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I have some criticism of this paper:

"A case study of cannabis use leading to a cardiac arrest

Marijuana as a Cause of Diffuse Coronary Vasospasm Leading to Cardiac Arrest

https://assets.cureus.com/uploads/case_report/pdf/64574/20230423-30312-u2fsrz.pdf"

"Marijuana is one of the most widely abused substances in the US. The effects of tetrahydrocannabinol (THC), the active ingredient in marijuana, have been well studied and reported substantially in the literature. When smoked, THC results in a rapid, dose-dependent tachycardia by 20-100%, an increase in blood pressure, and an increase in cardiac output by > 30%, leading to increased oxygen demand, which is augmented by the vasoconstriction from endothelial damage by smoking and activation of CB1 receptors by marijuana [3,4]..."

It's interesting to me that at least as far as the late1980s, marijuana was commonly found to produce a lowering of blood pressure, not an increase; and a tendency toward vasoldilation, not vasoconstriction. The physical effects of marijuana were commonly associated with dose-dependent symptoms like postural hypotension, not hypertension- much less hypertensive crisis or cardiac arrest. (Mild tachycardia was always generally acknowledged in the literature as a common physical effect of marijuana.)

I'm curious about when medical opinion began to shift on this, and what might have accounted for it.

In the case cited, the study reports the patient suffering from cardiac arrest as a 53-year old male with "a past medical history of hypertension, hyperlipidemia, and chronic obstructive pulmonary disease (COPD)". Also, the report of the incident says that "the patient woke up with severe shortness of breath unresponsive to albuterol inhalers"- indicating that the onset of the first symptoms of the acute physical distress appeared on their awakening, not in the immediate aftermath of marijuana ingestion.

The conclusion of the case incident study goes on to conclude that "In patients with low to absent risk for cardiovascular events, particularly pediatric and young adult patients, presenting with symptoms of MI/cardiac arrest, substance-induced (marijuana) MI should be suspected"- which, while possibly a warranted recommendation, has nothing to do with the case that was presented as possibly due to cannabis use. To my reading, the only evidence of a connection was the test result that " UDS was positive for marijuana"- but urine tests are not a reliable indicator of most recent use; they only indicate some amount of ingestion within the previous 7-30 days.

The report goes on to state that " Synthetic cannabinoids such as K2 and Spice are a rapidly emerging class of substances, usually undetectable on conventional urine drug screens (UDS), and becoming more widely available [1,2]." However, the report provides no context for this observation. It's possible that it was prompted by patient report, but if that was the case, no statements to that effect were included in the report.

The incident report goes on to state that "the patient was discharged eight days after admission on aspirin, statin, and diltiazem with close follow-up with cardiology. He was counseled to quit marijuana. Due to no other plausible etiology, the diagnosis of marijuana causing severe global coronary vasospasm was entertained with the possibility of a synthetic component."

I'm not sure how the clinicans arrived at the conclusion that the cardiac arrest could have "no other pluaible etiology", given the pre-existing medical conditions of already cited, of hpertension, hyperlipidemia, and COPD, based only on the UDS result of THC metabolites, which are not probative for recent use. I'm also unsure of why the study authors repeatedly brought up the synthetic THC analogs known as K2 and Spice, along with mentioning their undetectability by UDS unless there was some direct relevance to the case at hand that wasn't cited. It's unquestionable that the synthetic analogs have more dramatic effects and a more serious hazard profile in comparison with natural THC. But the case in question refers only to "marijuana."

It's also worth noting that of the total of 13 references cited by the study, only three were published prior to 2004.

The abstract of one of the references (11) made no mention of THC, marijuana, or cannabinoids; it appears to be a more generalized study of myocardial infarction cases, and the findings cited in the abstract are equivocal.

Another reference, from 1973, was a study of seven test subjects given oral THC at two different dose levels. At the higher dosage level, six of the subjects showed increased heartbeat- tachycardia- a well-known side effect of marijuana. Two of them showed ST and T wave changes, hardly an uncommon finding-- https://www.uptodate.com/contents/ecg-tutorial-st-and-t-wave-changes#! . One of the test subjects was shown to exhibit "premature ventricular contractions"- also known as "skipped beats", or a "flutterby." Not an optimal finding, but also one that is not uncommon in the total population- particularly in coffee drinkers, I note. None of the observed changes found in the seven subjects are commonly viewed as extraordinary or cause for alarm, in and of themselves. The study made no mention of myocardial complications or hypertensive effects.

