Last year, I wrote an article for KevinMD defending nicotine. My argument was straightforward: Nicotine had been unfairly demonized because of its association with cigarettes, and we’d largely ignored its potential therapeutic benefits. I still believe that.
But a few weeks ago, I underwent a coronary CT angiogram and discovered that I have coronary artery disease. Suddenly, my interest in nicotine was no longer entirely academic.
I enjoy nicotine. Not cigarettes. I don’t smoke or vape. I’m talking about an occasional 4 mg nicotine pouch, usually before playing tennis or paddle. I like the mild stimulation, the increased alertness, and perhaps the little psychological edge it gives me before a competitive game. It’s a small pleasure, but one I genuinely enjoy.
The day I learned I had coronary disease, I stopped using it. Immediately. I didn’t spend hours reviewing the literature or calculating risk. I just stopped.
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Which is interesting, because I’ve spent much of my career telling patients to make medical decisions based on evidence rather than fear. Apparently, that’s easier advice to give than to follow.
After the initial shock of my diagnosis wore off, I began wondering whether I actually needed to give up nicotine. Was there convincing evidence that an occasional pouch could precipitate a coronary event? Or was I reacting to the same assumptions about nicotine that I’d challenged in my original article? So I went back to the literature.
The problem with nicotine’s reputation
Nicotine has spent more than a century traveling in terrible company. Cigarette smoke contains carbon monoxide, oxidants, aldehydes, fine particulates, and thousands of chemicals implicated in vascular injury, inflammation, and thrombosis.
Nicotine is what keeps people smoking. But that doesn’t mean it’s responsible for all the cardiovascular damage associated with cigarettes.
I made the analogy in my earlier article that if caffeine had been delivered exclusively through a dirty pipe, we’d probably have spent decades warning people about the dangers of caffeine. It’s an imperfect analogy, but I still think it makes the point.
We’ve become so accustomed to associating nicotine with smoking that we sometimes discuss their cardiovascular effects almost interchangeably. They’re not interchangeable.
Nicotine certainly has physiological effects. It stimulates the sympathetic nervous system, increases catecholamine release, and can transiently elevate heart rate, blood pressure, and myocardial oxygen demand. It can also influence coronary vascular resistance.
But what I wanted to know was whether these physiological changes actually translate into more heart attacks or cardiovascular deaths when nicotine is delivered without cigarette smoke. That turns out to be a surprisingly difficult question to answer.
What the studies actually show
One small study examined the effects of nicotine gum in 17 patients with established coronary artery disease. Using quantitative coronary angiography, investigators found no measurable narrowing of coronary stenoses or adjacent normal segments after nicotine administration.
Another study administered a 4 mg nicotine tablet to 12 smokers at elevated cardiovascular risk and measured myocardial blood flow using PET imaging. Systolic blood pressure increased by approximately 5 mmHg and heart rate by 2 beats per minute, but resting myocardial perfusion regulation remained intact.
An earlier study in 8 healthy nonsmokers suggested that nicotine could modestly interfere with the increase in coronary blood flow needed to meet greater myocardial oxygen demand.
These aren’t large or definitive studies. But they certainly don’t establish that occasional low-dose nicotine causes clinically meaningful coronary ischemia.
What about actual cardiovascular outcomes? The EAGLES randomized trial enrolled more than 8,000 smokers and compared nicotine replacement therapy with varenicline, bupropion, and placebo. Major cardiovascular events occurred in fewer than 0.5 percent of participants, without a statistically significant difference among groups.
A 2023 systematic review examining 42 randomized studies similarly found no statistically significant increase in myocardial infarction, stroke, cardiovascular death, or arrhythmia among participants receiving nicotine.
There are limitations, of course. Many participants were smokers who had developed nicotine tolerance. Serious cardiovascular events were uncommon. And nicotine replacement trials weren’t designed to answer questions about occasional recreational use in people with established coronary disease.
