Parkinson’s has no cure; nicotine patches haven’t been proven an effective treatment

In May 2024, a Facebook reel with over 350,000 views claimed that nicotine patches can cure Parkinson’s disease. In the reel, chiropractor Bryan Ardis shared the alleged testimony of a person who claimed “all of his Parkinson’s symptoms disappeared” after using the patches for seven days and had “been told by his neurologist he no longer has Parkinson.”

The reel comes from an interview of approximately one hour and a half with Ardis for the Flyover Conservative podcast, which posted the reel on its Facebook account. The full interview was released in April 2024 on multiple video platforms, including Rumble, Banned.video, Bitchute, which together accumulated over 100,000 views at the time of writing, and on the donation platform Subsplash. The Flyover Conservatives also shared the interview on Instagram and Twitter.

Ardis was one of the proponents of a viral conspiracy theory claiming that COVID-19 was caused by synthetic snake venom, not SARS-CoV-2. Science Feedback and multiple other fact-checking organizations debunked this claim. He has also promoted nicotine patches to prevent or cure various medical conditions, including COVID-19, dementia, and brain tumors, despite the lack of scientific evidence supporting these uses.

Likewise, it is false that nicotine patches cure Parkinson’s, a chronic neurological disease that currently has no cure. While nicotine patches have been researched as a potential therapeutic strategy in people with Parkinson’s, the results from clinical trials don’t support their use for treating the disease. We explain below.

Parkinson’s disease has currently no cure

Parkinson’s disease is a disorder of the nervous system that causes a series of characteristic motor symptoms, including trembling (tremor) at rest, stiffness, slowness of movement, and impaired balance. These symptoms are due to the progressive loss of a specific type of neurons in a brain region called substantia nigra.

The substantia nigra is part of a broader network of brain structures jointly known as basal ganglia. The basal ganglia are responsible for controlling movement and coordination, a process regulated through dopamine signaling. In Parkinson’s, the loss of dopamine-producing neurons in the substantia nigra causes dopamine levels to drop up to a point at which the basal ganglia circuits can’t work correctly anymore. This is when the first motor symptoms appear.

Researchers still don’t know what causes these neurons in particular to die. Around 15% of Parkinson’s cases are caused by mutations in specific genes. However, the cause of the vast majority of cases is unknown. Some factors, such as pesticide exposure and brain injury, are associated with an increased risk of developing the disease^[1]. This suggests that Parkinson’s is a complex disease, likely arising from a combination of genetic and environmental factors that contribute to the risk.

Although the substantia nigra is the region most affected by Parkinson’s, the disease can also damage neurons producing neurotransmitters other than dopamine in different brain regions. This results in non-motor symptoms that are also common in people with Parkinson’s, such as depression, memory or sleep problems, and constipation^[2].

As Parkinson’s progresses, more and more neurons die, worsening the symptoms and making it increasingly difficult to carry out everyday activities without help.

Medication, surgery, and supportive therapies can temporarily ease some symptoms. The most common treatment is an oral medication called levodopa. When absorbed in the brain, levodopa turns into dopamine, partially reestablishing the function of the basal ganglia. However, there is currently no treatment that can stop or slow the progression of the disease. Therefore, any product claiming to cure Parkinson’s is simply a scam.

Smokers have a lower risk of Parkinson’s than non-smokers

As often happens with misinformation, Ardis’ claim contains a grain of truth. Dozens of epidemiological studies have consistently shown that cigarette smokers are much less likely to develop Parkinson’s compared to people who have never smoked^[3].

This association was first observed in a 1959 study by the U.S. Public Health Service on tobacco smoking and mortality. After analyzing almost 200,000 veterans, researchers found that smokers had a 64% reduced risk of dying from Parkinson’s compared to non-smokers^[4].

While epidemiological studies can’t demonstrate that smoking is indeed the cause of the reduced risk, additional evidence supports a causal link.

For example, the apparent protection of smoking increases with the dose and the years the person has been smoking^[5]. Conversely, people who quit smoking have a higher risk of Parkinson’s than active smokers, although still lower than that of people who never smoked. Some research has shown that passive smokers show a risk reduction similar to that of active smokers^[6], although the evidence in this regard is conflicting.

That said, this apparent protection isn’t a reason to start smoking. While smokers have a reduced risk of Parkinson’s, they are also much more likely to die from smoking-related cancers such as lung cancer^[7]. Smoking is also associated with an increased risk of other chronic diseases, including cardiovascular disease.

Moreover, the underlying cause of this inverse association between smoking and Parkinson’s is far from clear. While smoking might have a true protective effect, it is also possible that the observed effect reflects reverse causality. This phenomenon can lead to incorrectly identifying a cause as the effect and vice versa.

In other words, it is possible that smoking doesn’t reduce the risk of Parkinson’s but instead people with an increased risk of developing the disease are less likely to become smokers in the first place. For example, people at a high risk of Parkinson’s might be less sensitive to the addictive effect of nicotine.

