Must-read: ayahuasca in America

Ecuadorian ayahuasca shaman (Ammit Jack/

Ecuadorian ayahuasca shaman (Ammit Jack/

In the current (Sept 12) issue of The New Yorker. Ariel Levy writes about the drug-fueled South American shamanistic ritual ayahuasca (or yagé,) and how its plants and practices are being imported to “hip” American areas such as Brooklyn and Silicon Valley. As TPR has explained before:

Pharmacologically, ayahuasca is quite interesting. It is commonly made by macerating and boiling together parts of the plants Banisteriopsis caapi and Psychotria viridis. Neither of these plants, taken alone, has psychedelic properties. P. viridis does contain DMT, a psychedelic tryptamine that acts — as does LSD and mescaline — at the 5-HT2A receptor. However, because of first-pass metabolism, this compound is broken down by the enzyme monoamine oxidase before it ever reaches the systemic circulation. As it happens, B. caapi contains several beta-carbolines — harmine and harmaline — that act as monoamine oxidase inhibitors. These MAOIs prevent the breakdown of DMT.

Levy’s article, cleverly titled “The Drug of Choice for the Age of Kale,” traces the history of Americans’ fascination with ayahuasca back to the Dennis and Terence McKenna, who sought out ayahuasca in 1971 during a trip to Colombia and Peru. She actually could have gone back further, at least to William Burroughs who wrote The Yage Letters in the 1950s and 60s.

The actual ayahuasca “trip” sounds horrendous, and often involves a good deal of projectile vomiting. One friend told Levy that ayahuasca “takes you to the swampland of your soul.” Author Tim Ferriss calls one of his first “trips” “the most painful experience I’ve ever had by a factor of a thousand . . . I felt like I was being torn apart and killed a thousand times a second for two hours . . . I thought I had completely fried my motherboard.”

Finally, Levy goes to Williamsburg in Brooklyn to take part in an ayahuasca ceremony. I’ll leave you to discover how the ceremony played out when you read the article, but will just say that the author ends up covered in emesis. As to whether the experience was in the end positive or negative, the results are ambiguous.

To my mind, this is the most interesting tox writing in the popular press so far this year. A must-read.

Related posts:

Ayahuasca — a pharmacologically fascinating psychedelic brew

Ayahuasca for tourists

Case series: 8 patients exposed to phony alprazolam (Xanax) containing fentanyl and/or etizolam

3 out of 5 stars

Adverse Effects From Counterfeit Alprazolam Tablets. Arens AM et al. Ann Emerg Med 2016 Aug 8 [Epub ahead of print]


In March of this year,there were 9 deaths reported in Pinellas County, Florida (the Tampa/St. Petersburg area) associated with fake alprazolam (Xanax) tablets containing fentanyl. Earlier, similar counterfeit pills had been seen around San Francisco and in Monroe County Southern Illinois.

This letter, from the University of California-San Francisco and the California Poison Control System describes 8 cases — including 1 cardiac arrest — from that region. An additional victim found at the same location as two of the cases was pronounced dead at the scene. All 8 cases occurred during the two-and-a-half month period from october 15 to December 31, 2015.

Seven of the 8 patients had blood and/or urine positive for fentanyl. Four patients had serum positive for etizolam, a benzodiazepine analog that is not FDA-approved for medical use in the United States. Additional drugs identified in these patients included cocaine, levamisole, chlordiazepoxide, diphenhydramine, sertraline, and diazepam.

Cardiac effects seen in this case series included ischemia, biventricular heart failure with pulmonary edema, and reversible cardiac arrest.

Because of the mixture of drugs involved, it’s hard to draw definite conclusions from this case series, except as a reminder that fentanyl is showing up in a variety of phony medications sold on the street, including Norco. There are also suggestions that this phenomenon may have been responsible for the death of the musician Prince.

I did a Google search and could not find any reports of counterfeit alprazolam containing fentanyl after March 2016.

As the following picture from the San Francisco Health Department shows, the phony pills look quite similar to the real thing:

Xanax Counterfeit

State-of-the-art review of lithium poisoning: almost a must-read

Lithium4 out of 5 stars

Lithium Poisoning: State of the Art.  Baird-Gunning J et al. J Intensive Care Med 2016 Aug 11 [Epub ahead of print]


This is a very good paper, the best comprehensive review I can remember reading on lithium. It is up to date, with 78 references as recent as 2015. A major reason I liked it so much is that the authors are quire frank about how much we don’t know, and resist giving, for instance, mandates about when to start hemodialysis based on lithium levels. This is a temptation that the authors of the recent ExTRIP review  succumbed to. Interestingly, the two papers share an author (Sophie Gosselin).

However, I think the authors missed — or at least failed to emphasize — a key point. With lithium poisoning, as with all toxicology cases, the key to successful treatment begins with basic ABCs and supportive care. This includes adequate hydration, which is crucial.

There are many reasons why these patients — especially those with chronic lithium poisoning — present with significant and often under-appreciated volume depletion. The gastrointestinal manifestations of lithium toxicity include nausea, vomiting, and diarrhea. Because of these symptoms, along with lithium-induced mental status changes, fluid intake has typically been deficient. Because it can take days to weeks for chronic lithium toxicity to develop, this deficiency may have been going on for some time. In addition, chronic lithium poisoning often is set off initially by dehydration resulting from viral infections, gastroenteritis, drugs such as diuretics, or other causes. Finally, as the authors note, the most common renal side effect of lithium is diabetes insipidus and volume depletion.

