Treating Parkinson’s Disease with Ketogenic Diet: A Deep-dive Analysis
Parkinson’s disease (PD) is a progressive neuro-degenerative disorder that affects neurons that produce dopamine in the substantia nigra portion of the brain. The symptoms for PD usually takes years to develop.
The reduced production of dopamine leads to symptoms such as tremors, difficulty in movement, depression, confusion, and pain. It considerably reduces the quality of life of the patient.
Cause for Parkinson’s Disease
The primary cause of the disease is attributed to genetic disorders and/or environmental triggers such as infections, impact of insecticides, psychological stress, etc.
These conditions are known to impact the mitochondrial functions of the body due to excess oxidative stress. Usually, the body has agencies to counter the impact of oxidative stress. However, under severe stress, as observed in PD, the agencies cease to operate. This allows the production of free radicals (such as Reactive Oxygen Species) that damage the cells that produce dopamine in the brain.
How Can Ketogenic Diet Treat PD?
The Ketogenic diet helps the brain cells to shift from glucose, its usual source of energy, to ketones, produced in the liver due to restricted carb intake.
Ketones are proven to boost antioxidant activity in the brain and control the production of free radicals. This further reduces the stress and damage to brain cells and its ability to produce dopamine.
Considering the impact of ketones on the mitochondrial function of brain cells, Ketogenic diet has been considered an alternative treatment to reduce the conditions associated with PD.
Is there proof to support this claim?
Research on Keto’s impact on PD is at its very infancy and only a handful of studies on humans are available.
Note that Keto has been successfully used to treat epilepsy for more than a 100 years and there are numerous studies to support it.
Keto’s primary support relies on several animal studies in which rats depicting similar disorder as PD where infused with ketone bodies (mostly β-hydroxybutyrate or BHB). It was found that the introduction of BHB significantly reduced the concentration of free radicals.
In another human study, seven PD patients agreed to try Keto for a period of 28 days. They chose a strict diet wherein they consumed less than 20 gram of carb daily.
After 28 days, 5 of the 7 patients who stayed true to the diet reported remarkable improvement in their condition. They reported a drastic reduction in symptoms such as shaking, freezing, tremors, weakness, and pain. They even reported improvement in bowel movement and motor movement.
The remaining 2 patients who were not entirely true to the diet but did it off and on also reported mild improvement in their condition.
Although the sample size of the study was very small, it did provide strong insights into the affect of Keto on PD conditions.
It is still early days in the research for treatment of Parkinson’s disease through Ketogenic diet but limited studies and logical deductions do provide encouraging prospects.
Even if Keto does not have a direct impact in reducing the conditions associated with PD, it is still a healthier lifestyle for the patients with reduced oxidative stress on their brain.
‘D-beta-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson disease.’ Tieu K, Perier C, Caspersen C, Teismann P, Wu DC, Yan SD, Naini A, Vila M, Jackson-Lewis V, Ramasamy R, Przedborski S., Department of Neurology, Columbia University, New York, New York, USA (2003)
‘D-beta-hydroxybutyrate protects neurons in models of Alzheimer’s and Parkinson’s disease.’ Kashiwaya Y, Takeshima T, Mori N, Nakashima K, Clarke K, Veech RL, Division of Neurology, Tottori University Faculty of Medicine, Yonago, 683-8503 Tottori, Japan (2000)
‘Neuroprotective and anti-inflammatory activities of ketogenic diet on MPTP-induced neurotoxicity.’ Yang X, Cheng B., Department of Human Anatomy, Jining Medical College, 45 Jianshe Nanlu, Jining City, Shandong Province, People’s Republic of China (2010)
‘Ketones prevent synaptic dysfunction induced by mitochondrial respiratory complex inhibitors’ Do Young Kim, Johana Vallejo, and Jong M Rho, Barrow Neurological Institute and St. Joseph’s Hospital & Medical Center, Phoenix, Arizona, USA and Department of Physiology, Midwestern University, Glendale, Arizona, USA (2010)
‘The Role of Oxidative Stress in Parkinson’s Disease’ Vera Dias, Eunsung Junn, and M. Maral Mouradian, Center for Neurodegenerative and Neuroimmunologic Diseases, Department of Neurology, Rutgers – Robert Wood Johnson Medical School, Piscataway, NJ, USA (2014)
‘Etiology of Parkinson’s disease’ Anthony H.V. Schapira, University Department of Clinical Neurosciences, London, UK (2006)