Other Therapeutic Options

traffic-light-green-dan--01-800pxStrong scientific evidence:  It is sometimes difficult to prove the effectiveness of non-drug therapies, but these have been subjected to well-designed clinical trials, and pose little risk of patient harm.

Deep Brain Stimulation (DBS):  DBS really belongs in a category of its own; this surgical intervention, which involves precisely placing electrodes within the brain, has been refined over 2 decades.  Amazingly, the precise mechanism by which it works remains incompletely understood, but improves motor symptoms more than non-motor symptoms.  Adverse outcomes are relatively rare, but DBS is generally used for advanced Parkinson’s patients with poor response to available drugs.
Exercise:  If exercise were a drug, it would be a blockbuster. Many studies have shown that various forms of exercise (e.g., Tai Chi, bicycling, even Nintendo Wii Fit games) reduce Parkinson’s symptoms, including both motor and non-motor symptoms. The only debate at this point is whether exercise can actually slow disease progression. Available evidence doesn’t strongly support any one type of exercise vs. others, so do whatever you enjoy (and can do safely!).
Voice Training:  The deleterious effects of Parkinson’s on speech and swallowing can be mitigated with specialized training.  The best known intervention is LSVT, and this and other approaches have shown benefit in clinical studies.
Cognitive Behavioral Therapy:  Psychiatric impacts of Parkinson’s are under-treated, and among non-drug treatments, CBT has been subjected to the greatest clinical scrutiny, showing that patients likely derive benefit in treating depression and possibly anxiety, including CBT administered by telephone.


Some scientific basis, but further study required:  The supplements listed in this section have NOT been proven to benefit Parkinson’s patients. However, each has a reasonable scientific rationale with supporting pre-clinical and clinical or epidemiological evidence, and evidence-based guidelines are available for safe dosages. Creatine and co-enzyme Q10 would have been in this section a few years ago, but definitive clinical trials showed no benefit.

Nicotine:  Smoking decreases lifespan and increases risk for many diseases, such as cancer, but paradoxically, current or past smokers have a lower risk of Parkinson’s.  This strange observation has motivated lab research and clinical trials examining possible beneficial effects of nicotine on disease symptoms or progression.  Obviously these clinical trials do not involve patients smoking but rather using nicotine patches or gum, which have less potential for addiction because nicotine is released slowly.  Until definitive clinical results are available, the use of nicotine for Parkinson’s will undoubtedly remain controversial.
Caffeine:  Similarly, epidemiology suggests that drinking caffeinated beverages lowers risk of Parkinson’s; some patients also report that caffeine helps with symptom management.  While much more study is required, there are obviously no major patient safety concerns.
Vitamin D:  Low vitamin D levels are associated with increased risk of Parkinson’s.  One small but high quality study has shown some benefit of vitamin D3 supplementation for Parkinson’s patients.  Pending a definitive clinical study, vitamin D supplements can be considered, especially for patients with low blood levels, given the low cost and extensive clinical experience with its use.
N-acetyl cysteine:  Oxidative stress in dopaminergic neurons is associated with Parkinson’s pathology, and possibly contributes to progression of the disease.  Many attempts have been made to develop ‘anti-oxidant’ therapies, without success.  There are reasons to hope that N-acetyl cysteine might be a more effective anti-oxidant.  One preliminary clinical trial concluded in 2016 with some evidence for benefit, and definitive clinical trials are planned.
Cannabis (marijuana):  The scientific literature on this topic is a mess, in part because cannabis contains dozens of neuro-active compounds, with varying amounts in different strains.  Clinical trials thus far are not of sufficient quality to draw any firm conclusions.  I have included it in this category primarily on the basis of pre-clinical research, and its relatively well understood safety/adverse effects.  See also the research summary and webinar from the Parkinson’s foundation.  The legal status of cannabis is of course complex and evolving; the first cannabis-derived drug (for epilepsy) has recently received support from the FDA, and more may follow.


Insufficient evidence for safety and/or efficacy:  Some of these are probably safe, some may have a vaguely plausible scientific rationale, but none have good quality scientific evidence that they actually work (and in some cases there is strong evidence that they do not work).

Cinnamon:  In 2014, there were a flurry of web articles about cinnamon being a potential cure for Parkinson’s, apparently due to this study.  The science is not nearly strong enough to justify these headlines. Obviously, cinnamon is safe to use as a spice, but please don’t start doing the cinnamon challenge multiple times a day.
Acupuncture:  Numerous, mostly small studies have shown various benefits for Parkinson’s patients.  But almost all of these lack the key ingredient for a high-quality clinical study:  a control group, to account for the placebo effect.  The highest quality studies have not shown benefit vs. ‘sham’ acupuncture.
Gluten-free diet:  There are no high quality research studies or clinical trials supporting any role for gluten in Parkinson’s disease, or any patient benefit derived from eliminating it.  With respect to diet more broadly, an interesting study has shown that gut microbes could modulate Parkinson’s symptoms, complementing previous studies showing that Parkinson’s affects the gut.  There is no evidence at present supporting any particular diet.
Coconut oil:  I’m not totally sure where this came from, but there is no clinical research supporting claims of patient benefit, and the few tangentially related research studies are rather preliminary.
Co-enzyme Q10:  Q10 showed promise for slowing progression of the disease in research studies and early clinical trials, but a large and very expensive placebo-controlled trial unfortunately demonstrated no benefit.
Creatine:  Similarly, creatine showed promise for slowing progression of the disease in research studies and early clinical trials, but a large and very expensive placebo-controlled trial unfortunately demonstrated no benefit.
Inosine:  A phase 3 clinical trial, SURE-PD3, was terminated early, in late 2018, because an interim analysis indicated that it was unlikely to demonstrate an effect on disease progression.