Nicotine, Myocarditis and Heart Rhythm: Dr. Ardis on the Heart

Table of Contents

1. 1. What Dr. Ardis Says
2. 2. Myocarditis and Heart Rhythm: A Plain Primer
3. 3. The Cholinergic Anti-Inflammatory Pathway
4. 4. Nicotine in Viral Myocarditis: The Mouse Studies
5. 5. Nicotine in Autoimmune Myocarditis
6. 6. Vagal Tone, Vagus Stimulation and Atrial Fibrillation
7. 7. Nicotine’s Own Effects on the Heart
8. 8. Nicotine Through the Skin: Tobacco Leaves and Water
9. Safety Notes
10. Dr. Ardis’s Own Work
11. Key Research Papers
12. Connections
13. Featured Videos

1. What Dr. Ardis Says

Dr. Ardis set this out in a 2025 podcast appearance (Culture Apothecary) and in his book Moving Beyond the COVID-19 Lies: Restoring Health and Hope for Humanity. His statements on the heart come in two places.

Myocarditis: three days of nicotine, a healed heart by day 14

Speaking of the nicotine patch — for adults, he describes a 7 mg nicotine patch placed between the shoulder blades — Dr. Ardis states that nicotine is “also a cure for myocarditis in three days, and it actually reverses all the scarring on the heart caused by myocarditis by day 14.” He adds that the nicotine is needed only for those three days: “But you only have to use the nicotine for three days. … By day 14, the whole heart’s cured.”

A-fib and tachycardia after vaccination: the tobacco-leaf foot soak

Asked which single nicotine study he would most want funded if Robert F. Kennedy Jr., as Secretary of Health and Human Services, backed nicotine research, Dr. Ardis answers that the first would be heart disease. He describes people who developed atrial fibrillation after COVID-19 vaccination and could not get their heart rhythm back to normal. His method: steep a tobacco leaf in water, then put the feet in that water. He states that within 5 minutes the tachycardia disappears, and that the A-fib has not come back in the couple of years he has been watching:

A-fib disappears like forever, or forever now that we’ve seen for the last couple years, it just didn’t come back. Nicotine is releasing poisons out of the heart and correcting arrhythmias.

He calls this “really incredible to actually watch,” and says studies of myocarditis, tachycardia and A-fib “would be miraculous studies.” These are what he would ask Secretary Kennedy to encourage the CDC, the NIH and HHS to investigate.

His position in brief

1. Nicotine resolves myocarditis in three days of use.
2. Scarring of the heart from myocarditis is reversed by day 14, with nicotine needed only for the first three days.
3. Post-vaccination tachycardia disappears within 5 minutes of a foot soak in tobacco-leaf water, and A-fib has not returned over the following couple of years.
4. The mechanism, in his words: nicotine “releasing poisons out of the heart and correcting arrhythmias.”
5. Heart disease — myocarditis, tachycardia and A-fib — is the first area he would ask the CDC, NIH and HHS to study.

His wider framework — that the COVID-19 spike protein acts on nicotinic acetylcholine receptors and that nicotine holds those receptors first — is set out on the Nicotinic Acetylcholine Receptors and Cobra Venom and Nicotine pages.

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2. Myocarditis and Heart Rhythm: A Plain Primer

Myocarditis means the heart muscle itself is inflamed. The commonest causes are viruses — in laboratory research the classic one is coxsackievirus B3, an enterovirus that infects heart muscle cells. Inflammation brings in immune cells and chemical messengers called cytokines (TNF-α, IL-1β, IL-6, IL-17A and others). In small amounts they fight infection; in excess they injure the very muscle they are protecting. When inflamed muscle dies it is replaced by fibrosis — scar tissue that does not contract — and that scarring is what can leave a heart weaker after the inflammation has gone. Myocarditis is also a recognised, mostly short-lived reaction after mRNA COVID-19 vaccination, reported most often in young men; the site’s Myocarditis page covers causes, tests and treatment.

Heart rhythm is set by the heart’s own pacemaker, the sinus node, and then tuned by two branches of the autonomic (automatic) nervous system:

• The sympathetic branch — the “accelerator” — releases noradrenaline and speeds the heart.
• The parasympathetic branch — the “brake” — works mainly through the vagus nerve, which releases acetylcholine and slows the heart. “Vagal tone” is shorthand for how firmly that brake is being held, and heart-rate variability is one common way of estimating it.

