Cannabis and Cardiovascular Health: 7 Things the JAMA Study Missed

What one vascular study reveals—and what it gets spectacularly wrong—about cannabis and your heart

What You’ll Learn in This Post:

✔︎ What the new JAMA Cardiology study actually found about cannabis and cardiovascular health and what it didn’t. (PDF here)

✔︎ Why “endothelial dysfunction” (“reduced FMD”) isn’t the same thing as proven cardiovascular harm

✔︎ What the real science says about edibles, THC, and blood vessel function

✔︎ How poor controls, small sample sizes, and serum confusion limit the study’s conclusions

✔︎ Where the study stumbles—methodologically and clinically

✔︎ Why these results say little about guided medical cannabis use

✔︎  How to read cannabis and cardiovascular health headlines with a sharper, smarter eye

The Headline Heard Round the Internet

If you scanned headlines last week, you probably saw something like:

“Cannabis Might Damage Your Blood Vessels, Even If You Don’t Smoke It.”

It’s the kind of punchy, panic-tinged news that practically writes itself—and sure enough, it’s already spreading fast. But if you’ve been around long enough to see how cannabis research is often covered, you’ve probably developed a familiar reflex: read past the headline.

Because beneath the sensationalism, this study actually tells a much quieter story. One about a small group of people, a few blood tests, a couple fancy-sounding biomarkers—and a sea of unanswered questions.

Still, the buzz is real. And for anyone using cannabis regularly—whether for anxiety, pain, sleep, or something else—it’s worth asking: Is there a real cardiovascular risk here? Or is this just another example of flashy data getting more attention than it deserves?

Let’s pull the curtain back on the actual science, separate correlation from causation, and unpack what this study shows—and where it veers into foggy territory.

What the Study Found (And Didn’t)

The research—published in JAMA Cardiology—looks at the relationship between cannabis and cardiovascular health, specifically measuring a marker called flow-mediated dilation (FMD). In plain terms, FMD is a way to test how well your blood vessels respond to changes in blood flow—a proxy for vascular health, not a clinical diagnosis.

Credit to the authors:

Leila Mohammadi, MD, PhD; Mina Navabzadeh, PharmD; Nerea Jiménez-Téllez, PhD; Daniel D. Han, BA; Emma Reagan, BA; Jordan Naughton, BA; Lylybell Y. Zhou, BS; Rahul Almeida; Leslie M. Castaneda, BA; Shadi A. Abdelaal, MD; Kathryn S. Park, BA; Keith Uyemura, BS; Christian P. Cheung, MSc; Mehmet Nur Onder; Natasha Goyal, MD; Poonam Rao, MD; Judith Hellman, MD; Jing Cheng, MD, MS, PhD; Joseph C. Wu, MD; Gregory M. Marcus, MD, MAS; Matthew L. Springer, PhD

The study had 3 groups:

• Regular cannabis smokers

• Regular cannabis edible users

• Non-users as controls

Researchers measured FMD and a few other cardiovascular markers, then collected serum (a component of blood) to test how it affected lab-grown endothelial cells.

Here’s what made headlines:

• Cannabis smokers had significantly lower FMD than non-users (6.0% vs. 10.4%, P = .004)

• Edible users had even lower FMD (4.6%, P = .003)

• Serum from smokers suppressed nitric oxide production in endothelial cells (1.1 vs. 1.5 nmol/L, P = .004)

• The FMD decline was described as dose-dependent with reported cannabis use (correlation coefficient r = –0.7)

If you’re a journalist, those numbers are catnip. If you’re a patient, they’re unsettling. And if you’re a clinician like me, they’re… well, interesting. But also incomplete.

These findings may suggest that cannabis and cardiovascular health have a more complicated relationship than some assume—but they don’t show causation. They don’t track clinical outcomes like heart attacks, strokes, or long-term cardiovascular disease. They don’t adjust for lifestyle, diet, BMI, lipids, exercise, or even sex. And while nitric oxide is an important signaling molecule, changes at the cellular level don’t automatically translate to health outcomes.

To their credit, the researchers used a combination of human participant data and in vitro (lab dish) testing. That’s good science. But it’s also important to remember: lab-grown cells don’t eat cheeseburgers, don’t stress about rent, and don’t take CBD oil before bed. The real world is messier than the Petri dish.

Decoding the Measurements: What FMD and PWV Actually Tell Us

So, what exactly are these vascular tests everyone’s talking about? And what do they really say about cannabis and cardiovascular health?

Let’s start with FMD, or flow-mediated dilation. Imagine a healthy blood vessel like a flexible garden hose—it expands and contracts depending on how much water (blood) is flowing through. FMD tests how well a vessel widens in response to increased blood flow. Lower FMD values suggest the vessel isn’t responding as well, which can be an early sign of vascular dysfunction. Think of it like a check engine light—not a diagnosis, but a nudge to look deeper.

Then there’s PWV, or pulse wave velocity. This one’s more like a long-term report card. It measures how fast pressure waves move through your arteries. The stiffer your arteries, the faster the wave travels—so higher PWV values typically indicate worse vascular health. But here’s the twist: in this study, PWV didn’t show meaningful differences between cannabis users and non-users.