Supporting this hypothesis, people with Parkinson’s are able to quit smoking more easily than people without Parkinson’s^[8]. In fact, this has been proposed as an early sign of the disease similar to specific non-motor symptoms such as reduced olfaction, chronic constipation, sleep disorders, and depression.

Nicotine patches haven’t been shown to improve symptoms or slow the disease in people with Parkinson’s

Cigarettes contain many substances that could be involved in the inverse correlation between smoking and Parkinson’s risk. However, nicotine, the main active compound in tobacco, has the support of a plausible biological mechanism that could explain a hypothetical protective effect.

Nicotine is addictive, which is precisely how it might exert a protective effect against Parkinson’s. Basal ganglia have a role not only in movement control but also in addiction, a behavior that is modulated by dopamine. Nicotine stimulates the release of dopamine in several brain regions, including the basal ganglia. This release of dopamine in the basal ganglia causes a pleasant sensation (reward) that reinforces the addictive behavior (in this case, smoking)^[9].

But researchers hypothesize that the release of dopamine induced by nicotine can also protect the neurons in the substantia nigra from dying.

Indeed, preliminary studies have shown that oral or dermal administration of nicotine protects the neurons in the substantia nigra from damage in rodents and monkeys^[10].

However, two randomized controlled trials failed to demonstrate any improvement in motor symptoms or disease progression in patients treated with nicotine patches^[11,12]. Nicotine doses in these trials ranged from 35 to 90 milligrams (mg) per day, with a treatment duration of up to 28 weeks. However, the number of participants was small in both studies (32 and 40, respectively).

In 2023, the largest clinical trial on nicotine patches and Parkinson’s to date was published in the New England Journal of Medicine Evidence^[13]. The trial involved 163 participants from multiple centers in the U.S. and Germany who had been diagnosed with Parkinson’s within the previous 18 months and were therefore in the earliest possible stage of the disease. These patients still didn’t require dopamine replacement therapy, thus ruling out the possibility that such medication would mask any potential benefit from the nicotine patch.

The participants in the treatment arm received 90 mg of nicotine per day for one year, while those in the control group received placebo patches without nicotine. The researchers didn’t find any benefit from nicotine in terms of either symptoms or disease progression.

These negative results don’t necessarily mean that nicotine has no therapeutic value in Parkinson’s. However, they strongly suggest that contrary to the reel’s claim, nicotine patches aren’t an effective treatment, let alone a cure, for Parkinson’s.

Conclusion

Parkinson’s is currently a chronic, incurable disease. Therefore, claims that any product, including nicotine patches, cures Parkinson’s are false. Nicotine has demonstrated some neuroprotective effects in preliminary studies in animals. While these effects might serve as a starting point for developing new treatments for Parkinson’s, evidence so far indicates that nicotine patches aren’t effective as a Parkinson’s treatment.

REFERENCES

• 1 – Ascherio and Schwarzschild. (2016) The epidemiology of Parkinson’s disease: risk factors and prevention. The Lancet Neurology.
• 2 – Schapira et al. (2017) Non-motor features of Parkinson’s disease. Nature Reviews Neuroscience.
• 3 – Mappin-Kasirer et al. (2020) Tobacco smoking and the risk of Parkinson disease: A 65-year follow-up of 30,000 male British doctors. Neurology.
• 4 – Harold F. Dorn (1959) Tobacco consumption and mortality from cancer and other diseases. Public Health Reports.
• 5 – Chen et al. (2010) Smoking duration, intensity, and risk of Parkinson disease. Neurology.
• 6 – Nielsen et al. (2012) Environmental tobacco smoke and Parkinson disease. Movement Disorders.
• 7 – Yoon et al. (2023) Association between smoking and all-cause mortality in Parkinson’s disease. npj Parkinson’s Disease.
• 8 – Ritz et al. (2014) Parkinson disease and smoking revisited: Ease of quitting is an early sign of the disease. Neurology.
• 9 – Neal L. Benowitz (2010) Pharmacology of Nicotine: Addiction, Smoking-Induced Disease, and Therapeutics. Annual Reviews in Pharmacology and Toxicology.
• 10 – Quik et al. (2012) Nicotine as a potential neuroprotective agent for Parkinson’s disease. Movement Disorders.
• 11 – Vieregge et al. (2001) Transdermal nicotine in PD: A randomized, double-blind, placebo-controlled study. Neurology.
• 12 – Villafane et al. (2017) High-dose transdermal nicotine in Parkinson’s disease patients: a randomized, open-label, blinded-endpoint evaluation phase 2 study. European Journal of Neurology.
• 13 – Oertel et al. (2023) Transdermal Nicotine Treatment and Progression of Early Parkinson’s Disease. New England Journal of Medicine Evidence.