Tachycardia is a resting heart rate above about 100 beats a minute. Atrial fibrillation is a disorganised rhythm in the upper chambers that makes the pulse irregular; it can come and go (“paroxysmal”) or persist. An imbalance between the two autonomic branches and inflammation in heart tissue are both studied as contributors to A-fib, which is why the nervous system and the immune system meet in the research below.

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3. The Cholinergic Anti-Inflammatory Pathway

The research thread most often linked to nicotine and inflammation began at the Feinstein Institute in New York with Kevin Tracey’s group.

• Borovikova et al., 2000 (Nature). Acetylcholine, the vagus nerve’s main chemical messenger, lowered the release of the inflammatory cytokines TNF, IL-1β, IL-6 and IL-18 — but not the anti-inflammatory IL-10 — from human immune cells (macrophages) stimulated with bacterial endotoxin in culture. In rats given a lethal dose of endotoxin, direct electrical stimulation of the vagus nerve lowered TNF in the liver and blood and prevented shock. The authors described this as a previously unrecognised parasympathetic anti-inflammatory pathway.
• Wang et al., 2003 (Nature). The same group identified the receptor on the immune cell that receives the signal: the α7 subunit of the nicotinic acetylcholine receptor (α7 nAChR). Vagus-nerve stimulation lowered TNF production in ordinary mice but not in mice bred without α7. Because nicotine also switches on α7, this paper is the reason nicotine became a laboratory tool for activating the pathway.

The name “cholinergic anti-inflammatory pathway” comes from these papers: cholinergic means acting through acetylcholine. The pathway has since been studied in sepsis, arthritis, bowel inflammation and heart injury. The mouse studies of myocarditis in the next two sections were designed explicitly as tests of it.

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4. Nicotine in Viral Myocarditis: The Mouse Studies

A cardiology group at the Second Affiliated Hospital of Wenzhou Medical University in China (Li Yue-Chun, Li-Sha Ge, Cheng Zhi and colleagues) published a series of experiments in which BALB/c mice were infected with coxsackievirus B3 and given nicotine. In most of them a second group received methyllycaconitine (MLA), a drug that blocks α7, as a mirror-image test. All of this work is in mice; no human trial of nicotine for myocarditis was found in this review.

• Cheng et al., 2014 (PLoS One). In infected mice, nicotine improved survival, lessened the heart-muscle lesions seen under the microscope and lowered TNF-α and IL-6. Blocking α7 with MLA did the opposite: lower survival, worse lesions, higher cytokines. Nicotine raised phosphorylated STAT3, a signalling protein downstream of α7. The authors concluded that nicotine protected the mice from coxsackievirus B3 myocarditis through α7.
• Li-Sha et al., 2015 (Scientific Reports) — the dose study. Nicotine was injected at 0.1, 0.2 or 0.4 mg/kg three times a day for 7 or 14 consecutive days. Survival on day 14 rose with the dose and was markedly higher at 0.2 and 0.4 mg/kg than in untreated infected mice. The highest dose reduced heart inflammation and improved left-ventricular pumping function, and TNF-α, IL-1β, IL-6 and IL-17A fell in step with the dose. (A published erratum to this paper exists.)
• Li-Sha et al., 2016 (Life Sciences). Nicotine (0.4 mg/kg three times a day for 7 or 14 days) raised survival, lessened inflammation and improved left-ventricular function compared with MLA, and lowered TNF-α, IL-1β, IL-6 and IL-17A. The authors also reported that nicotine had no significant antiviral or antioxidant effect in these mice: the virus was not reduced; the inflammatory response was.
• Li-Sha et al., 2017 (Frontiers in Pharmacology). Cutting the right vagus nerve in the neck (vagotomy) made viral myocarditis worse — more lesions, more cytokines, weaker pumping — and giving nicotine reversed those changes. The authors read this as showing that the vagus nerve restrains inflammation in viral myocarditis, and that nicotine acts on α7 directly, even without an intact vagus nerve.
• De-Pu et al., 2018 (Virulence). Looking at which immune cells were shifted, nicotine increased the proportion of Th2 and regulatory T cells and decreased the inflammatory Th1 and Th17 cells in the spleen of infected mice, with less heart damage and cell infiltration. MLA had the opposite effect.

