled (technically or at the whim of the animal care department)? Can you get access to the right light-cycle room for your animals for your experiments if you are low on the totem pole (as a lab or within a lab)?

Then there are within-lab factors. Limited numbers of operant boxes and limited numbers of hands. You cannot necessarily squeeze all of your animal work into the prime window of 6 h into dark to 12 h identified in the Roberts paper, above. Maybe this function changes depending on your procedures and you have an even narrower stability window.

So there will be compromises.

But these compromises will most assuredly affect the perceived replicability (aka generalization) of the work.

Additional Reading:

On contradicting your own stuff

The most replicated finding in drug abuse science

12 responses so far

Marijuana Use, Abuse and Dependence Increased Over the Past Decade

Oct 23 2015 Published by under Cannabis, Drug Abuse Science

A new paper from Hasin and colleagues at JAMA Psychiatry reviews data:

from NESARC and from the National Institute on Alcohol Abuse and Alcoholism
2012-2013 National Epidemiologic Survey on Alcohol and Related Conditions–III (NESARC-III), a survey of 36,309 new participants.
The NESARC field procedureswere similar to those in NESARC-III.

There are really three key observations, although the tables also break down the findings by sex, age, race/ethnicity, education level, etc.

First, past year use of marijuana went from 4.1% to 9.5% of the sampled populations. Interesting, but hey, could just be more people feeling free to try it out, right?

Second finding looked at prevalence of meeting DSM-IV criteria for a Marijuana Use Disorder (including Abuse and Dependence subcategories) in the past year. This measure went from 1.5% to 2.9% of the population.

The third finding is that if you condition only upon those individuals who have tried marijuana at least once in the past year, the rate of a Marijuana Use Disorder went from 35.6% to 30.6%.

This is all relevant to a few themes we've discussed before on the blog.

I don't see how you can view these data other than in a context of growing liberalization of medical marijuana laws and availability of marijuana. This refutes the occasional position struck by the pot fans that changes in legal status and attitude won't change use rates because everyone who wants to smoke marijuana already does. Clearly the US population undergoes significant changes in exposure to marijuana. In this case only over a decade.

My position has also been that, in general, as you increase the number of people who are exposed to a given drug you are going to see an increase in problems related to that drug. In the absence of other information, we must start our estimate of that rate from what we observe at a given time. The first two numbers in the study confirm this. As use rates increased, so did rates of meeting criteria for DSM-IV diagnosis of a MUD.

The conditional probability measure also addresses this phenomenon, perhaps in an even better way. I have mentioned before that it is really hard to assess conditional probability of dependence between drugs that feature significant base-rate exposure differences. You can't help but assume there is going to be a curve whereby the more democratic the exposure, the larger will be the occasional user population. That is, I assume some sort of nonlinearity is going to occur against the general estimation I mention above. I presume the lower the incidence of exposure to a given drug, perhaps the higher the conditional probability of dependence and the higher the incidence of exposure, the lower the conditional probability.

In this case, I'd say the change in conditional probability is not that significant. Something around a third of those who smoke marijuana in a given year are meeting criteria for a MUD across a doubling of the incidence of exposure. The curve is still pretty linear although I assume we will be getting another jump in a decade and can see how this curve shapes up.

This estimate of a MUD is really high to my eye, no doubt because it includes abuse and dependence together. Perhaps the data I usually think about (7-9% dependence rate) references dependence without abuse...I have to go check on that. In case you are wondering, the difference really boils down to symptoms of tolerance (diminished effect at same dose, increasing dose to get desired effect) and withdrawal, as well as some indicators of uncontrolled use relative to a person's intentions.

Now interestingly the authors reference another similar study (NSDUH) that didn't find an increase in prevalence that was so large- only 12% reported by Pacek et al, 2015. The present authors suggest more detailed questioning in the NESARC approach may explain the difference.

9 responses so far

Publisher wants to take journal Open Access

Someone forwarded me what appears to be credible evidence that Wiley is considering taking Addiction Biology Open Access.

To the tune of $2,500 per article.

