Nearly six months of a ketogenic diet, one low in carbohydrates and high in fat, eased motor symptoms and anxiety and depression while improving cognition in a woman with mild Parkinson’s diseasea case study found.
These findings suggest that a ketogenic diet may offer an additional, non-pharmacological way of addressing Parkinson’s motor and non-motor symptoms, and support its further evaluation in appropriately controlled trials, the study’s author noted.
The case report, “Effects of a Ketogenic Diet on Symptoms, Biomarkers, Depression, and Anxiety in Parkinson’s Disease: A Case Study”Was published in the Cureus Journal of Medical Science.
Current pharmacological treatments often have little or no effect on these non-motor symptoms, and dietary approaches are gaining interest as potential add-on strategies for managing Parkinson’s.
The ketogenic, or keto, diet is a type of low-carb / healthy-fat (LCHF) diet with limited protein intake. A previous small trial showed that adopting a keto diet for 2.5 months was associated with greater reductions in patients’ non-motor symptoms relative to those assigned to a low-fat diet.
While the underlying mechanisms of these benefits remain unclear, the induced switch in the body’s energy source from standard glucose, or sugar, to fatty ketones may “sustain energy demands for the brain and reduce systemic and [brain] inflammation, especially in older persons with PD [Parkinson’s disease]”The author wrote.
Ketones are the fat-derived molecules produced by the liver to serve as an energy source when glucose (sugar) is not readily available.
A researcher with AT Still University of Health Sciences, in Arizona, described the case of a 68-year-old woman with mild Parkinson’s whose motor and non-motor symptoms were eased with the keto diet.
The woman, who could still move and perform daily activities without help, had slow leg movements, moderate hand tremors, and painful sensations in her feet. She also reported mild-to-moderate feelings of depression and anxiety, occasional sleep disturbances, high blood pressure, and issues with blood glucose control.
She was on standard Parkinson’s medication.
The woman was obese, and exercised two to three times a week with a personal trainer. She followed a standard diet, with reduced fat, but admitted tending to consume mostly processed foods and sugar.
A traditional ketogenic diet – consisting of 70–75% fats, 20–25% protein, and 5–10% carbs – was initiated for 24 weeks (nearly six months) with the help of a recommended food list, a cookbook with recipes and meal plans, and a food-tracking tool called the MyFitnessPal app.
A Keto-Mojo device was also provided for daily at-home measures of fasting glucose and ketone levels in the blood to help assess dietary compliance.
Assessments covering health biomarkers, disease severity, and anxiety and depression levels were also conducted before the diet (baseline measures), midway into the diet (12 weeks), and at the intervention’s end (24 weeks).
Health biomarkers included weight, body mass index (a ratio of weight to height), waist circumference, and the blood levels of HbA1C (a marker of glucose control), fasting insulin, triglycerides, HDL or ‘good cholesterol,’ and C-reactive protein, an inflammation biomarker.
Notably, based on her high HbA1C levels, low HDL, a waist circumference of more than 35 inches, and reported high blood pressure at baseline, the woman qualified for metabolic syndrome, a cluster of conditions that together increase the risk of heart disease, stroke , and type 2 diabetes.
Dietary compliance was confirmed from the start of the diet through week 24, with an average blood ketone reading of 0.5 nanomoles, indicating sustained nutritional ketosis – the state in which the body can use stored fat for energy most effectively.
Gradual improvements were observed in all health biomarkers at 12 and 24 weeks into the diet, including an increase in HDL levels and a drop in HbA1C, C-reactive protein, triglycerides, and fasting insulin levels. Reduced weight, waist circumference, and heart risk factors were also observed.
At the end of the 24-week keto diet, the woman “no longer met the criteria for a metabolic syndrome diagnosis,” the researcher wrote.
Notably, “PD can be associated with an increase in CRP [C-reactive protein] levels ”and even though the woman’s CRP levels“ were not significantly elevated at baseline, the 24-week results did indicate a reduction in this marker of inflammation, ”the author added.
The total score of the Unified Parkinson’s Disease Rating Scale, a measure of disease severity, was higher at the end of the diet, indicative of disease worsening. However, tremors had eased at 12 weeks and painful sensations in the lower extremities were reported to be moderately lower at 12 weeks, with no further reported improvement at 24 weeks.
Improvements in concentration and a reduction in depression symptoms, hand tremors, and painful sensations in the lower extremities were reported at week 12. Most of these benefits were sustained, without further changes, at week 24.
In agreement, depression symptoms, when specifically assessed with the Center for Epidemiologic Studies Depression Scale-Revised, were modestly reduced at the end of the diet. The Parkinson’s Anxiety Scale score, a measure of anxiety symptoms, was also lower at 12 and 24 weeks.
The clinical relevance of these improvements remains unclear, the report noted.
Findings suggest that the ketogenic diet may be “safe and effective for improving biomarkers of health, symptoms of depression, anxiety, and PD symptoms in patients with [mild] PD, ”the researcher wrote.
“Empowering individuals with PD through a more personalized nutritional approach to symptom management can be achieved by offering adjuvant treatment approaches together with medication therapy to reduce symptoms and improve function,” the report noted.
Future controlled clinical trials are needed to further evaluate the effectiveness of the LCHF / keto diet “in improving cognitive function and controlling or reducing symptoms of depression, anxiety, and both motor and nonmotor symptoms in PD,” the researcher concluded.