Medical Compass: Slowing Parkinson’s disease’s progression
Removing iron accumulation may improve results
By David Dunaief, M.D.
Patients with Parkinson’s disease (PD) suffer from a variety of movement disorders caused by a breakdown of brain neurons. While we don’t fully understand the causes of PD, we know that risk factors may include head trauma, genetics, exposure to toxins and heavy metals, and other issues, such as a sedentary lifestyle.
The prime culprit is dopamine deficiency that occurs in a region at the base of the brain (1). Because of this, the mainstay of medical treatment has been adding back dopamine; however, eventually the neurons themselves break down, and the medication becomes less effective.
Newer approaches include medications and deep brain stimulatory surgery, as well as modifying lifestyle, considering factors like iron, inflammation, CoQ10, and vitamin D. While the research is not conclusive, it is continuing. This provides us with hope and more options.
Iron accumulation
Iron accumulation is potentially harmful in neurodegenerative diseases such as Parkinson’s disease, as well as Alzheimer’s disease, macular degeneration, and multiple sclerosis, because of the oxidative damage it can cause.
In a small, yet well-designed, randomized controlled trial (RCT), researchers used a chelator to remove iron from the substantia nigra. An iron chelator is a drug that removes the iron. Here, deferiprone (DFP) was used at a modest dose of 30 mg/kg/d (2).
The chelator reduced the risk of disease progression significantly on the Unified Parkinson Disease Rating Scale (UPDRS) during the 12-month study. Participants who were treated sooner had lower levels of iron compared to a group that used the chelator six months later. A specialized MRI was used to measure the brain’s iron levels.
A subsequent small RCT of 22 early-onset PD sufferers found a trend for improvement at the same dosing of DFP, results did not achieve statistical significance by the conclusion of the six-month trial (3).
An iron chelator does not affect systemic levels of iron, only those in the substantia nigra region of the brain. The chelator may work by preventing degradation of the dopamine-containing neurons. Your physician may also recommend that you consume foods that contain less iron.
Inflammation
In a 2023 study, researchers tested 58 newly diagnosed PD participants’ blood and compared their results to 62 healthy control participants to compare inflammatory markers (4). Some PD-arm participants had additional testing done, including cerebrospinal fluid samples and brain imaging.
Researchers found that those with PD had significantly higher brain inflammation levels than those without PD in specific regions. Their blood and cerebrospinal fluid also had high inflammatory markers. These measures correlated with worse visuospatial and cognitive scores.
While this study provides hints of possible treatments, we need additional studies to confirm whether the inflammation is a cause or an effect of PD.
Regardless, adopting a low-inflammatory diet might help mitigate some symptoms of PD or slow its advancement.
CoQ10
In an RCT, results showed that those given 1,200 mg of CoQ10 daily reduced the progression of the disease significantly based on UPDRS changes, compared to a placebo group (5). Other doses of 300 and 600 mg showed trends toward benefit, but were not significant. This was a 16-month trial in a small population of 80 patients. In this study, CoQ10 was well-tolerated at even the highest dose.
Unfortunately, a 2022 meta-analysis of CoQ10 studies concluded that it was not universally beneficial, even if some studies showed benefits for specific patients (6). The authors concluded that a personalized approach to its administration and follow-up is critical.
Vitamin D
Vitamin D may play dual roles of both reducing the risk of Parkinson’s disease and slowing its progression.
A prospective study of over 3000 patients showed that vitamin D levels measured in the highest quartile reduced the risk of developing Parkinson’s disease by 65 percent, compared to the lowest quartile (7). This is impressive, especially since the highest quartile patients had vitamin D levels that were insufficient, with blood levels of 20 ng/ml, while those in the lowest quartile had deficient blood levels of 10 ng/ml or less.
In an RCT with 121 patients, results showed that 1,200 IU of vitamin D taken daily may have reduced the progression of PD significantly on the UPDRS compared to a placebo over a 12-month duration (8). Also, this amount of vitamin D increased the blood levels by almost two times from 22.5 to 41.7 ng/ml.
In a 2019 study of 182 PD patients and 185 healthy control subjects, researchers found that higher serum vitamin D levels correlated to reduced falls and alleviation of other non-motor PD symptoms (9).
Like other PD research, investigations into the role of Vitamin D are ongoing.
So, what are our takeaways? Though medication is the gold standard for Parkinson’s disease treatment, lifestyle modifications can have a significant impact on both its prevention and treatment. While each change in isolation may have modest effects, their cumulative impact could be significant.
References:
(1) uptodate.com. (2) Antioxid Redox Signal. 2014;10;21(2):195-210. (3) Sci Rep. 2017; 7: 1398. (4) Movement Disorders. 2023;38;5:743-754. (5) Arch Neurol. 2002;59(10):1541-1550. (6) J Pers Med. 2022 Jun; 12(6): 975. (7) Arch Neurol. 2010;67(7):808-811. (8) Am J Clin Nutr. 2013;97(5):1004-1013. (9) Neurologica. 2019;140(4):274-280.
Dr. David Dunaief is a speaker, author and local lifestyle medicine physician focusing on the integration of medicine, nutrition, fitness and stress management. For further information, visit www.medicalcompassmd.com or consult your personal physician.