Long-term observational studies of Swedish snus have also raised concerns about cardiovascular mortality. But snus contains other tobacco constituents, making it difficult to attribute those associations specifically to nicotine.
The literature is neither a clean bill of health nor the indictment I expected. We simply don’t have adequately powered cardiovascular outcome studies telling us whether an occasional 4 mg nicotine pouch increases the risk of myocardial infarction or stroke.
That’s not proof of safety. But it isn’t proof of danger, either.
When the physician becomes the patient
I’ve been a practicing internist and lipidologist for more than thirty-five years. I’ve watched medicine repeatedly mistake plausible mechanisms and changes in surrogate markers for proof of clinical benefit or harm. I’ve made some of those mistakes myself. Now I’m trying to avoid making another one, this time with my own health.
I understand perfectly well why someone with coronary disease might choose to avoid nicotine. It’s not essential. It’s addictive. It increases sympathetic activity, and we don’t know whether occasional use during vigorous exercise has meaningful cardiovascular consequences. Those are legitimate considerations.
But the patient in me wants something more specific. If I’m going to abandon something I enjoy, I’d like to know why.
Show me the evidence that an occasional nicotine pouch meaningfully increases my cardiovascular risk. Not simply that nicotine raises blood pressure for a short time or changes coronary vascular tone under laboratory conditions. Show me the outcomes.
And if we don’t have those data, let’s at least acknowledge that uncertainty rather than automatically converting it into a recommendation based on fear.
This is especially relevant because nicotine has potentially useful pharmacological properties. Studies have demonstrated modest improvements in certain measures of attention and cognitive performance, and small trials have explored its use in ADHD, depression, and cognitive impairment.
These aren’t established indications. I’ve occasionally used nicotine gum or lozenges off-label in carefully selected patients, but I don’t regard nicotine as a miracle drug or something everyone should start taking. Dependence remains a legitimate concern. Still, its potential benefits deserve the same scientific scrutiny as its potential harms.
So what have I decided?
When I received my coronary diagnosis, I immediately stopped using nicotine. That was an emotional decision, not an evidence-based one.
Having now spent time reviewing the literature, I’ve decided to resume using it occasionally, in moderation. Not because I’m convinced it’s harmless. I’m not.
I recognize that the studies don’t adequately address someone exactly like me: a 64-year-old man with coronary disease who uses a nicotine pouch before spending 90 minutes playing a vigorous racket sport. And I recognize that a small pleasure may not be worth even an uncertain additional cardiovascular risk.
But I’ve also concluded that the available evidence doesn’t justify treating an occasional 4 mg nicotine pouch as though I’d just smoked a cigarette.
I’m taking my coronary disease seriously. I’m treating my risk factors, staying physically active, and making changes supported by good clinical evidence. I also intend to continue enjoying my life. For me, that means occasionally using nicotine without spending the next 90 minutes on the court worrying that I’ve just invited a heart attack.
This is a personal decision, not a recommendation that patients with coronary disease should begin using nicotine. I may change my mind as better evidence becomes available. But I don’t want fear to make the decision for me.
I’ve spent thirty-five years encouraging patients to understand risks, weigh benefits, and make informed choices. Now I’m discovering how much harder that becomes when the patient is me.
Larry Kaskel is an internist and “lipidologist in recovery” who has been practicing medicine for more than thirty-five years. He runs a concierge practice in the Chicago area and serves on the teaching faculty at the Northwestern University Feinberg School of Medicine. He is also affiliated with Northwestern Lake Forest Hospital.
Before podcasts were even a thing, Dr. Kaskel hosted Lipid Luminations on ReachMD, building a library of more than four hundred shows featuring thought leaders in cardiology, lipidology, and preventive medicine.
He is the author of Dr. Kaskel’s Living in Wellness, Volume One: Let Food Be Thy Medicine, a book that blends evidence-based medicine with practical strategies for a longer healthspan. His current work focuses on rethinking the cholesterol hypothesis and exploring the infectious roots of atherosclerosis. More information is available at larrykaskel.com.