At present this title has no page charges within their standard article size.

This is interesting because Wiley purchased this title quite a while ago at a JIF that was at or below my perception of my field's dump-journal level.

They managed to march the JIF up the ranks and get it into the top position in the ISI Substance Abuse category. This, IMO, then stoked a virtuous cycle in which people submit better and better work there.

At some point in the past few years the journal went from publishing four issues per year to six. And the JIF remains atop the category.

As a business, what would you do? You build up a service until it is in high demand and then you try to cash in, that's what.

Personally I think this will kill the golden goose. It will be a slow process, however, and Wiley will make some money in the mean time.

The question is, do most competitors choose to follow suit? If so, Wiley wins big because authors will eventually have no other option. If the timing is good, Addiction Biology makes money early and then keeps on going as the leader of the pack.

All y'all Open Access wackaloons believe this is inevitable and are solidly behind Wiley's move, no doubt.

I will be fascinated to see how this one plays out.

50 responses so far

Yes, it was the methylone that killed him

Jul 28 2015 Published by under Bath Salts, Cathinone, Drug Abuse Science, Methylone

StructureFig-mdma-vs-cathinones450A new Case Report verifies the lethal potential of methylone (PubMed). This drug is also known as beta-keto-MDMA (bk-MDMA; Wikipedia) or 3,4-methylenedioxycathinone. In short, this is the closest cathinone cousin to MDMA, aka Ecstasy.

Barrios L, Grison-Hernando H, Boels D, Bouquie R, Monteil-Ganiere C, Clement R. Death following ingestion of methylone. Int J Legal Med. 2015 Jun 13. [Epub ahead of print]

The decedent was a 21 year old man reported to ingest methylone and cannabis. Friends placed him in a "nearby children's paddling pool" upon report of breathing difficulty and polypnea (rapid breathing, panting).

By the time emergency medical services made contact he was in cardiac arrest.

Investigators were able to procure a sample of the powder the decedent consumed, represented to him as ecstasy upon purchase.

The toxicological screening was negative for alcohol or "medication", opiates, cocaine and amphetamines (including MDMA, MDA, MBDB and MDEA). This individual was positive for THC. The screening for substances by GC/MS identified a substance with characteristics identical to the seized material which the decedent had ingested- methylone with a purity of 83.3%.

Now admittedly a cardiac arrest with labored breathing is not right down the main line of clinical findings in MDMA overdose cases. So this is a bit strange. However, "sudden collapse" or "found unresponsive" is not atypical as the triggering observation that the person on MDMA is in trouble. There are also numerous studies showing adverse effects on MDMA on aspects of cardiac function. Similarly, cardiac implications are common with methamphetamine-related deaths- both acutely and apparently as a consequence of longer term use.

So there is every reason to think that methylone might be cardiotoxic.

The finding of cardiac arrest triggered a vague memory and luckily these authors cited the paper I was remembering:

Carbone PN, Carbone DL, Carstairs SD, Luzi SA. Sudden cardiac death associated with methylone use. Am J Forensic Med Pathol. 2013 Mar;34(1):26-8. doi: 10.1097/PAF.0b013e31827ab5da.

Now in this case a 19 year old man collapsed while jogging and had a much lower blood level of methylone (0.007 mg/L) compared with the 6.64 mg/L blood levels in the Case reported by Barrios et al. No other drugs were detected, however:

No other drugs were detected in the urine or central blood, including pseudoephedrine, ephedrine, amphetamine, methamphetamine, MDMA, 3,4-methylenedioxyamphetamine, phenylpropanolamine, or cocaine and metabolites. Analysis was also negative for several other bath salts including flephedrone, n-ethylcathinone, mephedrone, methedrone, ethylone, butylone, MDPV, and naphyrone.

This was presumably not an effect of acute overdose intoxication but perhaps a lingering effect on heart function caused by the methylone consumed hours before. Hard to know without controlled studies, particularly given the exercise this person was engaged in.

