Archive for the 'Cannabis' category

Hyperemesis associated with synthetic cannabinoid products

Mar 07 2014 Published by under Cannabis, Drug Abuse Science

As you know, Dear Reader, a cyclical vomiting syndrome is often associated with chronic cannabis smoking. I've written about it a few more times (here, here, here) and you can check out additional posts at Addiction Inbox (here, here). I urge you to read through the comments posted under all of these blog entries. The numbers definitely rival the published Case Reports in number of affected individuals. Clearly there continues to be many folks suffering who go initially undiagnosed.

A Reader sent me a link to a medical diagnosis challenge published in the Well section of the New York Times recently which returned my interest to the topic. Mostly due to the following comment in the solution column:

Sure enough, there it was – two recent case reports describing several regular synthetic marijuana users who developed a syndrome that was indistinguishable from cannabinoid hyperemesis caused by the real stuff.

I had not seen any such reports so I went looking and found one of them on PubMed.

Hopkins CY, Gilchrist BL. A case of cannabinoid hyperemesis syndrome caused by synthetic cannabinoids. J Emerg Med. 2013 Oct;45(4):544-6. doi: 10.1016/j.jemermed.2012.11.034. Epub 2013 Jul 26.

By now, the diagnosis sounds very familiar. A 30 year old man presented at the ED with nausea and vomiting. He reported a prior history of such episodes, including gastro-enterology workups, scans, endoscopies, etc. Nothing that would explain his symptoms was ever found. The patient had found that hot showers relieved his pain and took several showers per day.

Naturally the patient had started using cannabis at the age of 13 and had been smoking several times per day for years.

Up until this point, everything is very familiar.

This particular individual had been cannabis free for 6 months due to legal surveillance under parole. After cleverly determining with over-the-counter tests that synthetic marijuana products (brand names of K2 and Spice were popular early in the cycle and have come to be familiar as semi-generic terms) didn't trigger cannabinoid positives:

...he quickly resumed his daily smoking habits and in the month before presentation was often smoking synthetic marijuana hourly, including waking up several times at night to get high.

The patient claimed that in the 2 months prior to presentation he'd been using "Scooby Snacks (sic)*" brand exclusively and provided some to the research team. This is cool because the team identified the cannabinoids in the product. It contained several, "JWH-018, JWH-073, JWH-122, AM-
2201, and AM-694" and they also found the patient's urine to be positive for JWH-018, JWH-073 and AM-2201.

As a bit of a sidebar, I really don't know why particular combinations are included in various synthetic cannabis products. It is unclear if it is accident of supply, illicit manufacturers who just throw stuff together at random, the end of the batches or something more intentional. There is an interesting paper from the Fantegrossi group (Brents et al, 2013) that suggests the possibility of synergistic effects.

Returning to the case report, on three month followup it was found the patient manged to remain abstinent and reported remission of his symptoms after the first 2 weeks.

Okay, so typical story for cannabinoid hyperemesis syndrome and in this case the patient had been exposed to multiple cannabinoid full agonists instead of delta-9-tetrahydrocannabinol prior to current episode. Of course his history suggests strongly that it was cannabis smoking that created his liability for the episodes in the first place.

One take-away message over the past several years is that we've rapidly gone from a point where nobody knows cannabis can cause a vomiting syndrome to some reasonable awareness. This is fantastic. The greater awareness, the greater the chances of rapid and accurate diagnosis. If you read the case reports you will see extensive and expensive gastrointestinal testing and diagnostic work in the history of many individual patients. Realization on the part of the patients that they should mention their cannabis smoking helps. Realization on the part of medical staff that they should ask about cannabis helps.

Knowledge can be a powerful bit of assistance for health care.

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*more likely Scooby Snax?

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Marijuana use rates in 12-17 year olds is highest in medical marijuana states

Dec 18 2013 Published by under Cannabis, Drug Abuse Science

The ONDCP twitter account just posted a very interesting graph on past-month marijuana use rates in the 12-17 year old adolescent population.
TeenMJbyState

This dovetails very nicely with a factoid being twittered today in the #MTF2013 hashtag which is covering the release of the mid-term data from the Monitoring the Future project.

this actually surprised me. That it was so low.

Of course, one's first suspicion is that states which are liberal enough to pass medical marijuana laws might have adolescent populations that are more likely to smoke marijuana anyway, i.e., regardless of the medical legalization. Be nice to see a workup on teen marijuana use in these states before and after they legalized medical marijuana.

