The relationship between an eating disorder (ED) and Postural Orthostatic Tachycardia Syndrome (POTS) is a frequently observed clinical challenge. Both conditions can profoundly disrupt daily life, affecting the body’s automatic functions and overall well-being. Eating disorders involve significant disturbances in eating behaviors, while POTS is a complex disorder of the autonomic nervous system. Examining the physiological chain of events offers clarity on how the severe physical stressors of an ED can trigger the development of POTS-like symptoms or unmask a pre-existing vulnerability.
The Clinical Connection Between Eating Disorders and POTS
Postural Orthostatic Tachycardia Syndrome (POTS) is a form of dysautonomia, a disorder affecting the automatic nervous system functions that regulate heart rate and blood pressure. It is diagnosed when a person experiences an excessive increase in heart rate—typically 30 beats per minute or more in adults—when moving from a lying to a standing position, without a corresponding drop in blood pressure. Individuals with eating disorders, particularly those involving severe restriction like Anorexia Nervosa, commonly exhibit orthostatic intolerance, which is the inability to tolerate upright posture. Research indicates a significant overlap, with nearly three quarters of adolescents diagnosed with POTS reporting restrictive eating patterns.
Symptoms such as dizziness, weakness, and lightheadedness upon standing are common to both conditions, creating a diagnostic challenge for clinicians. For a definitive POTS diagnosis, a patient’s nutritional status must be stabilized. The cardiac complications of an active eating disorder, including orthostatic tachycardia, are often reversible with recovery. Physicians may delay a POTS diagnosis if an active ED is present, recognizing that the severe physiological stress of the ED is likely driving the orthostatic symptoms.
Physiological Pathways: How ED Behaviors Drive POTS
Eating disorder behaviors, especially those involving severe calorie restriction, purging, or excessive exercise, create a state of profound physical stress that can directly lead to autonomic dysfunction. The body’s attempt to adapt to starvation and dehydration often initiates a cascade of events that manifests as POTS-like symptoms. A hypovolemic POTS phenotype—the type caused by low blood volume—is often observed in this patient group.
One of the most immediate consequences of restriction and purging is severe hypovolemia, or low circulating blood volume. Inadequate fluid and sodium intake, coupled with fluid loss from purging behaviors, reduces the total plasma volume. When a person stands up, gravity pulls the limited blood supply downward, and there is not enough volume to return to the heart and brain efficiently. The heart must then compensate by pumping much faster to maintain adequate blood flow to the brain, resulting in the excessive heart rate increase characteristic of POTS.
Severe nutritional deficiencies and prolonged weight loss can also contribute to autonomic neuropathy, or damage to the small nerve fibers. These fibers are responsible for regulating the constriction and dilation of blood vessels, a reflex essential for maintaining blood pressure when changing posture. When these nerves are impaired, the blood vessels in the lower body fail to constrict quickly enough upon standing. This pooling of blood exacerbates the low blood volume issue, further triggering the heart’s excessive compensatory response.
The prolonged inactivity and muscle wasting that can accompany severe illness lead to cardiovascular deconditioning. The heart muscle itself may become smaller, reducing its efficiency. A deconditioned heart and weakened skeletal muscles impair venous return, meaning less blood is mechanically pushed back up to the heart. This combination creates a scenario where orthostatic intolerance is almost inevitable, as the cardiovascular system cannot effectively manage the gravitational challenge of standing upright.
Navigating Treatment and Recovery
Successfully treating the orthostatic symptoms in patients with a co-occurring eating disorder requires a highly integrated, multidisciplinary approach. The first step is to address the underlying nutritional deficit and achieve stability, as many of the physiological abnormalities are reversible with weight restoration. As the body receives adequate nutrition, blood volume begins to normalize, and the severe stress placed on the autonomic nervous system is alleviated.
Weight restoration and nutritional rehabilitation often lead to a resolution or significant improvement of POTS-like symptoms, particularly those driven by hypovolemia and deconditioning. However, the process must be carefully managed by medical professionals to prevent complications such as re-feeding syndrome, which can involve dangerous shifts in electrolytes. Standard treatment protocols for POTS, such as encouraging high salt and fluid intake, can be challenging in the context of an active ED.
Once nutritional stability is reached, a graded exercise program is often introduced to address cardiovascular deconditioning. This usually starts with recumbent exercises, like swimming or recumbent cycling, to avoid orthostatic stress before progressing to upright activities. A collaborative team including physicians, dietitians, and mental health specialists is required to navigate the complexities of treating both the psychiatric components of the ED and the physical manifestations of the autonomic dysfunction.