Parkinson’s disease (PD) is the second most common neurodegenerative disease. Parkinson’s disease 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. There are no treatments available currently for delaying or preventing this neuronal damage that causes PD.
One of the potential theories of what causes this degeneration of the substantia nigra, is from mitochondrial dysfunction, specifically, impaired complex I activity of the electron transport chain.(VanItallie, 2005) Impairment of the mitochondrial results in decreased energy (ATP) production. As with most neuro-degenerative disorders there is probably also a component of increased inflammation. (Masino, 2016) Another theory is that there is increased oxidative stress. (Shaafi, 2015) This increased oxidative stress is from increased levels of reactive oxygen species. The antioxidant Glutathione is also decreased levels in patients with PD.(Cheng, 2009)
The ketogenic diet (KD) has been used for treatment for drug resistant epilepsy since the 1920s. There is 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, stroke, traumatic brain injury and even Parkinson’s disease. (Gano, 2014) Ketones are produced naturally from the liver under conditions of sustained low glucose levels, 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)
Ketones have several benefits that are potentially neuroprotective. One of the potential neuroprotective benefit of ketones in PD is from the improved energy (ATP) production. There are three different ways that using ketones instead of glucose as a fuel result in more ATP. First of all ketones have been shown to bypass the blocked pathway in the mitochondria that is damaged in PD, thus the previously damaged mitochondria are now able to produce ATP. (Gano, 2014) Secondly, ketones have also been shown to actually 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 from the anti-inflammation and anti-oxidant effects of ketones. 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 ketones. 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 less ROS and increased level of the antioxidant glutathione in the rats on the KD compared to those on normal diet. (Cheng, 2009)
So does this improved ATP production, decrease inflammation and decreased oxidative stress correlate with 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, how does this translate clinically in humans with PD? To date there is only one small human study, that I am aware of. 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, when exposed to neurotoxins that would typically cause PD, showed that ketones resulted in decrease inflammation, decrease ROS, and increase ATP production compared to animals on standard diets. These findings correlated with improved dopamine levels and improved motor function. There, however is limited data on how this translates to clinical benefits in PD patients. The one study using the KD in PD patients has encouraging results, but more studies are needed.
Currently one of the limitation is that the KD is very hard to stick with. Luckily there is another way to get into ketosis; 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?