Dr Maria Shapoval

Naturopathic Doctor

Ketogenic Diet for Parkinson’s Disease

Ketogenic diet may improve motor symptoms in patients with Parkinson’s disease. According to a small uncontrolled study (n=7) and a several animal studies the ketogenic diet has potential to improve mitochondrial function, which is implicated in Parkinson’s disease.

What is Ketogenic Diet?

The ketogenic diet was developed in the early 1920’s and demonstrated remarkable effect in controlling epileptic seizures. Today it is reserved for managing refractory seizures that are not responding to anti-convulsion medications. The focus of ketogenic diet is to switch the fuel – instead of burning carbohydrates, the main source of calories becomes fats. The utilization of fats as fuel results in increase in ketones, while at the same time reducing levels of glucose in the blood.

There a few different protocols for ketogenic versus modified-ketogenic diet, but the main feature remains – high fats, low carbohydrates. The ratio of fat to carbohydrates is where these protocols may differ. The typical ratio varies between 4:1 and 3:1 – that’s 4 grams of fat compared to 1 gram of carbohydrate + protein or 3 grams of fat to 1 gram of carbohydrate + protein. The higher the ratio the better the impact (in terms of seizures), but also the more complex or difficult the diet is to sustain. In terms of percentages – the ideal is carbohydrates at <10%, but some studies do include <20%. 


Additional Benefits

Since it’s initial development in the 1920’s the diet has been tried in a variety of different conditions and purposes. The ketogenic diet has shown consistent success in achieving weight loss, improving blood glucose in diabetes and seizure control in epilepsy. In terms of neurological conditions, the diet is being explores in the following conditions with some promising but still very preliminary results:

Alzheimer’s  ALS  Migraines   Traumatic brain injury
Autism  Stroke Dementia  Astrocytoma



In short we don’t know how this diet works on the brain, but there are several hypotheses. Here is a brief overview of some of the leading theories at this point:

  • Reduce alpha-synuclein accumulation in the brain. Alpha-synuclein is a protein that becomes damaged, or miss shaped, and starts to accumulate in the nerves of the substantia nigra that end up undergoing apoptosis. Several genetic studies have isolated mutated genes responsible for the accumulation, but these are not strongly represented in the actual clinical population. Thus the cause of the accumulation remains to be uncovered. What we do know is that this accumulation can cause or contribute to mitochondrial dysfunction and lead to increase in oxidative stress. (Michael J Fox Foundation: “Effect of Dietary Ketosis on Alpha-Synuclein Accumulation”, 2014).
  • Ketone bodies easily cross the blood-brain barrier and provide it with fuel. The extra dense fuel source may directly assist brain function through improved energy production, but may have additional effects. The ketone bodies include acetoacetate and beta-hydroxybutyrate. Both of these molecules have been shown to prevent neuronal cell death in conditions of stroke and hypoglycemia. They may also be involved in strengthening the blood brain barrier, which has been implicated in the pathogenic process of Parkinson’s disease – suggesting that the breach in the integrity of the barrier may be part of the cause of this condition.
  • Improve mitochondrial function and reduce production of free radicals (reactive oxygen species. This results in more ATP (energy molecule) being produced and prevents damage to the surrounding cellular structures via the free radicals. The mitochondria is a fuel center of the cell. It has a very important role to play in providing the necessary energy in order to power the cell. However, at the same time, the mitochondria is like a nuclear reactor. You really want to make sure it does not get damaged in any way shape or form, or the consequences could be very dire!


Impact on Parkinson’s Disease

The small uncontrolled study demonstrated a 46% reduction in the UPDRS scale (frequently used scale to assess improvement) in 5 of the 7 individual who participated in the study. The participants followed the ketogenic diet for 28 days. However, as this is a very small and uncontrolled study – we can’t be sure this was not due to the placebo effect.

Animal studies demonstrate protection against MPTP induced cell damage by protecting the mitochondria. Other studies report anti-inflammatory effects of ketones – providing neuroprotection in MPTP models of Parkinson’s disease. 

Another mechanism that can be explored is the impact of the ketogenic on the microflora of the digestive tract in patient’s with Parkinson’s disease. As more research supports the gut – brain connection as an important factor in the development of this condition – it becomes reasonable to wonder if regulating this microflora through diet could also regulate the condition itself. 



Thus, ketogenic diet may have therapeutic effects on Parkinson’s disease. However more research is needed to demonstrate the degree of effect and the ideal ratio of fats to carbohydrates.



  1. Stafstrom C. The ketogenic diet as a treatment paradigm for diverse neurological disorders. Frontiers in Pharmacology. 2012; 3(59).
  2. Vanitallie TB. Treatment of Parkinson disease with diet-induced hyperketonemia: a feasibility study. Neurology 2005; 64(4): 728-30
  3. Gasior M. Neuroprotective and disease-modifying effects of the ketogenic diet. Behav Pharmacol. 2006; 17(5-6): 431-439
  4. Wirrell E. Ketogenic ratio, calories and fluids: do they matter? Epilepsia. 2008; 49(Suppl 8): 17-19


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