The third reference cited from the 1970s consists only of a single excerpted paragraph from an article in Clinical Toxicology published in 1979- the reprint of the introduction to a referring to a single case of "pulmnary edeoma and myocradial infarction" connected by the authors with cannabis use. The original citation was found, copied, and republished online in 2008.

All of the other references cited are from 2004-2019.

I don't want to dismiss the possibility of cardiac complications from THC and marijuana out of hand. If there are authentic grounds for concern, I want to know about them. The THC strength of cannabis has increased markedly over the past 25 years- well beyond the limits achievable under natural conditions of cultivation. If that phenomenon has led to an increased hazard profile, I want to know the details. I think the recent increases in THC levels to above 15% and the concomitant absence of CBD has led to an increase in undesirable side effects in some respects.

But as far as cardiac complications, despite all of the pages devoted to the possibility in recent years, almost all of the clinical evidence I've read consists of series-of-one cases- and every few of those, at that. Reference to possible confounding factors has typically been cursory, or absent entirely.

I'm all in favor of researching cannabis for both its possible harms and its therapeutic benefits. But on this particular issue, I'm unimpressed by the strength of the evidence I've reviewed. I remain exceedingly skeptical that cannabis has a potential for cardiovascular harm that approaches that of tobacco, or even high doses of caffeine.

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Thanks for the comment. And yes, I agree that these case studies are often muddied (though not always).

But the reason it makes sense to me is because you see the same thing in the public health data. In cannbis users in general, you do see these increased signals for heart problems.

So while it's often impossible to tell for any one case study, it looks like it's true for some of them.

That being said, I think the heart risk is much less than for the other legal intoxicants of alcohol & tobaccoo, but it does appear to be there.

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Although that paper doesn't make much of a case for it, I think negative cardio effects are possible. But if so, I'd venture that it's most likely a recent side effect, due to (imo) pampering hybridized cannabis strains to produce THC levels far in excess of what they were before the late 1990s, which is when the super-strong indoor hydro hybrids began to take over the market. Possibly a result of the biphasic character of THC ingestion. I first heard the term "biphasic" in an article by Martin Lee, and it tracks well with my own experience. https://projectcbd.org/health/cbd-dosing/

The biphasic property of THC is its tendency of small amounts to produce a catalytic mind-altering effect with little body load, up to a point where larger amounts begin adding physical side effects, and the mind alteration has a heavier character that comes on much faster and can be disorienting, unpleasant, or even experienced as mentally unbalancing by new users and vulnerable temperaments.

When I first heard the saying "this isn't the same weed" back in the early 1990s, I scoffed; all sinsemilla from Humboldt or Hawaii meant was that two tokes did what it took an entire joint to achieve, back in the 1970s. (Still a little too powerful and hard to titrate, in my view.) By the end of the 1990s, I was taking half-tokes, and even cutting it with tobacco. The breeders and indoor cultivators had finally overdone it.

Since 2006, my consumption of cannabis/THC on an annual basis has varied between "total abstention", "rare", and "occasional." So I'm not expressing my skepticism of cardio problems as "denial" by a regular user. At 67, I'm so healthy it's bewildering. I just wish I could find some fresh terpene-rich Oaxacan semi-sinsemilla with a good cannabinoid balance and a THC level of 3.5%-5%. Outdoor grown, please; that's what the sun is there for. The legal market needs to grow out of its current overemphasis on THC potency. A take that I've expressed so many times that this screed looks like boilerplate to me.

I'm finding your Substack an invaluable resource, by the way. I had no idea that there was a one-stop clearinghouse for studies on cannabis and its chemical constituents. Lo and behold. And is this stuff ever being studied, nowadays! The research- once rudimentary- is beginning to show signs of maturity. Notwithstanding the bias that I occasionally detect with some studies, in the direction of "making cannabis wrong" as a priority.

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