That’s not a small detail.

If you’re going to make a case that cannabis and cardiovascular health are directly linked by way of vessel dysfunction, you’d expect both short-term and long-term vascular markers to tell the same story. But they didn’t. FMD dipped. PWV didn’t budge.

Why does that matter? Because FMD is sensitive—but not specific. It changes with things like sleep, caffeine, anxiety, hydration, recent meals, and yes, potentially cannabis. It’s a snapshot, not a story. PWV, on the other hand, reflects actual physical changes in the vessels—changes that accumulate over time and are much harder to influence with a few lifestyle quirks or daily habits.

That divergence raises a fair question: are we seeing a true signal of harm from cannabis? Or just noise?

If you’ve ever had a borderline cholesterol reading after a long vacation, you already know the answer: context matters.

 What the Study Gets Right

Let’s give credit where it’s due: not every study on cannabis and cardiovascular health goes this far in trying to measure something tangible. This one deserves recognition for attempting to do more than just collect self-reported surveys or make vague guesses based on insurance claims.

The authors used both human vascular testing and in vitro cellular assays. That’s not nothing. They looked at both cannabis smokers and edible users—an important distinction, since inhalation and ingestion affect the body very differently. And they didn’t just test people once—they took serum samples, exposed lab-grown endothelial cells to those samples, and looked for nitric oxide changes, which plays a key role in vessel health.

There’s also a fair effort to show a dose-response relationship. In other words, people who reported more frequent or intense cannabis use tended to show greater drops in FMD. That kind of pattern makes researchers—and reviewers—perk up. It suggests there may be a consistent effect worth examining.

And of course, any study that brings more attention to cannabis research helps chip away at decades of neglect. As we move toward fuller cannabis legalization and medical normalization, studies like this—warts and all—help make the case for deeper, better-funded science. That’s something every clinician, patient, and policymaker should want.

So yes, the methods are narrow. The sample is small. But the intent to explore real biological pathways deserves acknowledgment. We don’t need to agree with the conclusions to appreciate the effort.

Where the Study Falls Short

For all its ambition, this study has more blind spots than a rental SUV. When it comes to cannabis and cardiovascular health, conclusions only work if the road between cause and effect is clearly paved—and here, it’s full of potholes.

Let’s start with size: 55 participants. That’s not even enough to field a decent intramural soccer league, much less draw broad conclusions about millions of cannabis users. And of the 15 people in the edible group? Only one was a woman. That’s a staggering gender gap for a study trying to generalize about cardiovascular function.

Then there’s the serum. Researchers used whole serum—unfiltered. So, whatever was in those participants’ bloodstreams at the time (stress hormones, caffeine metabolites, inflammatory cytokines, dietary fats, unknown supplements, even lingering effects from sleep deprivation) could’ve influenced what happened in those endothelial cell cultures. That makes it impossible to say whether cannabis was the active ingredient—or just another part of the biochemical soup.

Missing controls are another issue. There were no adjustments for BMI, blood pressure, cholesterol, hormone levels, or lifestyle habits like exercise, sleep, or diet. That matters. These are not minor variables—they’re the heart of cardiovascular risk. Skipping them and pinning the results on cannabis is like blaming the sun for your sunburn without asking if you were wearing SPF 4 and holding a magnifying glass.

Even the language of “dose response” deserves scrutiny. The study assumes that the body’s internal response to cannabis is linear and identical from person to person. But we know that’s not how endocannabinoid systems work. Receptor density, metabolism, tolerance, product types—all of these shape how cannabis behaves in the body. Without accounting for that diversity, dose-response becomes a shaky claim.

And finally, the biggest gap: no clinical outcomes. No heart attacks, no strokes, no real-world disease endpoints. Just surrogate markers, mostly from lab tests. It’s like evaluating a new diet based solely on what’s in your fridge—not how your body actually feels, functions, or flourishes.

So yes, the findings are provocative. But are they conclusive? Not even close.

🔍 What Might Really Be Going On Here?

So, if this study isn’t the smoking gun for cannabis and cardiovascular health, what is it actually showing?

It might just be capturing the messy reality of real-world life—through a pretty narrow lens. The cannabis users in the study weren’t under clinical guidance. We don’t know what strains they used, how they dosed, how often they consumed, or why. Were they stress-eating THC gummies after midnight? Puffing through burnout while working two jobs? Self-medicating anxiety, insomnia, trauma?

Each of those scenarios could affect the vascular system. Each could alter serum contents. And none of them are controlled for here.

Then there’s diet. Someone eating processed food, skipping hydration, or carrying chronic inflammation will absolutely show different FMD values—regardless of cannabis use. Same goes for acute stress, poor sleep, or high caffeine intake. These are everyday, invisible variables that affect endothelial function just as much—if not more—than cannabinoids do.

Another likely factor: metabolic individuality. Our endocannabinoid systems are as unique as fingerprints. Two people could take the same dose of THC and experience wildly different effects on mood, blood vessels, or nitric oxide levels. Without filtering for these physiological differences, the study treats all cannabis users as interchangeable—which they aren’t.