Since lithium is eliminated through the kidneys, establishing adequate renal perfusion is essential. This requires “filling the tank.” Although the authors certainly mention fluid resuscitation, they spend very little time on it, and give no suggestions on how to optimize volume repletion.It is astounding that they spend more time discussing sodium polystyrene sulfonate, for which they have decidedly little enthusiasm.

Since many patients who present with chronic lithium toxicity are elderly and/or have concurrent medical problems — including cardiac disease — some clinicians are reluctant to administer adequate volume repletion. Fortunately, we now have a safe and easy technology to guide us in these efforts. I am, of course, talking about ultrasound. In a recent “Toxicology Rounds” column in Emergency Medicine News, I talked about Toxicologic Ultrasound in Shock and Hypotension — the TUSH exam — and how visualizing the inferior vena cava can provide important information about volume status in salicylate toxicity. The same holds true with lithium poisoning. By not discussing bedside ultrasound at all, this article is — despite all the recent references — at least 10 years behind the times.

Still, the paper is well worth reading and referring to.

Related posts:

Hemodialysis in lithium poisoning: what is the evidence?

Hemodialysis in lithium poisoning: there is no evidence. Full stop.


Elephant-tranquilizer (carfentanil)-tainted heroin showing up in Ohio

4 out of 5 stars

Human Health Hazards of Veterinary Medications: Information for Emergency Departments. Lust EB et al. J Emerg Med 2011 Feb;40:198-207


Yesterday, Canadian police announced that, earlier in the summer, they had seized one kilogram of carfentanil contained in a package labelled “Printer Parts” shipped from China and addressed to a man in Calgary.

Carfentanil is frequently, and accurately, referred to as an “elephant tranquilizer.” It is a fentanyl analog with a potency 10,000 times that of morphine (or 100 times that of fentanyl.) It is not approved for any medical indication in humans but is used by veterinarians to sedate large animals such as elephants and horses.

The lethal amount of carfentanil is reported to be about 20 μg in humans, which led the police in Canada to claim that the 1 kg seizure contained 50 million deadly doses. It’s unclear if the substance seized was actually pure carfentanil. If it was, that would present an extreme hazmat risk, since the drug can be absorbed after inhalation or through mucus membranes or broken skin.

I had missed this valuable article by Lust et al when it was published in 2011, but came across it when I found it was virtually the only paper available describing the toxicity of carfentanil. The authors note that in animals, the drug has rapid onset and undergoes hepatic metabolism and renal elimination. Manifestations of carfentanil exposure, consistent with opioid toxicity, include mitosis, altered mental status, and respiratory depression. Larger than usual doses of naloxone may be required to reverse the effects of the drug. Areas of mucus membrane or skin exposure should be irrigated abundantly with cool water. (Hot water will increase blood flow to the area and possibly accelerate absorption.)

Other veterinary medications discussed in this article are clenbuterol, ketamine, tilmicosin, testosterone, estradiol, dinoprost,  and cloprostenol.

By the way, recent news about carfentanil has not been limited to the seized shipment in Canada. As the news story from WKRC in Cincinnati at the top of this post reports, carfentanil has been identified in samples and specimens associated with a number of recent overdose cases in the Akron area. Carfentanil-laced heroin has also been associated with at least one fatality in Ohio.

Further reading:

Everything You Should Know About Carfentanil (



Seven cases of laboratory-confirmed exposed to the synthetic cannabinoid MDMB-CHMICA

sweetleafherbalbend3.5g-1-300x3003 out of 5 stars

Clinical toxicity following analytically confirmed use of the synthetic cannabinoid receptor agonist MDMB-CHMICA. A report from the Identification Of Novel psychoActive substances (IONA) study. Hill SL et al. Clin Toxicol 2016 Sep;54:638-643.


MDMB-CHMICA is a synthetic cannabinoid receptor agonist (SCRA) with strong affinity for the CB1 receptor. It has to date not been banned in may localities, and is available on the street under labels such as “AK47 Loaded,” “Manga Hot,” “Black Diamond,” and “Sweet Leaf Obliteration.” It use has been associated with fatalities.

This case series, from the United Kingdom, describes 7 cases of laboratory-confirmed exposure to MDMB-CHMICA. The most interesting cases are the first three, which involve exposure to MDMB-CHMICA alone without any identified coingestants:

Case 1: A 41-year-old man collapsed after smoking a substance labelled “Sweet Leaf.” On arrival at hospital he was described as “drowsy,” with bradycardia and a respiratory acidosis. He did well with observation and supportive care only.

Case 2: A 16-year-old man lost consciousness at a bus station after smoking a product called “Sweet Leaf.” On presentation to the emergency department he had mildly depressed mental status and a respiratory acidosis. He also did well and was discharged after 18 hours observation

Case 3: A 33-year-old man was brought to the emergency department after being observed having a seizure. At the scene he had a Glasgow Coma Score of 3/15 and tachycardia (120 bpm.) On arrival at hospital his mental status had improved by he was described as agitated, paranoid, and violent. Laboratory work-up showed a respiratory acidosis. The patient improved over several hours and signed out against medical advice. Although he denied any recreational drug use,a blog sample tested positive for MDMB-CHMICA alone.

It’s hard to square these relatively mild cases of MDMB-CHMICA exposed with the occasional reports of fatalities that have appeared in the forensic literature. (For examples, click here and here.) It might be a matter of dose, undetected co-ingestants, or individual susceptibility.

The authors’ conclusions:

” . . . these analytically confirmed cases suggest that MDMB-CHMICA can cause a reduction of level of consciousness associated with hypercapnia, confusion, heart rate disturbances, mydriasis and in some cases convulsions and behavioral disturbances…