Genetics of POTS / Dysautonomia
POTS (Postural Orthostatic Tachycardia Syndrome) and dysautonomia involve dysfunction of the autonomic nervous system, causing abnormal heart rate and blood pressure responses. POTS is among the most commonly reported Long COVID conditions and has genetic contributors.
This page is for educational and informational purposes only. Not a diagnostic tool. Always consult a qualified healthcare provider.
What is POTS / Dysautonomia?
The autonomic nervous system (ANS) regulates involuntary physiological functions including heart rate, blood pressure, digestion, and temperature regulation. POTS is characterised by an excessive increase in heart rate upon standing (≥30 bpm in adults), often accompanied by dizziness, palpitations, brain fog, and fatigue. Long COVID has dramatically increased the prevalence of POTS-like presentations. Proposed mechanisms include autoantibodies against adrenergic receptors, small fibre neuropathy, hypovolaemia, and impaired baroreflex function. Genetic variants in adrenergic signalling, norepinephrine transport, and autonomic regulatory pathways may predispose individuals to dysautonomia.
Biological pathways commonly discussed in relation to POTS / Dysautonomia
Research into Postural Orthostatic Tachycardia Syndrome and Dysautonomia has highlighted several biological pathways that may be relevant. Genetic variants within these pathways may influence individual susceptibility, symptom severity, or the trajectory of the condition.
Adrenergic Signalling
Adrenergic receptors (ADRA1A, ADRB1, ADRB2) mediate responses to adrenaline and noradrenaline. Variants may alter autonomic tone and cardiovascular responses to postural change.
Norepinephrine Transport
The norepinephrine transporter (NET, encoded by SLC6A2) clears norepinephrine from synapses. Reduced NET function increases sympathetic signalling and is associated with hyperadrenergic POTS.
Baroreflex Function
The baroreflex detects blood pressure changes and adjusts heart rate and vascular tone. Impaired baroreflex sensitivity may contribute to orthostatic intolerance.
Autoantibody Adrenergic
Autoantibodies against adrenergic and muscarinic receptors have been detected in POTS patients. Genetic immune variants may influence susceptibility to generating such autoantibodies following infection.
Key genes studied in relation to POTS / Dysautonomia
The following genes have been studied in relation to Postural Orthostatic Tachycardia Syndrome and Dysautonomia. These genes span the biological pathways most commonly discussed in this area of research.
29 genes total studied in relation to POTS / Dysautonomia across the ChronicDNA dataset.
Genetic variants commonly discussed
The following genetic variants (SNPs) are found in genes that have been studied in relation to POTS / Dysautonomia. Each variant represents a position in the genome where individuals may carry different alleles.
62 variants total across genes studied in relation to POTS / Dysautonomia.
How personal DNA data may provide educational insights
Consumer DNA files from 23andMe, AncestryDNA, and MyHeritage contain raw SNP data. When you upload your file to ChronicDNA, the analysis engine checks your genotype against a curated panel of 80+ genes selected for their relevance to Long COVID, ME/CFS, and connected biological pathways - some of which may relate to areas such as POTS / Dysautonomia.
This is not a diagnostic service. Genetic variants do not determine whether you have POTS / Dysautonomia, nor do they predict your clinical outcomes. The report is educational - it explains which variants you carry, what the research says about them, and how they fit into the biological pathways most relevant to chronic illness. All results should be discussed with a qualified healthcare provider.
Related conditions and pathways
POTS / Dysautonomia shares biological pathways and genetic associations with the following related conditions and areas of research.
Frequently asked questions
What is POTS and why does it occur in Long COVID?
POTS is a form of autonomic dysfunction where the heart rate increases excessively upon standing. In Long COVID, proposed mechanisms include autoantibodies against adrenergic receptors, small fibre neuropathy, and reduced blood volume. Genetic variants in autonomic regulatory pathways may predispose individuals to developing POTS.
Which genes are studied in relation to POTS?
Key genes include SLC6A2 (NET), ADRA1A, ADRB1, ADRB2, COMT, DBH, and CHRNA7. These cover norepinephrine handling, adrenergic signalling, and acetylcholine neurotransmission relevant to autonomic regulation.
Is POTS hereditary?
Familial clustering of POTS has been reported, suggesting a genetic component. Variants in norepinephrine transporter and adrenergic receptor genes have been identified in POTS patients. However, POTS often arises from complex gene-environment interactions, particularly post-viral triggers.
How is dysautonomia different from POTS?
Dysautonomia is a broad term for any dysfunction of the autonomic nervous system. POTS is a specific form of dysautonomia characterised by orthostatic tachycardia. Other dysautonomias include orthostatic hypotension, neurocardiogenic syncope, and autonomic neuropathy.
Related articles
- Long COVID Dysautonomia: What Your Genes May Reveal
Explore how genes in the autonomic nervous system may relate to Long COVID dysautonomia, including POTS, heart rate changes and orthostatic intolerance.
- Long COVID POTS: Symptoms, Testing and Genetics
Learn how Long COVID POTS affects heart rate, how standing and tilt table tests assess it, and which genes research is exploring.
Explore DNA insights
If you already have DNA data from 23andMe, AncestryDNA, or MyHeritage, upload your raw file to ChronicDNA and receive a personalised educational report covering genes studied in relation to POTS / Dysautonomia and connected biological pathways.
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29 genes · 62 variants analysed in relation to POTS / Dysautonomia