Even more subtle: if some of the participants were former tobacco users (as several were), we can’t be sure that cannabis is the main actor in their vascular story. Tobacco’s effects linger—especially in the endothelium. And mixing smoking histories muddies the water.

Even without tobacco in the picture, it’s difficult to isolate cannabis as the sole vascular actor. Variables like diet, stress, sleep deprivation, or unreported substance use could all influence endothelial outcomes—and serum testing can’t fully disentangle those threads.

So while this paper tries to frame a clean causal link, the truth is messier. We’re likely looking at a swirl of overlapping behaviors and biologies—poorly filtered, loosely measured, and conveniently attributed to one green scapegoat.

What It Means for Medical Cannabis Patients

If you’re a medical cannabis patient—or care for someone who is—this study might sound a little unsettling. But here’s the context you didn’t get in the headlines: this research says very little about how cannabis works when it’s used thoughtfully, therapeutically, and under clinical supervision.

The participants in this study weren’t following any guided treatment plan. There were no tracked doses, no cannabinoid ratios, and no attention to timing, goals, or concurrent medications. That matters. Because the way cannabis behaves in a weekend smoker hitting mystery flower from a friend’s vape is not how it behaves in a patient using 1:1 tinctures before bed to manage anxiety or taper off opioids.

When used with care, cannabis can be gentle on the body and supportive of the cardiovascular system—especially when it replaces more harmful substances like alcohol, tobacco, or sedating pharmaceuticals. But this study doesn’t measure that. It doesn’t explore what happens when you use balanced formulations, take breaks to reset tolerance, or match cannabinoid profiles to patient goals. It looks at a narrow slice of unregulated, unguided use and draws wide conclusions.

That’s why the conversation about cannabis and cardiovascular health needs nuance—and why physician involvement is so critical. We need more research, yes—but also more real-world data, more physiological context, and more honesty about how lifestyle, stress, and comorbidities factor into the equation.

The takeaway for patients? Don’t panic. Don’t overreact. And don’t confuse lab-based noise with personalized clinical guidance. The best outcomes still come from knowing yourself, knowing your products, and having someone knowledgeable in your corner.

Why Studies Like This Still Matter

Despite its flaws, this study isn’t worthless. In fact, it might be just what we need—if not for the reasons it thinks.

Any research that probes the relationship between cannabis and cardiovascular health adds to the bigger picture. We need better data. We need sharper tools. And we need to keep asking hard questions—even when the answers are fuzzy. This study raises a legitimate one: could certain patterns of cannabis use affect early vascular function? Maybe. But that’s a question, not a verdict.

What matters is what we do next. Sensational headlines don’t help patients—or clinicians. They don’t guide safer use. They don’t clarify risk. They just amplify uncertainty and make it harder for thoughtful voices to be heard. But if studies like this spark better research design, more transparent data, and a push for smarter clinical tools? Then we all benefit.

In that sense, this study is a kind of progress. A flawed first draft in a long overdue conversation. One that needs less noise and more nuance.

The Real Takeaway: Less Fear, More Context

Cannabis and cardiovascular health deserve real study—not just real headlines. This paper flirts with that mission, but misses the mark on clarity, scope, and causality. It asks a good question, but answers it in shorthand, with too many assumptions and too little precision.

Here’s the bottom line: A modest drop in a surrogate marker like FMD—without clinical events, without multivariable controls, and without a purified mechanism—doesn’t equal danger. It equals a data point. One that belongs in a much larger, more human conversation.

For patients, the message isn’t “cannabis damages your heart.” The message is: We’re still learning. And we need better research—more representative, more personalized, more nuanced. Because the real-world impacts of cannabis depend on who’s using it, how it’s used, and why.

So don’t let this paper scare you. Let it sharpen your thinking. Ask questions. Demand evidence. And above all, don’t mistake correlation for conclusion—especially when the real conclusions deserve a bit more care.

Related Work (similar past article critiques): 

Understanding Cannabis Cardiovascular Risk: My Response to Recent Claims (November 2023)

Understanding the Limitations of “Association of Cannabis Use With Cardiovascular Outcomes Among US Adults” (March 2024)

5 Alarming Truths About Cannabis and Heart Health (March 2025)

External Work – Related

American College of Cardiology Press Release Statement

Nature Reviews: Cardiology, The relationship between cannabis and cardiovascular disease: clearing the haze

NIH Public Statement

📎 Editorial Addendum (June 2025)

Since the publication of this article, one of the study authors reached out with clarifying points, including a correction regarding participant history: none of the study participants were former tobacco smokers. That line has now been removed from this post to reflect the accurate dataset.

Additional concerns were raised about interpretations presented here—for instance, the assumption that the authors claimed a linear and uniform physiological response to cannabis, or the critique that use of whole serum obscures whether cannabis was the active agent. These points reflect interpretation rather than error and may stem from differing views on study design and intention. The authors also noted that although no statistical adjustments were made for BMI, blood pressure, or cholesterol, there were no appreciable differences in these variables between study groups.

These clarifications do not alter the broader clinical questions raised, but they do underscore the importance of precision in scientific dialogue. I appreciate the constructive exchange.