Rationale for Nicotine Patch in Treatment of Long-COVID and Vaccine Injuries

Test subjects with long-COVID treated with nicotine patches had documented improvement in multiple domains including neurological, cognitive, cardiovascular, and general well-being.

By Peter A. McCullough, MD, MPH | Courageous Discourse

In my practice, most patients with post-acute sequelae after SARS-CoV-2 infection and COVID-19 vaccination are on the McCullough Protocol Base Spike Detoxification: nattokinase, starting dose 2000 units twice a day; bromelain, 500 milligrams a day; and curcumin, 500 milligrams twice a day. The word “base” is important because it signifies that in addition to triple therapy with nattokinase, bromelain, and curcumin, other drugs and interventions can be added to reduce the intensity and duration of symptoms while the root cause of the syndrome (Spike protein) is being cleared from the body.

Leitzke summarized the literature on post-acute sequelae being related to residual SARS-CoV-2 interactions with the ACE-2 receptor as well as nicotinic acetylcholine receptors (nAChR).

Changeux et al. (2020) recently proposed a ´nicotine hypothesis´, which implicates the propensity of SARSCoV-2 to not only bind to ACE2-receptors (ACE2R) but to nicotinic AChRs, as well (Changeux et al. 2020). Viral particles competing with acetylcholine for nAChR binding in order to enter the human body may lead to primary neuro infection (Changeux et al. 2020; Steardo et al. 2020). Furthermore, among the severe and fatal cases of COVID-19, the proportion of nicotine consumers was significantly lower than non-consumers of nicotine (Miyara, et al. 2020). Since nicotine may protect nAChRs from viral attachment, therapeutic nicotine application was proposed in the management of acute COVID-19 infections (Changeux et al. 2020). This argument is convincingly supported by the cohort study of Hippisley-Cox et al. (2020), with a total of 8.28 million participants (including 19,486 confirmed COVID-19 cases), showing lower odds for COVID-19 infection and COVID-19-related ICU stay in association with smoking (Hippisley-et al. 2020).

Nicotine binds to nAChR and works to competitively antagonize Spike protein while at the same time upregulating nAChR.

Is the post-COVID-19 syndrome a severe impairment of acetylcholine-orchestrated neuromodulation that responds to nicotine administration?

Marco Leitzke¹

“From a clinical perspective, nicotine application leads to functional improvement of vigilance, locomotor activity, cognition, respiratory function, cortical blood flow, EEG activity and pain resilience, as well as gastrointestinal and cardiovascular regulation in animals (Lloyd and Williams 2000). French et al. (1999) demonstrated a long-lasting (up to 72 h after nicotine exposure) increase of neurotrophic nerve growth factor (NGF) mRNA after nicotine administration to the hippocampus, suggesting long-term neuroprotective effects of nicotine (French et al. 1999). Nicotine works as a ligand with high affinity and profound intrinsic activity on nAChRs (Gottiet al. 2006), improving the responsiveness (Buisson and Bertrand 2001) and activity (Lloyd and Williams 2000) of these core receptors of neuromodulation substantially.”

Leitzke presents four cases of mainly young persons with long-COVID syndrome treated with nicotine patches 7.5 to 15 mg/24 with documented improvement in multiple domains including neurological, cognitive, cardiovascular, and general well-being. I have had several patients tell me “brain fog” and general lassitude improves with the use of nicotine patches. We cannot make any therapeutic claims since large, prospective, double-blind, placebo-controlled randomized trials have not been performed with nicotine. However the rationale and empirical evidence appears strong and would support future trials.

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