8 responses so far

Transitioning to cannabis dependence

Nov 04 2013 Published by under Cannabis, Drug Abuse Science

The conditional probability of dependence on a given drug is a question that is of substantial interest to users, parents of users, public policy makers and heath care providers. After all, if people simply stopped using a drug once a problem arises then many of the negative effects could be avoided. There is a fair degree of correlation between meeting diagnostic criteria for dependence and someone failing to stop using a drug despite clear and growing negative consequences. (Indeed this is one of the dependence criteria). Therefore, we must consider dependence to be a target of substantial interest.

It can be difficult to estimate the conditional probability of dependence in humans because we mostly have cross-sectional data to work with. And so we must infer conditional probability from dividing the currently dependent population by some denominator. Depending on what one uses for the denominator, this estimate can vary. Obviously you would like some population that uses the substance but what represents a level of "use" that is relevant? One time ever? Use in the past 12 months? Use in the past 30 days?

A new paper by van der Pol and colleagues uses a prospective design to provide additional data on this question.

The authors recruited 600 frequent cannabis users, aged 18-30, and assessed them for cannabis dependence at start, after 18 months and after 36 months using the:

Composite International Diagnostic Interview (CIDI) version 3.0 (Kessler and Ustun, 2004), and required the presence of three or more of seven symptoms within the 12-month period since the previous interview (without requiring the presence of all symptoms at the same time). It should be noted that the CIDI includes a withdrawal symptom, which is not included in the DSV-IV manual.

The study defined "frequent" use as 3 or more times per week for 12 months or more. This is important to remember when trying to assess the conditional probability. It all depends on what you construe as an at-risk population. Here, I'd say these were already rather confirmed cannabis fans.

The authors were interested in the very first incidence of dependence and so therefore excluded subjects who had ever met criteria, this left 269 subjects at intake (retention in the study left N=216 at 18 mo and N=199 at 36 mo). This is another point of interest to me and affects our estimation. Three or more times per week for 12 months or more and 45% of them had never previously met criteria for dependence. There are two ways to look at this. First, the fact that a lot of similarly screened users had already met criteria for dependence suggest that this remaining population was at high risk, merely waiting for the shoe to drop. Conversely it might be the case that these were the resistant individuals. The ones who were in some way buffered from the development of dependence. Can't really tell from this design....it would be nice to see similar studies with various levels of prior cannabis use.

There were 73 cases of cannabis dependence of the 199 individuals who were followed all the way to 36 months, representing a conditional probability of transitioning to dependence of 36.7% within 3 years.

Now, of course the authors were interested in far more than the mere probability of meeting dependence criteria. They assessed a number of predictor variables to find differences between the individuals that met criteria and those that did not. Significant variables included living alone, mean number of prior cannabis use disorder symptoms, a continual smoking pattern per episode, using [also] during the daytime, using cannabis to "cope", child abuse incidents, motor and attentional impulsivity and recent negative life events. For this latter, followup analysis identified major financial crisis and separation from someone important as driving events.

As the authors point out in the discussion, the predictors differ from those identified from a more general population. This makes sense if you consider that the range on numerous variables has been seriously restricted by their catchment criteria. The amount of cannabis exposure, for example, did not predict transition to dependence in this study--perhaps because it was well over the "necessary if not sufficient" threshold. This underlines my theme that the denominator matters a lot to our more colloquial estimates of the risks of dependence on cannabis.

Another issue identified in the discussion was the choice to start at 18 years of age for the captured population. Cannabis use frequently starts much earlier than this and many studies of epidemiology suggest that initiation of drug use in the early teens, mid teens, late teens and early twenties confers substantially different lifetime risk of dependence. "The earlier someone starts using, the more likely to become dependent" is the general findings. The authors cite a study showing that the mean age of meeting cannabis dependence criteria for the first time is 18. This is at least consistent with the fact that 65% of their collected sample had previously met criteria for dependence. No study is perfect or gives us the exact answer we are looking for, of course.

A final note on estimating the conditional probability of dependence in the population that uses cannabis 3 or more times per week for over a year. Of the original sample, 331 had already met dependence criteria and were excluded because the interest here was on the first time dependent. If we ignore those 70 people lost to followup during the study, and add the 73 to the 331 then we end up with 76% of those individuals smoking that much cannabis who have already, or will soon, meet dependence criteria.

