Parkinson's disease is linked to body fat loss and a shift in how the body produces energy.
Unintentional weight loss is common in Parkinson's disease, yet doctors still do not fully understand why it happens. Researchers in Japan examined whether changes in the body's energy chemistry could help explain this pattern.
Enjoying this research? Get deeper insights like this delivered every other week.
Every other week our Premium Members receive deep dives like this alongside Rhonda's commentary and 8+ other hand-picked papers.
The study included 91 people with Parkinson's disease and 47 healthy adults with a similar age and sex distribution. Researchers measured body fat and muscle using bioelectrical impedance analysis, a method that estimates body composition by passing a small electrical current through the body. After an overnight fast, they analyzed blood samples to examine molecules involved in how the body produces and uses energy.
- People with Parkinson's disease weighed less than controls, mainly because they had less body fat. Muscle mass was not clearly different between groups.
- Blood levels of lactic acid and succinic acid were lower in Parkinson's. These molecules are part of glycolysis and the Krebs cycle, two linked processes cells use to extract energy from glucose.
- Ketone bodies, specifically acetoacetic acid and 3-hydroxybutyric acid, were higher in Parkinson's disease. Ketone bodies are fuel molecules made from fat when the body relies less on glucose.
- Within the Parkinson's disease group, higher ketone levels were associated with lower body mass index (BMI).
- Markers of amino acid breakdown, including 2-hydroxybutyric acid and 2-oxobutyric acid, were also elevated in Parkinson's disease patients, suggesting that protein-derived fuels may contribute more to energy supply in Parkinson's disease.
- The phospholipid phosphatidylcholine, a fat molecule found in cell membranes, was higher in Parkinson's disease and increased with more advanced disease stages.
Together, these findings suggest a shift in energy production and use. Signals of reduced glucose use suggest that cells may not be extracting energy from sugar as efficiently. In response, the body appears to rely more on breaking down stored fat and amino acids for energy. This pattern may reflect impaired mitochondrial function, although reduced calorie intake, increased energy expenditure, or medication effects could also contribute. At the same time, higher levels of phosphatidylcholine indicate broader changes in how lipids are handled as the disease advances. This phospholipid contains fatty acids that can influence membrane stability, oxidative stress, and the clumping of proteins such as alpha-synuclein (a hallmark of Parkinson's disease), raising the possibility that altered lipid composition may be linked not only to energy balance but also to disease progression.
Future long-term studies using more precise body composition analysis methods could determine whether these metabolic changes occur early and predict weight loss. If confirmed, blood-based metabolic markers might help clinicians identify patients at higher risk of nutritional decline and guide targeted dietary or metabolic therapies in Parkinson's disease. In Aliquot #114 and Aliquot #115, I discuss supplements and lifestyle factors that boost mitochondrial function and production.