Postural Orthostatic Tachycardia Syndrome (POTS) is a complex condition classified as a disorder of the autonomic nervous system. This dysfunction, known as dysautonomia, manifests primarily when moving from a lying or seated position to standing upright. Upon standing, individuals with POTS experience an excessive and sustained increase in heart rate, often accompanied by symptoms like dizziness, lightheadedness, and profound fatigue. The body’s ability to maintain stable blood glucose levels is also a function heavily influenced by this same nervous system. Therefore, the connection between this circulatory disorder and the stability of blood sugar warrants a closer examination of metabolic function in those with POTS.
The Hormonal Link Between POTS and Glucose Regulation
The central mechanism linking POTS and blood sugar stability lies in the overactivity of the sympathetic nervous system, often referred to as a hyperadrenergic state, particularly upon standing. When a person with POTS stands, the body struggles to maintain blood flow to the brain, leading to an exaggerated compensatory response. This response involves the excessive release of stress hormones, most notably norepinephrine, which acts as both a hormone and a neurotransmitter.
Norepinephrine levels can be significantly elevated in a subset of POTS patients, sometimes exceeding 600 picograms per milliliter (pg/mL) while standing. This hormonal surge activates the primal “fight or flight” mechanism, whose metabolic goal is to rapidly provide fuel for immediate action.
To achieve this, norepinephrine directly influences the liver, triggering a process called glycogenolysis, the breakdown of stored glucose into circulating glucose. This acute hormonal signaling can cause a transient elevation in blood glucose levels as the body attempts to fuel the perceived energy demand created by the circulatory stress.
Furthermore, the continuous or frequent activation of this hyperadrenergic state introduces a chronic metabolic challenge. The body is repeatedly exposed to high levels of hormones that favor glucose release and counteract the actions of insulin. This constant hormonal signaling creates an environment that predisposes individuals to challenges in maintaining balanced glucose metabolism.
Understanding Dysglycemia in POTS Patients
The persistent hormonal imbalance in POTS patients can lead to two distinct, yet related, forms of dysglycemia, or abnormal blood sugar regulation. One significant outcome is the development of reduced insulin sensitivity, which is the precursor to insulin resistance, even in individuals who are not overweight or otherwise prone to type 2 diabetes. Chronic exposure to stress hormones like norepinephrine and cortisol blunts the ability of insulin to effectively move glucose from the bloodstream into the cells for energy.
Studies have shown that while fasting glucose levels may appear normal in POTS patients, insulin resistance often becomes apparent only after the body is challenged with a sugar load, such as during an oral glucose tolerance test. Individuals with POTS often exhibit a significantly lower Matsuda Index, a measure of insulin sensitivity, compared to healthy controls. This suggests that the problem is not a lack of insulin production, but rather the body’s reduced responsiveness to the insulin that is produced.
The other common metabolic issue is reactive hypoglycemia, characterized by a rapid drop in blood sugar levels after a meal. This can occur when a high-carbohydrate meal causes a swift surge in glucose, prompting the pancreas to release an excessive amount of insulin. Due to the autonomic dysfunction, this insulin release may be overcorrected or poorly timed, leading to a precipitous and symptomatic drop in blood glucose, sometimes several hours after eating.
The symptoms of this low blood sugar, such as lightheadedness, tremors, and a rapid heart rate, can closely mimic the orthostatic symptoms of POTS, making diagnosis challenging. In some patients, the autonomic dysfunction contributes to rapid gastric emptying, which accelerates the absorption of carbohydrates and further exacerbates this cycle of sharp glucose spikes and subsequent crashes.
Dietary and Lifestyle Management
Managing blood sugar instability in the context of POTS requires a focused approach that addresses both metabolic and circulatory needs simultaneously. A foundational strategy is to replace large, infrequent meals with small, frequent meals. This approach helps prevent the significant blood sugar spikes that trigger an exaggerated insulin response and subsequent crash.
The composition of meals is equally important; individuals should focus on consuming complex carbohydrates, which are digested slowly, alongside adequate amounts of protein and healthy fats. Pairing protein and fat with carbohydrates helps to slow the rate of glucose absorption, thereby moderating the post-meal glucose rise. Foods high in refined sugars and simple carbohydrates should be reduced, as they can exacerbate both post-meal tachycardia and glucose instability.
Hydration and electrolyte management, which are cornerstones of POTS treatment, also indirectly support metabolic stability. Increasing fluid intake to 2 to 3 liters per day, along with a high sodium intake—often between 3,000 and 10,000 milligrams daily—is recommended to expand blood volume. A larger blood volume can help stabilize overall circulation, potentially reducing the hyperadrenergic stress response that contributes to dysglycemia.
When considering exercise, which is beneficial for insulin sensitivity, the timing must be carefully coordinated with POTS symptoms and medication schedules. Furthermore, any pharmacological interventions for glucose control, such as medications for insulin resistance, must be managed in close consultation with a specialist, as many POTS medications, including beta-blockers, can also affect glucose metabolism. A coordinated care plan ensures that treating one condition does not inadvertently worsen the other.