How the studies were set up. In these experiments nicotine was given by injection several times a day for 7 or 14 consecutive days, beginning around the time of infection, and survival, heart inflammation, cytokines and pumping function were measured at about day 7 and day 14. The specific study behind a three-day course and scar reversal by day 14 is not identified here; related published work is listed below.

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5. Nicotine in Autoimmune Myocarditis

Not all myocarditis is viral. In autoimmune myocarditis the immune system attacks the heart’s own proteins. A Heidelberg group tested the cholinergic pathway in this form.

• Leib et al., 2011 (Circulation Research). A/J mice were immunised with cardiac troponin I, a heart protein, to provoke autoimmune myocarditis. Nicotine was given in drinking water at two concentrations (12.5 or 125 mg/L) for either 3 days or 21 days after the first immunisation. Untreated mice developed extensive heart inflammation and fibrosis with high IL-6 and TNF-α. Oral nicotine reduced inflammation in the heart muscle, lowered IL-6 and TNF-α, and turned down a set of inflammatory chemokines and their receptors. It also lowered several proteins commonly involved in heart failure (matrix metalloproteinase-14, natriuretic peptide precursor B, TIMP-1 and osteopontin). Neostigmine, a drug that raises acetylcholine by another route, did not change the course of the disease.

This is the one study found here whose design includes a three-day nicotine arm; the abstract reports the nicotine-treated groups together and does not single out the three-day group’s results. It is a model of autoimmune, not post-vaccination, myocarditis, and it was carried out in mice.

Reviews that gather this work include Cheng, Li-Sha and Yue-Chun (2016), “Autonomic Nervous System in Viral Myocarditis: Pathophysiology and Therapy,” and Lu and Wu (2021), “Cholinergic modulation of the immune system — a novel therapeutic target for myocardial inflammation.”

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6. Vagal Tone, Vagus Stimulation and Atrial Fibrillation

The closest human research to Dr. Ardis’s A-fib observation tests the same nerve pathway with electricity rather than nicotine. A branch of the vagus nerve reaches the skin of the outer ear at the tragus (the small flap in front of the ear canal), so a mild current there stimulates the vagus without surgery. A group at the University of Oklahoma tested this “low-level tragus stimulation” (LLTS).

• Stavrakis et al., 2015 (Journal of the American College of Cardiology). Forty patients with paroxysmal A-fib who were having an ablation procedure were randomised to 1 hour of tragus stimulation (20 Hz) or sham. A-fib was then induced by pacing under anaesthesia. With stimulation, the induced A-fib lasted on average 6.3 minutes less than at baseline, and its cycle length lengthened; neither changed in the sham group. Blood TNF-α and C-reactive protein fell only in the stimulation group.
• Stavrakis et al., 2020 (TREAT AF, JACC: Clinical Electrophysiology). A double-blind, sham-controlled trial in 53 people with paroxysmal A-fib: an ear clip on the tragus (active) or the earlobe (sham) for 1 hour a day for 6 months. At 6 months the median A-fib burden, measured by two-week continuous ECG monitoring, was 85% lower in the active group than the sham group, and TNF-α was 23% lower. Heart-rate variability changed with active stimulation, and no device-related side effects were observed.

These trials show A-fib being reduced over an hour (in the laboratory) and over months (at home) by stimulating the vagus nerve, together with a fall in inflammatory markers — the same nerve-to-immune link described in section 3. They used electrical stimulation, not nicotine, and they did not study post-vaccination A-fib. No published study of a tobacco-leaf foot soak for A-fib or tachycardia was found; the specific observations Dr. Ardis describes are his own clinical reports.

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7. Nicotine’s Own Effects on the Heart

Nicotine acts on more than one kind of nicotinic receptor. Besides α7 on immune cells, it stimulates receptors in the nerve relay stations (ganglia) of both autonomic branches and in the adrenal glands. The net effect on the circulation, as summarised by Neal Benowitz and Adam Burbank of the University of California, San Francisco (Trends in Cardiovascular Medicine, 2016), is mostly sympathetic: nicotine releases noradrenaline and adrenaline, which raises heart rate, raises blood pressure and increases the force of the heart’s contraction, while narrowing some blood vessels, including in the skin. Their review concludes that the risks of nicotine without tobacco smoke are low compared with smoking, but are still of concern in people with cardiovascular disease.

