The way the Keto diet works is that it mimics the fasting state to induce ketone production from high levels of long chain triglycerides in the body which will be used as the primary energy source when carbohydrates (CHO) are not available.  The physiology of the diet is that it modifies a person's metabolism into it’s fasting state.  With a shortage of glucose in the body, which is the normal energy supply, the body must identify an alternative energy source and thus utilizes ketone bodies (acetone, 3-hydroxybutyrate, and acetoacetate - all products of ketogenesis) [27].  

 

In the KD, calorie consumption is usually 8% CHO intake, 90% Fat, 7% protein (PRO), as where the average diet is 55 CHO, 30 FAT, and 15 PRO.  The emphasis of the KD is long chain fatty acids which provide 90% of the energetic value, with very little protein and even less carbs [27].  Although studies have shown that the application of this diet works for children with Epilepsy, seniors with PD is a completely different population and thus, a population with completely different nutritional needs and physiological systems.  One must consider the population since although the diet works well for one group, it does not necessarily mean it will work for another.     

 

Another big issue is adherence to the diet which is difficult to meal plan and prepare. Due to these factors alone many other diets have emerged which are similar to KD in their approaches and concepts of deriving energy from fat.  Research has been done on diets providing extremely high medium chain triglycerides (MCT) as an alternative to KD which induce similar metabolic effects.  This MCT version allows for an increase in ketone bodies without the extreme changes in diet as KD.  One of the more popular versions of a KD is the Atkin’s diet.  In the Atkin’s diet consumption of fat is 70%, protein 25, and CHO 5%.  Even with this minor adjustment, compliance to the diet is generally inconsistent and most likely due to difficulty in maintaining a rigid diet and as a result of imminent gastrointestinal issues which occur from KD.

 

However, there is much positive research pointing to the efficacy of application of a KD, including improved cognitive and physical function in animal studies, and other benefits observed in improved metabolic abnormalities.  Unfortunately, most of these encouraging studies were done on animal models and although positive success rates were observed with application of the KD in animal studies, it is important to note that conclusions were not based on actual Parkinson’s diseased animals.  Due to a lack of understanding of the etiology of PD development and progression, researchers opted to induce a neurotoxin which mimicked the PD condition.  Therefore, since studies were conducted on animal models using not actual PD, the conclusions cannot be validated conclusively.    

 

Nevertheless, it is difficult to ignore the neuroprotective aspects of the KD as it’s introduction to disease induced mice showed high neuroprotective capability and a slowing down or complete cessation of the disease process.  This of course would be attractive to the medical and Parkinson’s community.  However, it is important to note that the neuroprotective benefits are the result of  high levels of ketone bodies, and extremely low blood glucose levels.  This condition permits the KD to be efficacious as a neuroprotective agent.  

 

Mitochondrial dysfunction and oxidative stress are significant features of brain degenerative diseases like Parkinson’s.  Imbalance of oxidant and antioxidant are characteristic in the pathophysiology of PD.  Oxidative stress is noted to cause a degeneration or imbalance of dopaminergic neurons which is characteristic of PD [27].   Noting that oxidative stress can be the result of increased free radicals in the body, it is important to correlate the benefits of the KD in that high levels of ketone bodies improve mitochondrial respiration (increasing NADH oxidation and hindering mitochondrial permeability).  In part, the high levels of glutathione peroxidase in the brain (hippocampus region) contribute to the antioxidant action of the KD and block neurodegenerative changes in this region [27].  Other aspects of the KD which may contribute to neuroprotective influence is the increased ability to reduce cell death (apoptosis), reduced inflammatory conditions and free radical suppression.

 

Aside from the potential neuro-protective benefits of the Keto diet, simply due to an increase of ketones in the body from triglyceride sources, low protein consumption (approximately 7%) improves bioavailability of dopaminergic treatments [27].  A study group who followed the KD for eight weeks indicated improvements in non-motor symptoms.  

 

However, there are adverse effects from following the KD.  Among these problems include first long term adherence due to its rigid structure, and include but are not limited to: constipation, nausea, vomiting, increased dehydration, hypoglycemia, heightened cholesterol and triglyceride levels, increased risk of pancreatitis and hepatitis, elevated uric acid in the system, excessive liver enzymes (transaminases), a reduction in bone mineral density, optic nerve neuropathy, and atherosclerosis [27].  This is indeed a heavy list of side effects to gain enhanced neuroprotective benefits from this diet.  Further, the KD induces a loss of appetite which further exacerbates a higher risk for malnutrition, to which people with Parkinson’s disease are already predisposed.  

 

Finally, gradual loss of muscle mass and strength (sarcopenia) tend to accompany advanced age, and people with neurodegenerative conditions.  As of 2019, the scientific community still lacks to report any long term studies on humans, which would support dietary lifestyle changes exclusively to a strict Keto diet.  Perhaps a better path is to eat a nutritious, well rounded diet high in antioxidant foods and/or include high quality antioxidant supplements, explore the addition of nutrient dense superfoods, and exercise to improve cellular respiration and the production of ATP.