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van der Pol P, Liebregts N, de Graaf R, Korf DJ, van den Brink W, van Laar M. Predicting the transition from frequent cannabis use to cannabis dependence: A three-year prospective study. Drug Alcohol Depend. 2013 Jul 22. pii: S0376-8716(13)00228-7. doi: 10.1016/j.drugalcdep.2013.06.009. [Epub ahead of print]. [Publisher, PubMed]

25 responses so far

More cannabis hyperemesis Cases

Oct 28 2013 Published by under Cannabis, Drug Abuse Science

There was a twitt from Dirk Hansen today

which pointed to Chen and McCarron in Current Psychiatry. This paper seems to be a set of diagnostic and therapy recommendations and contains an example Case Report.

This triggered a bunch of the usual incredulity, in this case from @drogoteca.

those two are but the tip of this person's denialist iceberg on cannabis hyperemesis. He or she is quite convinced that this cannot be a real outcome of chronic pot smoking.

It can and is.

For background, I've discussed the evidence for a cyclical vomiting syndrome associated with cannabis use here, here and here. Also see Dirk's post.

For grins I thought I'd see if there were any new Case reports and found several I had not seen before.

Hickey and colleagues (2013) report a Case of Cannabis Hyperemesis Syndrome that was treated with haloperidol:

A 34-year-old man well known to our ED arrived with epigastric pain, nausea, and vomiting for 4 days. He had been unable to tolerate anything orally but reported temporary relief only with long hot showers. He came to the ED that night to be admitted because he knew his symptoms would not improve, and he was always admitted in the past when his symptoms were so severe. He denied fevers, chills, diarrhea, hematemesis, melena, or hematochezia.

The patient's history was significant for similar symptoms every 2 to 3 months for approximately 10 years. He reported daily cannabis use since 1992, with only short intervals of abstinence resulting in complete resolution of his vomiting. He has been admitted to our hospital from the ED 7 times and had multiple unremarkable diagnostic tests including 3 computed tomographic scans, an esophagogastroduodenoscopy, and several specialty consults. He has also been admitted to several other local hospitals for cyclical vomiting. Other than substance abuse, he has no known psychiatric history. A diagnosis of CHS was finally made in 2012, a few months before this ED arrival.

Mohammed and colleagues (2013) reported a Case (which they are at pains to point out is from the Caribbean) that resolved with abstinence.

A 26-year-old Caucasian male presented to our center with a
1-week history of severe colicky epigastric pain heralded by significant nausea for 3 weeks. He had approximately 20 episodes of bilious vomiting daily with numerous bouts of retching. He admitted to smoking 4 “joints” or marijuana cigars every day for the last 2 years, and denied alcohol and tobacco use. He had 4 similar episodes over the last 6 months. During
these admissions, he was rehydrated and abdominal imaging revealed no abnormalities. His ongoing nausea was relieved
by taking hot showers, of which he took up to 15 times per day, sometimes for more than an hour.

...

The diagnosis of CHS was made and he was counseled on abstinence from marijuana. Though he refused to enter a substance
abuse program, he remained cannabis-free and on follow-up at 1, 3 and 6 months revealed no recurrence in symptomatology.


Enuh and colleagues (2013)
report a case from the US.

A 47-year-old African American male with a history of epilepsy and drug addiction presented to the hospital with a seizure complicated by nausea, vomiting, and severe abdominal pain. He was known to be diabetic, hypertensive, and addicted to marijuana for 30 years. He smoked two to three “blunts” (cigar hollowed out and filled with marijuana) most days and occasionally up to eight blunts daily. The drug was last taken on the day of his admission.

He immediately went to the bathroom and remained under a hot shower with the exception of two 15-minute breaks for the rest of the day. He believed that a warm shower could relieve his nausea and vomiting. He stated that it made him feel better than medication. Intravenous ondansetron was of limited benefit. It was difficult to persuade him to exit the shower for the rounds and physical examination. Receiving medication and eating were problems because of this compulsive showering. The same event of entrenching himself in the shower had happened 2 months prior to his hospitalization for a grand mal seizure. Abstinence from marijuana during the hospital stay made the patient’s nausea, vomiting, and obsessive warm showering resolve after 3 days.

Not as satisfying as it could be with respect to the workup and the post-hospitalization followup, of course. But interesting.

