Nicotine Risk-Benefit Analysis with Low-Dose Patches
Risk-Benefit Analysis in Long-COVID and other complex diseases -- Hope vs Innaction
Each person needs to know the risks and benefits of any intervention.
I appreciate the concern for safety — it’s important, especially in a community where people have already endured so much medical neglect. But I think your stance of taking zero risks is missing the other side of the risk/benefit equation.
Yes, nicotine is vasoactive (although it increases bloodflow to the brain and other major organs). Yes, we should be cautious with anyone who has underlying cardiovascular disease. But the blanket framing of “this could go bad fast” doesn’t reflect the actual data we now have.
We published an N=231 study on nicotine use in Long COVID and ME/CFS. This isn’t just scattered anecdotes anymore. The majority of participants reported sustained improvement in symptoms such as fatigue, brain fog, orthostatic intolerance, and post-exertional malaise.
Beyond symptom reports, there are well-documented mechanistic reasons why low-dose nicotine may be beneficial in post-viral and neuroimmune disease contexts:
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Reduces maladaptive Default Mode Network (DMN) hyperactivity → improves focus, reduces rumination/overthinking.
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Anti-inflammatory effects via the “cholinergic anti-inflammatory pathway” → dampens cytokine release.
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Supports mitochondrial and NAD+ function → nicotine can upregulate NAD biosynthesis, important in energy metabolism.
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Reduces pain and hyperalgesia → nicotinic acetylcholine receptor agonism reduces central sensitization and neuropathic pain.
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Improves autonomic balance → stabilizes orthostatic intolerance and dysautonomia symptoms.
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Neuroprotective potential → evidence from Parkinson’s, Alzheimer’s, and ulcerative colitis research suggests reduced neurodegeneration and improved gut-immune regulation.
In other words, patients aren’t simply “getting a stimulant buzz.” They’re tapping into known, biologically plausible pathways that overlap directly with Long COVID pathophysiology.
And here’s the ethical question:
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Doing nothing is not neutral. People are losing jobs, families, and in some cases their will to live. Suicide and euthanasia rates in this community are tragically real.
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The actual harm profile of low-dose transdermal nicotine is modest and well-characterized.
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The potential upside — restoration of function in a neglected disease — is enormous.
This is not to say nicotine is for everyone. People with significant cardiovascular disease, arrhythmias, or clotting history should only consider it under medical guidance. But painting nicotine patches as a reckless gamble, when the alternative for many is despair and decline, is itself harmful.
Finally, the next step is already underway. We are preparing a patient-led longitudinal study to track outcomes systematically and in real time. This will provide much stronger data than our retrospective work and move the discussion forward with evidence rather than speculation.
So the question isn’t just “what could go wrong?” It’s also “what is happening if we keep doing nothing?”
Moreover, if there is funding, I would love to do research on the long-term negative effects of low-dose nicotine patch use. This and many other questions are yet to be answered. However, the answer to “what is happening if we keep doing nothing?” is clearly worse. The biggest current danger with low-dose nicotine is the risk of a strong Her/Verx sickness reaction when people try to go too fast.
Thanks for reading :-).
Check out our research and some of the links to topics involving low-dose nicotine for complex neuro-immune diseases like Long Covid and MECFS.
Troy Roach
linktr.ee/thenicotinetest
"Take care of yourself, and if you can, take care of someone else too," Stephen Dubner
Selected References
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Sutherland MT, Riedel MC, Flannery JS, Yanes JA, Fox PT, Stein EA, Laird AR. Nicotine differentially modulates default mode network across resting state, working memory, and attentional tasks. Neuropharmacology. 2021;184:108438. PubMed
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Tracey KJ. The inflammatory reflex. Nat Rev Immunol. 2002;2(6): 533–541. PubMed
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Dollerup OL, Chubanava S, Agerholm M, Søndergård SD, Altıntaş A, Møller AB, et al. Nicotinamide riboside augments the NAD metabolome and induces transcriptomic and anti-inflammatory signatures in human skeletal muscle. Cell Metab. 2018;27(6): 1297–1311.e4. PubMed
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Shi Y, Weingarten TN, Mantilla CB, Hooten WM, Warner DO. Nicotine as an analgesic: paradox or promise? Anesthesiology. 2010;113(2): 438–446. PubMed
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Giladi N, Honigman S, Korczyn AD. Transdermal nicotine in dysautonomia: a pilot study. Clin Auton Res. 2007;17(4): 217–221. PubMed
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Quik M, Wonnacott S. α6β2 and α4β2* nicotinic acetylcholine receptors as drug targets for Parkinson’s disease.* Pharmacol Rev. 2011;63(4): 938–966. PubMed