Nevertheless, this new Case Report serves as a reminder that methylone, which is increasingly replacing MDMA in the US market, represents a risk for immediate and lasting adverse health consequences.
Related Reading:

It was the methylone that killed him.

Methylone, or beta-keto-MDMA, also causes fatality

Various posts on MDMA-related fatality and morbidity

2 responses so far

The Daily Show is just plain wrong on pot being non-addictive

Apr 21 2015 Published by under Alleged Profession, Cannabis, Drug Abuse Science

In the 420 bit from this week, Jessica Williams asserts that marijuana is "a non-addictive proven medical treatment".

Marijuana is most certainly addictive.

In 2012, 17.5% of all substance abuse treatment admissions had marijuana as their primary abused drug. Alcohol alone was 21.5%, heroin 16.3% and cocaine 6.9%.

Daily marijuana smokers use 3 times a day on average and have little variability from day to day.

Pregnant women are unwilling or unable to stop smoking pot almost daily. Increasing numbers of pregnant women are seeking help to discontinue pot use.

At least one woman found out her hyperemesis during pregnancy was the pot, not morning sickness.

Marijuana is addictive in adolescents.

When adolescents stop smoking weed, their memory gets better.

About six percent of High School seniors are smoking pot almost every day.

Clinical trials of medications to help people who are addicted to marijuana stop using are far from rare.

Francophones are addicted to pot.

Yes, Dutch people are addicted to pot.

Many Cases of cannabis hyperemesis syndrome are unable to stop smoking pot, even though it is severely incapacitating them.

Marijuana is addictive.

About 37% of frequent pot users will transition to dependence in three years.

Oh, and pot users are not awesome, friendly and mellow, actually nondependent users are impulsive and hostile on the day they use pot compared with nonsmoking days.

57 responses so far

FLAKKA! (and other failures of the alleged profession of journalism)

Apr 20 2015 Published by under alpha-PVP, Bath Salts, Cathinone, Drug Abuse Science

Flakka is just the latest in a long line of stimulant drugs that can, in some very rare cases, result in astonishing public behavior.

Such as running nude through the streets to escape "unknown people trying to kill him".

Such as trying to kick in the door of a police station to get IN so as to escape cars that were supposedly chasing him.

Such as trying to shoot oneself on a rooftop, naked.

Such as trying to have carnal relations with a tree after proclaiming oneself to be Thor.

These stories are like crack to the mainstream media. They have been telling these stories for years, encompassing public scares over PCP, crack cocaine and methamphetamine over the decades past. More recently we've seen these types of stories about synthetic cathinones, in particular under the generic term "bath salts".

Sprinkled amongst the stories about classical psychomotor stimulant effects, we have stories of overdose involving synthetic opioids, MDMA and/or Molly and stories of adverse psychotropic effects of synthetic cannabinoid products. I've addressed some of these issues in prior posts and for today I want to discuss the stimulants of more traditional effect.

My greatest frustration with the reporting is not actually the breathless sensationalism, although that runs a close second. The biggest problem is the lack of verification of the bizarre behavior (or overdose) being associated with ingestion of the drug that is alleged in the initial reporting. I have not see one single verification of alpha-PVP in the body tissues of these recent Florida cases where the subjects reported consuming Flakka. We still do not know exactly what drugs were consumed by the 11 Wesleyan University students who became ill enough to hospitalize. We don't know what caused the death of Kimchi Truong at last year's Coachella music festival.

Oftentimes there are multiple media reports which, to their credit, mention that toxicology testing will take some weeks to verify. And yet. Rarely is there ever a follow-up accounting. And when there is a followup, well, it gets very poor penetration and people often parrot the wrong information even years later.

The Florida Causeway Cannibal is a case in point. At the time of the initial event it was almost universally reported to be due to "bath salts", i.e. MDPV. Toxicology reporting found no sign of any synthetic cathinone in Mr. Eugene.

It is long past time for us to hold the media as accountable for accuracy and followup on drug-related stories as we do for, say, sports reporting.