Sofka and Lerfald (2013) report a series of four Cases. All had histories of chronic cannabis use, all used hot showers to alleviate symptoms and all had negative GI scans and other clinical workups. One individual was reported to have ceased cannabis use and had remained symptom free. The other three were reported as continuing their cannabis use and continuing to have symptoms. Frustratingly, the authors do not specify the followup duration for any of the cases.

Gessford and colleagues (2012) report a Case that is significant for the comment on the efforts to find a cause prior to the identification of CHS:

A 42-year-old Caucasian female, who has routinely been seen at our institution for nausea, vomiting and abdominal pain since 2003, presented with the complaint of nausea, vomiting and abdominal pain. She stated that the symptoms occurred this time after eating four bites of ice cream. ...

Her physical exam was normal except for some mild epigastric tenderness which she attributed to her excessive vomiting. Laboratory studies including a comprehensive metabolic panel, amylase, lipase, and complete blood count were normal except for anemia, which had improved since her last admission. Urine studies, including urinalysis, were normal with a urine drug screen positive for delta-9-tetrohydrocannabinol (THC), benzodiazepines and opiates. Abdominal and chest x-rays were normal.

During the course of her admission, further investigation into her history revealed chronic marijuana use. She reported that long hot showers provided the only relief for her pain and nausea. She claimed that she took so many showers that her bathroom was growing excessive amounts of mold and mildew. Research into her medical records revealed an even more disturbing fact: excessive radiation exposure and medical cost. In total, she has had in excess of 97 abdominal x-rays, eight abdominal CT scans, two abdominal MRIs, an abdominal MRA, small bowel follow-through, three gastric emptying studies, four esophagogastroduodenoscopies (EGD), and three colonoscopies. Since 2003 these tests produced two abnormal findings: (1) the two most recent gastric emptying studies at 224 and 180 minutes (gastroparesis) and (2) gastritis/duodenitis on EGD. Throughout her complete sevenyear work-up, celiac sprue, peptic ulcer disease, Barrett's esophagus, porphyrias, ischemic bowel disease, appendicitis, ulcerative colitis, Crohn's disease and H. pylori infection have been excluded. The patient's medical record indicated that since 2005 she has had 97 emergency room visits. Additionally, since 2007 she has had 42 admissions.

Emphasis added. This is a feature of many of the clinical Case Reports that cannot be ignored. The lack of awareness of cannabis as the causal agent is costly. In terms of the dollar costs of diagnosis and care and in terms of the drugs and invasive diagnostic procedures administered to the patient.

I don't have access to Morris and Fisher (2013) which the Abstract states reports a single Case.

In trolling around on Google I ran across this comment in a pot user forum:

As far as symptoms are concerned, they began about 3 years ago when I would wake up feeling nauseated. Shortly after the nausea started, I'd vomit once and (after smoking) I would feel better. This continued off and on without me giving it much thought until February of this year, when I was floored by intractable vomiting for about 48 hours. I couldn't keep anything down (not even water), and the only time I felt like I didn't want to die was when I was in a hot shower. When the vomiting and nausea finally relented after that first episode, I chalked the experience up to acute gastroenteritis. However, about three days later, I woke up feeling nauseated. I went to work as usual, but by noon I was throwing up unstoppably again and had to go home. By the time evening came around, I could eat light food like white rice and slept. But as soon as I awoke the next morning, I had the same stomach pains and nausea. Again I went to work and again the unstoppable vomiting kicked in right around midday. The only thing that brought relief was a hot shower or bath. So long as I was under hot water, I felt alright.

This person details a history of medical workups and a bit of the recur/remit presentation before ending up with his conclusion:

At this point, I have been completely abstinent from ze herb for 5 days and I have already noticed improvement. Although I, too, was skeptical about CHS at first, I just do not know what else could be causing the problem. Although I absolutely love to get high, at my current weight/height (I am 6'1" and 129lbs now) I am quickly running out of options. If I can't find a solution to this problem soon, it will literally kill me. And I'll be damned if I gonna become the first known death directly related to marijuana consumption.

Naturally, the other forum users express the usual incredulity we see from the leegalizeetmon crowd. It's worth a read.

