The mechanisms underlying POTS are not well understood. Though heterogeneous in nature, patients often present with symptoms that include fatigue, orthostatic lightheadedness and tachycardia, "brain fog", shortness of breath, and sleep disruption. The central mediator that links observations in disease entities similar to POTS is energy use and balance driven by mitochondrial health. Mitochondrial dysfunction (i.e. respiration defects, reactive oxygen species (ROS) generation, and structural abnormalities) are hallmarks of currently defined syndromes that resemble POTS symptomatology. Many patients with POTS have underlying immune system dysfunction, which, when treated, may improve the patient's overall health. Though autoimmunity has been demonstrated in POTS, overall immune dysregulation may be broader and include immune cell exhaustion and persistent inflammatory cytokine responses. Immune dysfunction including cellular exhaustion and persistent inflammation has been linked to mitochondrial function. Therefore, we hypothesize that a unifying feature of POTS results from latent or continued mitochondrial/immune dysfunction which then impacts multi-organ energy imbalance and immune homeostasis. Understanding and targeting mitochondria utilizing established, novel, and directed approaches including time-restricted eating (TRE) will help to unravel common etiologies and help us to better diagnose, manage, and treat POTS.
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AI-rewrites the medical criteria so a patient or caregiver can understand them. Always confirm with the trial site.
Conduct a pilot clinical trial with POTS patients to assess if TRE can improve Quality of Life.
Timeframe: Change from Baseline quality of life questionnaire at 14 weeks