The largest randomised safety trial of the nicotine patch in heart patients is Joseph et al., 1996 (New England Journal of Medicine): 584 smokers with cardiovascular disease at 10 Veterans Affairs medical centres were given a 10-week course of transdermal nicotine or a placebo patch. Over 14 weeks, a serious event (death, heart attack, cardiac arrest, or hospital admission for worsening angina, arrhythmia or heart failure) occurred in 5.4% of the nicotine group and 7.9% of the placebo group, a difference that was not statistically significant. The authors concluded that transdermal nicotine did not significantly increase cardiovascular events in these high-risk outpatients. The trial enrolled people who were also smoking less or quitting, and it measured safety, not a treatment effect on rhythm.

Put plainly: nicotine at the receptors on immune cells is studied as an anti-inflammatory; nicotine at the receptors in nerves and adrenal glands is a stimulant that speeds the heart. Both happen at once, and how they balance depends on dose, route and the person.

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8. Nicotine Through the Skin: Tobacco Leaves and Water

Nicotine dissolves in water and passes through skin — the property every nicotine patch relies on. The best-documented example of skin absorption from the tobacco plant itself is an occupational illness called green tobacco sickness, seen in workers who handle wet, uncured tobacco leaves.

• Gehlbach et al., 1974 (JAMA) described “green-tobacco sickness” as an illness of tobacco harvesters. The same group later reported (1979, Archives of Environmental Health) that protective clothing reduced nicotine absorption in harvesters.
• Arcury et al., 2008 (American Journal of Industrial Medicine) studied 304 Latino farmworkers in North Carolina. Green tobacco sickness, which the authors note affects about a quarter of tobacco workers, was present in 18.4%. Workers with a rash were about three times as likely to have it (multivariate odds ratio 3.30), and itch and small wounds were also linked — broken or irritated skin lets more nicotine through.

The illness typically brings nausea, vomiting, dizziness, headache and weakness, and can include changes in heart rate and blood pressure; it is most common when leaves are wet with dew or rain, because water carries nicotine off the leaf and onto the skin. A foot soak in tobacco-leaf water is, in physiological terms, a deliberate version of the same route. How much nicotine such a soak delivers has not been measured in any study found here, and it would vary with the leaf, the water, the time, the temperature and the skin.

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Safety Notes

• Children and pets. Nicotine is poisonous in small amounts to young children and to dogs and cats. Keep patches — new and used — tobacco leaves and any tobacco-steeped water out of reach. Fold used patches sticky-side in before throwing them away. If a child or pet swallows or chews nicotine, call a poison centre (in the US, 1-800-222-1222) or a vet at once.
• Who should not use nicotine without their own doctor’s direct supervision: pregnancy and breastfeeding; a recent heart attack, unstable angina, a serious or uncontrolled arrhythmia, or uncontrolled high blood pressure; and anyone with other conditions listed on the protocol page.
• Heart rhythm problems need a diagnosis. A new fast or irregular heartbeat, chest pain, fainting or breathlessness can be a medical emergency; A-fib also raises the risk of stroke, which is managed separately from the rhythm itself.
• Skin exposure adds up. As green tobacco sickness shows, wet tobacco leaf on skin delivers nicotine with no fixed dose. Nausea, vomiting, dizziness, headache, sweating or a pounding heart are signs of too much nicotine; remove the source and wash the skin.

The full list of contraindications, interactions and warning signs is on the Nicotine Patch Protocol page.

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Dr. Ardis’s Own Work

• Moving Beyond the COVID-19 Lies: Restoring Health and Hope for Humanity — his 2024 book, where the nicotine framework is set out at length.
• Dr. Bryan Ardis Hub — the wing’s main page: his nicotine hypothesis, snake-venom theory and the pages built around them.
• The Dr. Ardis Show — official site

