Ketogenic diet good for Parkinson's?
New evidence showed that a high-fat, low-carbohydrate ketogenic diet could help improve symptoms in patients with Parkinson's disease (PD), so did a low-fat, high-carbohydrate diet.
Both diets led to improvements in motor and nonmotor symptoms, but those on ketogenic diet had greater improvements in nonmotor symptoms.
The nonmotor symptoms (ie, mood disorders, cognitive changes, hallucinations, and delusions) in PD can be more troublesome and disabling than motor symptoms as those are usually unresponsive to dopamine replacement therapy. PD is characterized by failure of the mitochondria to produce neuron energy hence, research is targeted at improving mitochondrial biogenesis through ketogenic diet.
Dr Matthew Phillips and colleagues from the Waikato Hospital in Hamilton, New Zealand sought to compare ketogenic diet vs low-fat diet among 47 PD patients in their hospital clinic. Patients were randomized to a low-fat or ketogenic diet for 8 weeks. Those on ketogenic diet were older (mean age 64.29 years vs 61.48 years) and with a slightly higher mean Hoenh and Yahr* score (2.13 vs 1.78) and MDS-UPDRS** scores. Of the 47 patients, 38 completed (20 in the low-fat diet, 18 in the ketogenic diet) the study. All patients were assessed by the same neurologist, who was blinded to the randomization, on the same day and time. [International Congress of Parkinson’s Disease and Movement Disorders (MDS) 2018, abstract 12]
Both diet groups had significant reductions in MDS-UPDRS scores (parts 1-3: where part 1=non-motor daily living experiences, part 2=motor daily living experiences, part 3=motor examination), but only the ketogenic group showed reductions in part 4 (motor complications). “The largest between-group improvements were seen for urinary problems, pain, fatigue, daytime sleepiness, and cognitive impairment,” Phillips said. “Notably, these represent some of the more disabling, less levodopa-responsive nonmotor symptoms in Parkinson’s.” The magnitude of reductions in MDS-UPDRS scores for parts 2-4 did not differ between groups.
As expected, bedtime glucose levels were higher in patients who consumed the low-fat diet vs those on the ketogenic diet. Blood ketone levels were also higher with ketogenic diet at 1.2 mmol/L, which is “well-within the range of physiological ketosis, a state in which neurons are obtaining energy from glucose and ketones, so the neurons are sort of running like hybrid engines,” said Phillips.
“Every patient in the keto[genic] group improved in their nonmotor symptoms. Not one got worse or stayed the same,” Phillips said. “This suggests that a ketogenic diet may be a good complement to levodopa therapy in PD.”
The most common adverse effects reported were excessive hunger in the low-fat diet group and intermittent but transient exacerbations of PD tremor or rigidity in the ketogenic diet group.
Experts however said the short duration of the trial, the possibility of a placebo effect, as well as the absence of a real control group were some of the study caveats. Larger and longer randomized controlled trials are warranted to establish if ketogenic diet has a complementary role in the treatment of PD and how long PD patients could stay on ketogenic diet.