Found this study interesting, with some relevance to the discussion about rehabilitation and deconditioning in the thread on the Putrino/Systrom/Wust preprint, in terms of the risks of making assumptions about poorly understood phenomena.
Study finds that weight loss in Parkinson’s, previously thought due to “muscle loss, poor nutrition, or deeper metabolic changes,” is due to change in metabolic function that cause selective loss of body fat, but not muscle mass, potentially opening new pathways for treatment:
“…This fat loss is a consequence of a deeper metabolic failure. Key metabolites, such as lactic acid and succinic acid were significantly reduced, indicating impaired glycolysis and dysfunction of the TCA cycle—the body’s primary ‘’main engine’’ for adenosine triphosphate production. This failure means that glucose can no longer be efficiently converted into usable energy.
As a result, the body activates an alternative survival mechanism. Markers of ketone bodies, including acetoacetic acid, were elevated, along with metabolites associated with amino acid catabolism, demonstrating activation of an “emergency engine” that relies on fat and protein breakdown to sustain energy production. In other words, when carbohydrate metabolism fails, the body is forced to burn fat to survive.”
“The study suggests a need to rethink nutritional and therapeutic strategies for PD. Interventions that stabilize glycolysis, improve mitochondrial function, or prevent excessive reliance on fat-derived ketone bodies may represent entirely new treatment approaches, distinct from conventional dopamine replacement therapy.”
Study finds that weight loss in Parkinson’s, previously thought due to “muscle loss, poor nutrition, or deeper metabolic changes,” is due to change in metabolic function that cause selective loss of body fat, but not muscle mass, potentially opening new pathways for treatment:
“…This fat loss is a consequence of a deeper metabolic failure. Key metabolites, such as lactic acid and succinic acid were significantly reduced, indicating impaired glycolysis and dysfunction of the TCA cycle—the body’s primary ‘’main engine’’ for adenosine triphosphate production. This failure means that glucose can no longer be efficiently converted into usable energy.
As a result, the body activates an alternative survival mechanism. Markers of ketone bodies, including acetoacetic acid, were elevated, along with metabolites associated with amino acid catabolism, demonstrating activation of an “emergency engine” that relies on fat and protein breakdown to sustain energy production. In other words, when carbohydrate metabolism fails, the body is forced to burn fat to survive.”
“The study suggests a need to rethink nutritional and therapeutic strategies for PD. Interventions that stabilize glycolysis, improve mitochondrial function, or prevent excessive reliance on fat-derived ketone bodies may represent entirely new treatment approaches, distinct from conventional dopamine replacement therapy.”