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Key Research Papers

1. Borovikova LV, Ivanova S, Zhang M, Yang H, et al. (2000). Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin. Nature. — PubMed PMID: 10839541
2. Wang H, Yu M, Ochani M, Amella CA, et al. (2003). Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammation. Nature. — PubMed PMID: 12508119
3. Cheng Z, Li-Sha G, Jing-Lin Z, Wen-Wu Z, et al. (2014). Protective role of the cholinergic anti-inflammatory pathway in a mouse model of viral myocarditis. PLoS One. — PubMed PMID: 25396421
4. Li-Sha G, Jing-Lin Z, Guang-Yi C, Li L, et al. (2015). Dose-dependent protective effect of nicotine in a murine model of viral myocarditis induced by coxsackievirus B3. Sci Rep. — PubMed PMID: 26507386
5. Li-Sha G, Jing-Lin Z, Li L, Guang-Yi C, et al. (2016). Nicotine inhibits the production of proinflammatory cytokines of mice infected with coxsackievirus B3. Life Sci. — PubMed PMID: 26851533
6. Li-Sha G, Xing-Xing C, Lian-Pin W, De-Pu Z, et al. (2017). Right Cervical Vagotomy Aggravates Viral Myocarditis in Mice Via the Cholinergic Anti-inflammatory Pathway. Front Pharmacol. — PubMed PMID: 28197102
7. De-Pu Z, Li-Sha G, Guang-Yi C, Xiaohong G, et al. (2018). The cholinergic anti-inflammatory pathway ameliorates acute viral myocarditis in mice by regulating CD4(+) T cell differentiation. Virulence. — PubMed PMID: 30176160
8. Leib C, Göser S, Lüthje D, Öttl R, et al. (2011). Role of the cholinergic antiinflammatory pathway in murine autoimmune myocarditis. Circ Res. — PubMed PMID: 21597011
9. Stavrakis S, Humphrey MB, Scherlag BJ, Hu Y, et al. (2015). Low-level transcutaneous electrical vagus nerve stimulation suppresses atrial fibrillation. J Am Coll Cardiol. — PubMed PMID: 25744003
10. Stavrakis S, Stoner JA, Humphrey MB, Morris L, et al. (2020). TREAT AF (Transcutaneous Electrical Vagus Nerve Stimulation to Suppress Atrial Fibrillation): A Randomized Clinical Trial. JACC Clin Electrophysiol. — PubMed PMID: 32192678
11. Benowitz NL, Burbank AD (2016). Cardiovascular toxicity of nicotine: Implications for electronic cigarette use. Trends Cardiovasc Med. — PubMed PMID: 27079891
12. Joseph AM, Norman SM, Ferry LH, Prochazka AV, et al. (1996). The safety of transdermal nicotine as an aid to smoking cessation in patients with cardiac disease. N Engl J Med. — PubMed PMID: 8943160
13. Gehlbach SH, Williams WA, Perry LD, Woodall JS (1974). Green-tobacco sickness. An illness of tobacco harvesters. JAMA. — PubMed PMID: 4479133
14. Arcury TA, Vallejos QM, Schulz MR, Feldman SR, et al. (2008). Green tobacco sickness and skin integrity among migrant Latino farmworkers. Am J Ind Med. — PubMed PMID: 18181197

PubMed Topic Searches

1. PubMed: Nicotine and viral myocarditis
2. PubMed: Cholinergic anti-inflammatory pathway in myocarditis
3. PubMed: Vagus nerve stimulation and atrial fibrillation
4. PubMed: Green tobacco sickness

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Connections

• Dr. Bryan Ardis Hub — the wing’s main page: his nicotine hypothesis and snake-venom theory
• Nicotine Patch Protocol — dosage, placement, tapering and the full contraindications list
• Nicotinic Acetylcholine Receptors — the receptor pharmacology behind his hypothesis, α7 included
• Vaccine-Injury Recovery — his protocol for post-vaccination symptoms, myocarditis among them
• The Nicotine Hypothesis — nicotine as an anti-inflammatory, decoupled from smoke
• Cobra Venom and Nicotine — his account of the receptor venom and nicotine share
• Nicotine Patches for Long COVID — the 2023 case reports he cites
• Myocarditis — the site’s full page on heart-muscle inflammation
• Atrial Fibrillation — causes, stroke risk and treatment
• Arrhythmia — the heart-rhythm disorders in one place
• Vagus Nerve and Autonomic Retraining — vagal tone and tachycardia in POTS
• The Nicotine Patch: Skin to Bloodstream to Receptor (Animation) — nicotine moving from patch through skin into blood

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