I also ran across this blog post from a person claiming to be an ER doc:

Since I have become aware of this association between marijuana use and CVS type presentations it has been my “good fortune” to care for nearly a dozen patients in the emergency department who self-reported diagnosis of CVS. Curiously, of these patients about 10 admitted active marijuana use, and the 2 who denied it had positive urine screenings for marijuana. This does not exactly make a case series, but is certainly another interesting observation. Of course, since the prevalence of marijuana use in our Emergency Department seems to approach 100% sometimes, this also may not be a statistically significant association!

I conclude with points I made in prior posts. At the moment, this syndrome is clearly quite rare considering estimates for chronic cannabis users worldwide. Some of this is due to lack of diagnosis..the Case Reports make very clear that an extended history of diagnostic investigation of more usual gastric disorders is typical prior to the identification of cannabis as the causal agent. But even so, very likely this is a rare reaction. Given that, it is not impossible that there is some as-yet-undetermined source of the chronic vomiting that is merely correlated with cannabis use. [In the event your imagination fails you, people tend to suggest moldy weed, herbicide/pesticide and/or contamination from smoking devices as causes.] Nevertheless, it appears to me to be likely that as we accumulate more and more Cases separated by time and place, which involve individual users with a variety of phenotypes and environmental circumstances, which present similar clinical pictures and which seem to have chronic cannabis smoking (not synthetic marijuana products, for example) as the only commonality.... well it becomes very difficult to sustain any alternative hypothesis.

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Hickey JL, Witsil JC, Mycyk MB.Haloperidol for treatment of cannabinoid hyperemesis syndrome. Am J Emerg Med. 2013 Jun;31(6):1003.e5-6. doi: 10.1016/j.ajem.2013.02.021. Epub 2013 Apr 10. [link]

Mohammed F, Panchoo K, Bartholemew M, Maharaj D.Compulsive showering and marijuana use - the cannabis hyperemisis syndrome.Am J Case Rep. 2013 Aug 23;14:326-8. doi: 10.12659/AJCR.884001. [PMC link]

Enuh HA, Chin J, Nfonoyim J. Cannabinoid hyperemesis syndrome with extreme hydrophilia. Int J Gen Med. 2013 Aug 19;6:685-7. doi: 10.2147/IJGM.S49701. [OpenAccess link]

Sofka S, Lerfald N. Cannabinoid hyperemesis syndrome: A case series. W V Med J. 2013 May-Jun;109(3):20-3.
[link]

Gessford AK, John M, Nicholson B, Trout R. Marijuana induced hyperemesis: a case report. W V Med J. 2012 Nov-Dec;108(6):20-2. [link]

85 responses so far

Driving test

Feb 24 2013 Published by under Cannabis, Uncategorized

10 responses so far

Some data on simple possession raps for three of my Readers

Dec 21 2012 Published by under Cannabis, General Politics

This is from a bit by David Frum:

20121221-074922.jpg

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Presumption of vocational impairment

Dec 08 2012 Published by under Cannabis, Drug Abuse Science, General Politics

Per this article, the question of private employers dealing with off-hours behavior deemed legal by the State.

Gee... If we only had some way to determine if users of marijuana are likely to be vocationally impaired. If only there were some way to get that information. So that we could come up with some guidelines. And do things based on reasonable approximations of fact rather than agenda based random reaction (on either side).

Wouldn't that be useful?

What? What's that you say?

"Science"?

25 responses so far

Estimating the populations at risk for dependence on marijuana versus cocaine

Oct 08 2012 Published by under Cannabis, Cocaine, Drug Abuse Science

The recent fax (yes, they still call it this despite it arriving via email attachment) from CESAR (Vol 21, Issue 40; October 09, 2012) puts us back on an occasional theme of this blog.
They have adapted data from the latest update from SAMHSA's National Household Survey on Drug Abuse. This figure shows the number of past year users of selected illicit/recreational drugs.
Interestingly, marijuana use continues to trend up from the approximate plateau of 2002-2007, while use of cocaine is trending downward. Even the nonmedical use of prescription drugs (which has been a big problem overdose-wise) is relatively flat. Rounding slightly, we're looking at some 30 million past year users of marijuana compared with 4 million past year users of cocaine.

So why is this interesting? Well, as we've covered in the past the notion of conditional probability of dependence is a key issue for parents and policy makers and yet we have really poor estimates on that. Direct studies are usually limited in scope and the big-scale epidemiological stuff is too imprecise- i.e., rarely are there good diagnostics of dependence. So we sometimes have to infer things based on, e.g., daily use rates versus annual rates. Something like that. Fortunately the more precise studies and the broader interpretive efforts tend to agree.

