What is Parkinson’s Disease?
Parkinson’s Disease (PD) is a progressive neurological condition generally indicated by nerve cell damage and cell death. It results from a deterioration of dopamine producing cells in the brain (an area known as substantia nigra).
This lack of dopamine in the brain is what produces the symptoms of the disease such as tremors, rigidity and slowness of movement. Other symptoms, which can also occur in some people with Parkinson’s disease, include tiredness, confusion, depression and pain. The disease itself significantly impacts an individual’s quality of life.
What Causes Parkinson’s Disease?
The specific cause of PD is believed to be genetic abnormalities and/or environmental triggers such as infections (1). These causes affect mitochondrial function by increasing oxidative stress in the body, which is believed to be a key driver in the deterioration of the dopamine producing cells in the brain (2).
Under normal conditions, when oxidative stress occurs in the body, there are systems that are available to help counteract the negative effects. However, when the system becomes over loaded (as in the case of PD), they are unable to deal with the pressure and so free radicals (also known as Reactive Oxygen Species; ROS) are formed which cause cell death and destruction.
Is there a Cure for Parkinson’s Disease?
There is currently no cure for Parkinson’s disease with only a select few drugs and treatments available to best help manage the symptoms.
How Can the Ketogenic Diet Help Patients with Parkinson’s Disease?
In normal adults, the brain generally relies on the metabolism of glucose for its energy. The only other substrate that it can use is that of ketone bodies produced when following the ketogenic diet.
The ketogenic diet (KD) is a high-fat, moderate protein, low-carb diet that makes your body switch from glucose to fat and ketones as fuel. KD has been used as a treatment in refractory epilepsy for over 50 years and now there is a growing interest in the use of the KD for treatment in PD.
There exists a growing body of evidence to show that the KD and specifically ketone bodies, can exert neuroprotective activity within the brain. Namely, studies that have been done in cells and animal models, have demonstrated that the ketones can promote antioxidant activity (3).
This antioxidant activity is what helps to decrease the free radical formation in the mitochondria and so protecting the cells from oxidative stress and injury (4).
Due to the proposed impact that ketones can have on mitochondrial function, it is hypothesised that they may be warranted as a treatment within PD.
The Effect of Ketone Bodies — Animal Studies
In animal models, a certain type of substrate (known as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; MPTP) has been found to mimic that of PD. This means that researchers have been able to investigate the impact that ketone bodies may have on the disorder.
In one study (5), tissue cells of rats containing MPTP were infused with the ketone body β-hydroxybutyrate. It was found that the ketone body could protect the mitochondria from the toxicity caused by the MPTP by decreasing free radical production.
Another similar study also demonstrated that the ketone body D-β-hydroxybutyrate protects the neurons in the brain from cell damage (6).
The Effect of Ketone Bodies — Human Study
Whilst most of the work looking at the effect of ketone bodies in the treatment of PD has been done in cell and animal models, there is one small study that has been carried out in humans. Seven patients with PD volunteered to follow a KD for 28 days at home.
Only 5 out of the 7 completed the 28 days but the results showed a positive impact on PD scales (UPDRS). Symptoms that were shown to improve included resting tremors, freezing, balance, gait, mood and energy levels (7).
Although this is a very promising study, the limitations of the study do need to be highlighted. It is of course a very small sample size and even of the sample size, only 5 out of 7 could stick with the diet.
Likewise, the diet was only carried out for 28 days, so not really mimicking what it would be like to follow a KD as a lifestyle change. The KD that was followed was of the strictest 4:1 variety (90% of calories as fat, 2% from carbohydrates and 8% from protein). This could be what caused the low adherence rates.
From the work that has been carried out in adults with epilepsy, we can see that the same neuroprotective effects can still be found from a Modified Atkins Diet (8).
Meaning that for future research, placing people on a less restrictive form of the KD may warrant similar results with better attrition rates.
From the data that we have already on the ability of ketone bodies to help mend and protect neurons from oxidative damage, the Ketogenic Diet as a therapy option for the use in Parkinson’s disease would therefore appear to be very promising.
Many more well designed studies in human populations would be needed before a specific conclusion could be drawn.