A number of studies suggest that dietary nicotine might have the ability to slow the progress of Parkinson’s disease.
However, up-to-date research from the Michael J. Fox foundation suggests that while pre-clinical studies suggest a link between nicotine, it is not a clinically useful intervention for Parkinson’s.
In this article, we investigate the available evidence that explores a link between nicotine and Parkinson’s, as well as its limitations.
However, much of this research consists of animal studies or questionnaire studies of the wider population. Many studies are also unclear as to whether the nicotine, other chemicals in tobacco smoke, or alternative factors are responsible for blocking the action of Parkinson’s.
In late 2018, a randomized-controlled trial produced high-quality evidence that showed direct doses of nicotine via patches to be an ineffective treatment for Parkinson’s.
Certain species of Solanaceae, a flowering plant family, are edible and contain nicotine. People might be more familiar with these plants under the name nightshade.
This family includes peppers, chilis, and tomatoes. Researchers have been examining the potential of this dietary form of nicotine as a treatment for Parkinson’s.
The study, led by Dr. Susan Searles Nielsen and her colleagues from the University of Washington in Seattle, included 490 participants with Parkinson’s disease and a control group of 644 individuals who did not have the disease.
The researchers gave the participants questionnaires asking about their diet and tobacco use.
They found that people who ate higher levels of edible Solanaceae faced a lower risk of Parkinson’s disease in comparison to those who did not eat as much. Of all the foods containing nicotine, the best protection seemed to come from eating peppers.
The protective effects of food that contains nicotine were most noticeable in people who had never used other tobacco products.
Dr. Searles Nielsen advised the following about the study:
“Our study is the first to investigate dietary nicotine and risk of developing Parkinson’s disease. Similar to the many studies that indicate tobacco use might reduce risk of Parkinson’s, our findings also suggest a protective effect from nicotine, or perhaps a similar but less toxic chemical in peppers and tobacco.”
In the conclusion of the study, however, Dr. Nielsen concedes that despite the relationship between tobacco smoke or some constituents of nightshade plants and a lower risk of developing Parkinson’s, she could not say whether the effects were a result of nicotine directly.
Dr. Nielsen advises that further research would be necessary to confirm nicotine as an effective, safe treatment for Parkinson’s.
Scientists know that some of the tremors of Parkinson’s result from a loss of neurons that produce dopamine.
Although scientists do not yet understand the death of neurons, certain biological events that occur during the disease progression have helped them identify the process.
Some proteins in cells fold incorrectly. The body of a person who does not have Parkinson’s discards these cells. In people with Parkinson’s, the body seemingly does not remove misfolded cell proteins from the system.
These proteins then build up within cells, eventually killing them.
A 2016 study in the Journal of Neuroscience examined how nicotine affects dopaminergic neurons.
By simulating the conditions that cause proteins to misfold, the study authors found that the dopaminergic neurons were more resistant to the toxic effects of the proteins in the presence of nicotine.
The authors suggest that nicotine may reduce both the level of incorrect protein production and the buildup of misfolded proteins in cells.
If this is the case, then the findings suggest that nicotine-based medicines that do not pose the health risks associated with smoking may warrant further investigation for use among people with Parkinson’s.
In 2015, geneticists at the University of Alabama (UAB) attempted to map (resource no longer available at www.nature.com) the genetic mechanisms that might support an association between nicotine exposure and reduced risk of Parkinson’s.
Their study found that regular smokers had a 25 percent lower risk of Parkinson’s, in comparison with people who had never smoked.
The UAB study identified a gene, SV2C, which may play a role in reducing Parkinson’s risk among regular smokers.
This gene is “biologically plausible,” the authors explain, because nicotine enhances the release of dopamine through synaptic vesicles, which form the part of the neuron that stores neurotransmitters. These are chemical messengers that send information between the brain, nervous system, and tissues throughout the body.
SV2C encodes a synaptic vesicle protein in a part of the brain called the substantia nigra. The development of Parkinson’s damages this area of the brain.
The study authors suggest that future treatments may address this gene, and nicotine has helped medical scientists identify SV2C as a potential avenue of treatment.
However, this research does not suggest nicotine as a treatment for Parkinson’s.
Parkinson’s disease is a progressive condition that increasingly disrupts function in the brain.
Parkinson’s disease causes degeneration in the central nervous system, disrupting movement, thought processes, and coordination.
The loss of brain cells that produce dopamine, an important neurotransmitter, causes the effects of this disease.
Symptoms develop gradually and may begin with small tremors in one hand. Parkinson’s symptoms might include:
- facial, hand, arm, and leg tremors
- balance difficulties
- slower movement
- stiff limbs
No cure is available for Parkinson’s. To date, treatment and medication can only ease some of its symptoms.
While dietary nicotine may in future yield more positive results, current high-quality evidence does not support nicotine as a treatment for Parkinson’s