Roughly speaking the conditional probability of alcohol dependence is on the order of 4%, for cannabis on the order of 8-10% and for stimulants, including cocaine, on the order of 15%.

So, applying these rough estimates to the past-year data above, we end up with something on the order of 600,000 dependent on cocaine and 2,400,000 dependent on marijuana. If you dropped the estimate of conditional probability for marijuana to the 4% of alcohol, you still end up with 1.2M people dependent on marijuana.

My point, as always, is that the definition and scope of a "drug dependence problem" is going to depend on frame of reference. One important frame of reference in my view is the number of people who are affected. This, btw, is why we think of alcohol dependence as such a huge problem even though just about every estimate suggests the conditional probability of dependence is one of the lowest. Because the percentage of the entire population exposed to alcohol on a regular basis is so large, the number of people who are dependent is relatively large.

22 responses so far

Transgenerational effects of exogenous cannabinoid exposure

Sep 11 2012 Published by under Cannabis

A paper in the October issue of the Journal of Psychopharmacology will be of interest to my readership. It looks at the consequences of exposure to an exogenous cannabinoid agonist

Byrnes JJ, Johnson NL, Schenk ME, Byrnes EM. Cannabinoid exposure in adolescent female rats induces transgenerational effects on morphine conditioned place preference in male offspring.J Psychopharmacol October 2012 26: 1348-1354, first published on April 19, 2012 doi:10.1177/0269881112443745 [ PubMed ]

In this study the authors exposed 23 day old (adolescent) female Sprague-Dawley rats to a three day, twice per day regimen of WIN 55,212-2 which is a full agonist at the CB1 receptor. The more familiar exogenous cannabinoid, Δ9-tetrahydrocannabinol (THC) is a partial agonist at the same site. The authors waited until the animals were adult (60 days), bred them and then examined the subsequent male off-spring of these mothers. They assay of interest was the Conditioned Place Preference test which is one common method to assess subjective drug liking in rats and mice.

The idea is to take a chamber which is divided into two or there sections by dividers and doors (in this case it was a three-chamber apparatus). The chambers are differentiated by salient stimuli such as the floor texture or type, wall stripes (horizontal vs vertical), etc. You let the subject explore at will in pre-conditioning baseline studies. Then, you conduct a series of conditioning sessions in which the animal is injected with a drug and then confined in one of the chambers. On other sessions the animal is injected with the drug vehicle only and confined to the other chamber. In this case, there were three active drug and saline conditioning sessions. Finally, on a later test day the animal is allowed once again to freely explore all of the chambers. The amount of time it spends in each chamber is recorded and the relative preference for the drug-paired chamber over the saline-paired chamber can be expressed, typically as a difference in amount of time, or the percentage of the total time, spent exploring the drug-paired chamber.

The figure presents Conditioned Place Preference data for the adult male offspring (WIN-F1) of mothers which were exposed to WIN 55,212-2 in adolescence and in the control group (VEH-F1) of adult male offspring of mothers treated twice a day for three days with the drug vehicle. There were three different place conditioning levels with groups of animals from the VEH and WIN treated dams place conditioned (in adulthood) with saline, 1 or 5 mg/kg of morphine. As expected, the chamber preferences of animals "conditioned" with vehicle were indistinguishable, i.e., they spent approximately equal time in each chamber. Animals conditioned with morphine, however, spent more time in the drug-paired chamber than in the vehicle-paired chamber.

Interestingly, there was a group difference which depended on the maternal treatment. The offspring of the WIN treated mothers appeared more sensitive to the rewarding effects of morphine because they expressed a conditioned place preference after 1 mg/kg training, unlike the adult offspring of VEH exposed dams. Although I'm not showing it here, the study also looked at adolescent male offspring and found a similar enhancement of morphine place-preference conditioning in the offspring of WIN exposed dams.

The translational take-away is pretty clear and fairly frightening. It suggests that one of the reasons for familial patterns of substance abuse may not simply be down to genetic legacy but may have something to do with drug exposures of the mother.

