Research & Education

Ketogenic Diet & Parkinson’s Disease

Neuromuscular and neurodegenerative illnesses are devastating for obvious reasons: loss of independence reduced quality of life financial strain emotional effects (such as depression) and the toll these conditions take on loved ones particularly if one or more of them assume a caregiving role. Conditions such as multiple sclerosis ALS and Alzheimer’s disease are even more difficult to navigate because there are essentially no effective pharmaceutical interventions. There may be drugs to reduce or relieve symptoms in the short term but these do nothing to address the root cause(s) of the conditions nor to stop or prevent future decline.

Fortunately there is a growing awareness that what many neurodegenerative conditions have in common is some degree of mitochondrial dysfunction. Although how these conditions ultimately manifest in the body may differ a common—and nearly universal—characteristic is impaired mitochondrial energy generation. This being the case there are therapeutic strategies ripe for exploration and research which may hold promise and potential for many conditions that are otherwise intractable and extremely difficult to treat. 

The ketogenic diet is one such strategy that may be beneficial for Parkinson’s disease. It has already shown great promise for other neurodegenerative issues. Animal studies and preliminary studies in humans indicate that ketogenic diets—especially when combined with a rich intake of ketone-boosting medium-chain triglycerides—may improve quality of life in ALS patients. This approach has also proven quite promising for Alzheimer’s disease and Terry Wahls MD skyrocketed to fame in the functional medicine community after her TED Talk in which she shared her account of reversing her progressive multiple sclerosis via diet and lifestyle interventions which included raising serum ketone levels.

While there is some degree of genetic susceptibility behind some of these conditions Dr. Wahls noted “70 to 90% of the risk for diabetes heart disease cancer and autoimmunity is due to environmental factors. The genes do not drive most chronic diseases. It is the environment. It is time we stop blaming our genes and focus on the 70% under the individual’s control. That is the real solution to the health care crisis.” If this is true for diabetes heart disease cancer and autoimmunity then there’s reason to suspect environmental factors have a powerful influence over whether some of these genetic tendencies for neurological issues manifest as chronic illness. 

For Parkinson’s disease (PD) specifically symptoms stem primarily from the death of dopamine-secreting neurons. While there are drugs that are effective—at least in the short term—their efficacy wanes over time. Moreover some Parkinson’s medications—specifically the dopamine receptor agonists—come with truly disturbing potential side-effects. Not totally surprisingly these include behavioral and personality changes that may be associated with the role of dopamine in the “reward” pathways: compulsive gambling shopping and eating and hypersexuality. (Researchers believe these issues are under-reported by patients and caregivers and are under-recognized by the treating physicians.) 

The death of dopaminergic neurons may be due in part to defects in complex I of the mitochondrial electron transport chain. If so then any intervention that boosts mitochondrial efficiency may help improve PD symptoms and if implemented early enough in the disease progression perhaps it would have potential to prevent or at least delay further loss of neurons. Studies with very small cohorts suggest that at the very least dietary ketosis improves scores on the Unified Parkinson's Disease Rating Scale.

The ketogenic diet may exert its benefits via multiple mechanisms. It is anti-inflammatory and boosts mitochondrial antioxidant capacity by inducing expression of mitochondrial uncoupling proteins which reduce the production of reactive oxygen species (ROS). Additionally ketone bodies may be directly neuroprotective by increasing ATP levels and the ketogenic diet has been shown to increase mitochondrial biogenesis.

An in vitro study indicated that elevated levels of the ketone body β-hydroxybutyrate (β-OHB) may protect neurons in models of PD (induced by 1-methyl-4-phenylpyridinium [MPP] which causes death of dopaminergic substantia nigral cells resulting in a syndrome indistinguishable from Parkinson’s disease). When incubated with β-OHB at a concentration of 4.0 mM neurons exposed to MPP showed reversal of the negative effects of the MPP (disappearance of dendrites and shrinkage of cell bodies). Compared to untreated control cells (healthy neurons) there were no significant differences in the cells exposed to MPP and β-OHB. Although these were cultured neurons this finding is extremely promising. A blood ketone concentration of 4.0 mM would be difficult but not impossible to achieve on a well-formulated ketogenic diet. It may be even easier to reach that level with a ketogenic diet combined with MCT oils.

Much remains to be understood about the potential for the ketogenic diet and/or exogenous ketones to have a significant impact on Parkinson’s disease patients. Dr. Wahls’s website features “success stories from individuals who experienced significant improvement by implementing the diet and lifestyle interventions (no increase in medication) Dr. Wahls wrote about in her book. Even so caution is obviously warranted. But that caution should be exercised as more research is conducted in this area so that anecdotes can be turned into hard data that may one day benefit PD patients.