Ketones and Parkinson’s Disease

Parkinson’s disease (PD) is the second most common neurodegenerative disease. It is a progressive neurodegenerative disorder, characterized by tremors, slowness of movement, rigidity and problems with balance. These symptoms are believed to be due to the degeneration of the dopaminergic neurons in the substantia nigra. The mechanism of this neurodegeneration in PD remains unclear. (Masino, 2016) Currently, there is only symptomatic treatment, not any treatment for delaying or preventing this neuronal damage in PD.


One of the potential theories of the causes of this degeneration of the substantia nigra is from mitochondrial dysfunction, specifically, impaired complex I activity of the electron transport chain.(VanItallie, 2005) This results in decreased energy (ATP) production. As with most neuro-degenerative disorders there is probably also a component due to increased inflammation. (Masino, 2016) Another theory is due to increased oxidative stress. (Shaafi, 2015) This increased oxidative stress is from increased levels of reactive oxygen species from the decreased levels of the antioxidant Glutathione.(Cheng, 2009)

The ketogenic diet (KD) has been used for treatment for drug resistant epilepsy since the 1920s. There is now mounting research that ketones are neuroprotective thus ketones and the KD are increasingly being studied in a number of other neurological disorders; including Alzheimer’s dementia, ALS, autism, cancer, traumatic brain injury and even Parkinson’s disease. (Gano, 2014)   Ketones are produced naturally from the liver under conditions of low glucose, such as times of starvation or when on a ketogenic diet. The ketogenic diet is a high fat, low carbohydrate diet that metabolically shifts the body from using glucose to ketones as it main source of fuel. When present, ketones are the preferred fuel source for the brain. (Cunnane, 2011)

One potential neuroprotective benefit of ketones in PD is the from the improved energy (ATP) production of ketones. First of all ketones have been shown to bypass the blocked pathway in the mitochondria that is damaged in PD thus the previous damaged mitochondria are now able to produce ATP. (Gano, 2014) Ketones have also been shown to stimulate new mitochondrial to form. (Gasior, 2006) Lastly, ketones are a more efficient source of energy (produce more ATP) per unit of oxygen compared to glucose.

Another potential neuroprotective benefit of ketones is the anti-inflammation and anti-oxidant effects. This has been shown in several different animal model of PD. One study looked at mice, which were treated with the neurotoxin MPTP. MTPT causes a neurodegeneration of the dopamine neurons similar to what is seen in PD. The mice which were treated with KD prior to injection with MPTP, were shown to have had decreased pro-inflammatory cytokines (interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha) levels in the substantia nigra. Importantly, this resulted in preserved levels of dopamine and protection against the motor dysfunction typically caused my MPTP. (Yang, 2010)

In another study using the rat model of PD induced by 6-OHDA also showed neuroprotective effects of the KD. The KD pretreated rats were found to have the dopaminergic neurons of the substantia nigra protected from the neurotoxicity of the 6-OHDA. The researchers felt that this was possibly due to decrease oxidative stress. They found that there was an increased level of the antioxidant glutathione level in the rats on a KD compared to those on normal diet. (Cheng, 2009)

So does this improved ATP production, decrease inflammation and decreased oxidative stress correlate to a clinical improvement? A recent study looked just at that. In the PD model of rats, the rats feed a KD had improved motor function compared to rats feed a normal diet. (Shaafi, 2016)

So the next question then is if then translates in humans. To date there is only one human study, that I am aware of, which is a small clinical study. This study placed 7 PD patients on a KD, 5 of which remained on the KD for 28 days. Those 5 patients had on average a 43% reduction of their Unified Parkinson’s Diseases Rating scale. The clinically improved symptoms included: resting tremor, freezing, balance, gait, mood and energy level.(VanItallie, 2005)

In summary, animal studies have shown that ketones decrease inflammation, decrease ROS, and increase ATP production. Thus, ketones may have a neuroprotective effect in PD. There is limited data in animal and human studies of the use of KD resulting in improved motor function but the results are encouraging. The limitation of KD is related to the restricted diet itself.

There is a possible solution to accomplishing ketosis, but without the negative aspects of the the very restrictive ketogenic diet:  the use of *ketone supplement.   This supplement, which is a blend of ketone salts, that puts your body into a state of therapeutic ketosis within 60 minutes of drinking it without having to be on a strict ketogenic diet. Now, this ketone supplement is not an approved treatment by the FDA for treatment of PD or any other disease. However, based on what the research suggests for PD and other neurological conditions, if something as simple as drinking this supplement could help, why not give it a try?



Cheng, B. (2009). Ketogenic diet protects dopaminergic neurons against 6-OHDA neurotoxicity via up-regulating glutathione in a rat model of Parkinson’s disease. Brain Research , 1286, 25-31.
Cunnane, S. E. (2011). Brain fuel metabolism, aging and Alzheimer’s disease. Nutrition (27), 3-20.
Gano, L. (2014). Ketogenic diets, mitochondria, and neurological diseases. Journal of Lipid Research , 55, 2211-2228.
Gasior, M. (2006). Neuroprotective and disease-modifying effects of the ketogenic diet. Behavioral Pharmacology , 17, 431-439.
Masino, S. A. (2016). Ketogenic Diet and Metabolic Therapies. (S. A. Masino, Ed.) Oxford.
Shaafi, S. (2015). Modulatory role of ketogenic diet on neuroinflammation; a possible drug naive strategy to treatment of Parkinson’s disease. Advances in Bioscience and Clinical Medicine , 3 (4), 43-47.
Shaafi, S. (2016). The efficacy of the ketogenic diet on motor functions in Parkinson’s disease: A rat model. Iranian Journal of Neurology , 15 (2), 63-69.
VanItallie, T. (2005). Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study. Neurology , 65, 728-730.
Yang, X. (2010). Neuroprotective and Anti-inflammatory Activities of Ketogenic Diet on MPTP-induced Neurotoxicity. Journal of Molecular Neuroscience , 42, 145–153.
*These products are not intended to are not intended to diagnose prevent treat or cure any disease. If you are under medical supervision for any allergy, disease, taking prescription medications or you are breastfeeding contact your medical provider before adding any new supplements to your daily regimen.
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