29 responses so far

More cannabis hyperemesis Cases emerge

Aug 15 2012 Published by under Cannabis, Drug Abuse Science

Just as our most fervent defender of pot posted the most scientifically offensive clause in the legalization initiative defeated by California voters:

5. Cannabis has fewer harmful effects than either alcohol or cigarettes, which are both legal for adult consumption. Cannabis is not physically addictive, does not have long term toxic effects on the body, and does not cause its consumers to become violent.[DM- policy statement, false, false, distraction]

a comment on an older post returned our attention to the cannabis hyperemesis syndrome.

The past year I started smoking a lot more than ever before.
I'm 21, and every single morning I wake up with the worst upset stomach. It gets all the way to the point where I'm running to the bathroom to throw up and nothing ever comes out. The doctors think its in my head. Awesome. When this first began happening I would just make myself throw up but once I began it wouldn't stop for hours and I had to be taken to the emergency room. I feel like I'm dying!! But of course I feel completely better when I go smoke. It's insane!

So I trotted over to PubMed to see what is new, if anything, with cannabis hyperemesis. I found three new CaseReport publications that I had not seen before including:

Nicolson SE, Denysenko L, Mulcare JL, Vito JP, Chabon B. Cannabinoid hyperemesis syndrome: a case series and review of previous reports. Psychosomatics. 2012 May;53(3):212-9. Epub 2012 Apr 4. PubMed

Luther V, Yap L.A hot bath to calm what ails you: the Cannabis Hyperemesis Syndrome. Acute Med. 2012;11(1):23-4. PubMed

Bagdure S, Smalligan RD, Sharifi H, Khandheria B. Waning effect of compulsive bathing in cannabinoid hyperemesis.Am J Addict. 2012 Mar-Apr;21(2):184-5. doi: 10.1111/j.1521-0391.2011.00209.x. Epub 2012 Feb 7. PubMed

There are a total of 6 individuals reported (20-27 yrs of age, 2 female), all of whom presented to medical services (New York, 4; London, 1; Amarillo, TX, 1) with repeated and severe vomiting. All Cases had been smoking marijuana for many years with at least daily smoking in recent months to years. Five of the cases identify multiple uses per day, the sixth just indicates daily smoking.

Medical workups for all six indicated no other detectable gastrointestinal causes. All six Cases include multiple episodes of repeated vomiting in the past which had resulted in emergency department visits or hospitalizations for that patient.

All six had been using hot showers to control their symptoms, selected quotes from different Cases are illustrative:

he persistently demanded to use our showering facilities...He continued to demand to use the showering facilities, and oddly seemed more settled after bathing.

Several times during the interview, he went to the bathroom to put his head under the hot shower, which he said improved his

Ms. B complained that the hospital showers were not warm enough because the best way to relieve her symptoms was to take extremely hot, hour-long showers four times daily.

Three of the cases have evidence that ceasing marijuana smoking prevented further episodes of cyclical vomiting. Three show evidence that returning to marijuana smoking after abstinence led to recurrence of symptoms. Two cases had no followup evidence.

As this evidence starts to accumulate, we need to remember one thing about the Case Reports which is that there is a severe publication/selection bias in this sort of thing. Physicians' motivations to publish are not like ours and what strikes one group of physicians to bother to publish a Report is entirely opaque to me. It is, however, likely only the tip of the iceberg. As a second caution, it may also be the case that their is a bias for the publication of "clean" Cases. For only bothering when the individual Case seems to fit this growing profile to a T. Thus, it may make things about this syndrome appear more clear cut, more severe, etc. This goes both ways but one thing I would be concerned about are those Cases that are indeed caused by chronic cannabis use but are not diagnosed because they don't seem to fit the Case Report literature.

Perhaps hot bathing/showers are not always involved? Perhaps the use history is not as severe as it was for this most recent set of six cases? Perhaps there are some cases in which marginal gastro-intestinal concerns have interacted with a lesser degree of chronic cannabis smoking to push an individual over the threshold to cyclic vomiting symptoms?

There is always the unknown factor. People have proposed unknown toxins in the past...contamination of the cannabis being used. Still not impossible, especially given the apparent rarity of the syndrome. But, I would argue, as the cases occur across time and geography this becomes less likely. You would think that contamination might surround particular drug supplies (in time and space) in a way that might turn up as a geographic patient cluster.

For now, however, the evidence is reasonably strong and it is most certainly growing. Obviously, I think it is well past time for scientists with models that are relevant to emesis to get cranking and start up some studies. Unfortunately rats don't vomit so it is going to require some specialized animal models, perhaps the ferret.

30 responses so far

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