Postural Orthostatic Tachycardia Syndrome (POTS) is a disorder of the autonomic nervous system (ANS), which controls involuntary bodily functions. POTS primarily impacts the regulation of heart rate and blood pressure when changing position, leading to symptoms like dizziness, fatigue, and a rapid heartbeat. Many individuals with POTS report feeling shaky or weak, sensations commonly associated with low blood sugar (hypoglycemia). This raises the question of whether the underlying dysfunction in POTS directly causes drops in blood glucose levels. The relationship is complex, rooted in the ANS’s control over both circulation and metabolic stability.
The Autonomic Nervous System’s Role in Glucose Control
The ANS is the body’s master regulator, controlling circulation and tightly managing glucose homeostasis—the process that maintains blood sugar within a narrow range. This control involves the sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). Both branches send nerve fibers to metabolic organs like the pancreas and liver, influencing glucose release and storage.
The sympathetic branch, associated with “fight or flight,” generally increases blood glucose. It inhibits insulin release while promoting glucagon secretion, which signals the liver to release stored glucose. Conversely, the parasympathetic branch, linked to “rest and digest,” stimulates the pancreas to release insulin, facilitating glucose uptake by cells. This dynamic prevents both high and low blood sugar.
Since POTS is a form of dysautonomia (ANS malfunction), its pathology overlaps with glucose regulation. Any disorder disrupting the ANS can destabilize the balance between glucose storage and release.
Mechanisms of Glucose Instability in POTS
Although POTS is not a primary endocrine disorder, autonomic dysfunction creates conditions leading to glucose instability. Many POTS patients show signs of carbohydrate metabolic dysfunction during glucose tolerance tests. The chronic hyperadrenergic state, common in many POTS subtypes, involves elevated stress hormones (norepinephrine and adrenaline).
These hormones, released by the sympathetic nervous system, can reduce insulin sensitivity, making glucose uptake less efficient. A specific proposed mechanism is reactive hypoglycemia, a temporary drop in blood sugar several hours after eating. This is often linked to rapid gastric emptying, a form of gastrointestinal dysmotility seen in dysautonomia.
When food moves too quickly into the small intestine, it triggers an exaggerated insulin spike. This excessive insulin causes blood glucose to drop below normal levels, resulting in symptomatic hypoglycemia. Furthermore, the dysregulation causing orthostatic intolerance may impair the body’s counter-regulatory response to falling glucose.
A healthy body uses the sympathetic nervous system to quickly mobilize stored glucose from the liver when blood sugar drops. If the sympathetic response is delayed or impaired by dysautonomia, the body fails to initiate this rescue mechanism promptly. This dysregulation of timing and response, rather than a direct cellular disease, is the primary link between POTS and blood sugar fluctuations.
Other Factors Contributing to Hypoglycemia in POTS Patients
Since the link between POTS and low blood sugar is often indirect, ruling out other conditions and external factors is important for accurate diagnosis. Adrenal insufficiency, where the adrenal glands do not produce enough cortisol, frequently overlaps with dysautonomia. Cortisol is a hormone directly involved in raising blood sugar, and a deficiency impairs the body’s ability to prevent hypoglycemia.
Medications prescribed for POTS can also influence glucose metabolism. Beta-blockers, used to control heart rate, may mask typical hypoglycemia warning signs like shakiness and palpitations. Diet composition, often modified for POTS patients to include high salt and fluid intake, also plays a role in sugar stability.
Mast Cell Activation Syndrome (MCAS) is another common co-occurring condition. Mast cells release chemical mediators that are hypothesized to interfere with insulin signaling pathways in some individuals. Therefore, not all low blood sugar symptoms experienced by a POTS patient are solely a consequence of the autonomic disorder, necessitating investigation into these related factors.