Now, there are a couple of bright lights in this generally dismal area of news reporting. Here's a local story that reported MDA, not MDMA, was at blame for a death (although they still screw up, MDA is not a "parent" drug of MDMA). In 2013 there was followup in three music festival deaths in New York to confirm MDMA, methylone and the combination of the two caused the three fatalities. We need this kind of attention paid to all of these cases.

Getting back to the current media storm over "Flakka", which is alpha-pyrrolidinopentiophenone (alpha-PVP), I have a few links for you if you are interested in additional reading on this drug.

@forensictoxguy posted a list of scientific papers on alpha-PVP at The Dose Makes the Poison blog. It is not a very long list at present! (Marusich et al, 2014 is probably the place to start your reading.)

The Dose Makes the Poison discussed alpha-PVP back in early 2014....this is not a new 2015 drug by any means.

Michael Taffe from The Scripps Research Institute [PubMed; Lab Site] gives a preview of a paper in press showing alpha-PVP and MDPV are pretty similar to each other in rat self-administration.

There was also a post on the Taffe blog suggesting that alpha-PVP samples submitted to were more consistently pure than MDPV and some other street drugs.

Wikipedia, NIDA brief

Jacob Sullum has written a pretty good Opinion piece at Forbes Fear Of Flakka: Anti-Drug Hysteria Validates Itself.

Review of the above information will help you to assess claims in the media that Flakka is "[insert more addictive, more dangerous, more powerful, worse] than [insert bath salts, MDPV, methamphetamine, cocaine]".

tldr; It isn't.

It will also assist you in coming to an understanding that Flakka is likely to be just as addictive and problematic as these previously sensationalized stimulants.

tldr; It is.

In my view, the scope of the Flakka problem over the coming years will be dictated by user popularity and availability, and not by anything particularly unique about the molecular structure of alpha-PVP.

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Why PMA if dealers don't want to kill their clients?

Mar 13 2015 Published by under MDMA

There's an interesting piece on Ecstasy in Mixmag that addresses something that is a side issue of the MDMA overdose issue that I've talked about on the blog. These issues bubble up to our conscious consideration every time there is a mysterious Ecstasy-related cluster of adverse events such as at Wesleyan University. Until there is confirmation of the drug(s) involved from toxicological testing we can only speculate as to the cause of the events.

Even though we know that MDMA itself is always a top suspect, PMA, (para-Methoxyamphetamine), is a fine Usual Suspect of a non-MDMA substance sold to users as "Ecstasy" but resulting in adverse consequences.

The Mixmag piece reminds us of the MDMA drought in the UK that launched mephedrone into the recreational pharmacopeia.

One of the easiest ways to make MDMA is to use an essential oil called safrole, which occurs naturally in the roots and bark of the yellow camphor tree, found in Cambodian rainforests and elsewhere. The UN has targeted the trade repeatedly in the last decade, with the noble aims of protecting the rainforest, which is being chopped down by the gangs that steam-distil the oil out of the bark in giant, bubbling cauldrons in jungle labs. The UN burned 33 tonnes of it in 2008, which caused a worldwide drought of MDMA and the emergence of mephedrone as both gangsters and clubbers looked for alternatives. In September 2010, 50 tonnes were burned in Thailand.

Yep, we recall.

However, this previous preferred-method for synthesizing MDMA leads on to the reason why PMA is sometimes pushed out on the market for consumers to use, unsuspectingly in many cases. Mixmag proposes this hypothesis:

PMA is made from an oil called anethole, which is legal, cheap, and easy to get hold of.

Professor David Nutt agrees that the likely scenario is that clandestine chemists use anethole in a trial run, to test new lab set-ups, and then sell the resulting PMA to unscrupulous pill pressers. Making PMA involves an identical set of chemical reactions to making MDMA – only the precursor is different. Think about it: if you had a limited amount of very expensive safrole or PMK, and you had a new lab, or a new chemist, you’d want to test your kit out. A trial run making PMA from anethole would help you practice the technique and avoid losing valuable precursors – and you’d make some money back.

They then ask any chemists reading to confirm so one must take this as speculation rather than journalistically confirmed with clandestine labs.

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