Genetics of Chronic Pain
Chronic pain is a common and debilitating feature of Long COVID, ME/CFS, fibromyalgia, and connective tissue disorders. Genetic variants in pain perception, neuroinflammation, and sensory neuron genes may influence individual pain thresholds and central sensitisation.
This page is for educational and informational purposes only. Not a diagnostic tool. Always consult a qualified healthcare provider.
What is Chronic Pain?
Pain is mediated by nociceptive sensory neurons that detect tissue damage and transmit signals to the brain. In chronic pain conditions, the pain processing system becomes sensitised — generating pain signals disproportionate to peripheral input. Central sensitisation, involving altered synaptic strength in the spinal cord and brain, is a proposed mechanism in fibromyalgia, ME/CFS, and Long COVID-associated pain. Genetic variants in ion channels (TRPV1, TRPA1), neurotransmitter systems (COMT, OPRM1), and inflammatory mediators may influence pain thresholds and susceptibility to central sensitisation.
Biological pathways commonly discussed in relation to Chronic Pain
Research into Chronic Pain and Pain Sensitisation 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.
Nociception
Nociceptive neurons detect potentially damaging stimuli via ion channels such as TRPV1 and TRPA1. Variants affecting channel sensitivity may alter pain thresholds.
Central Sensitisation
Central sensitisation involves amplification of pain signals in the spinal cord and brain. Neurotransmitter variants (COMT, MAOA) and glutamate receptor genes may influence this process.
Neuroinflammation
Inflammatory mediators including prostaglandins, bradykinin, and cytokines sensitise nociceptors and amplify pain signalling. Variants in COX enzymes, kallikrein, and cytokine genes may influence pain-related inflammation.
Endocannabinoid Opioid
The endocannabinoid and opioid systems modulate pain perception. Variants in OPRM1 and cannabinoid receptor genes may influence analgesic responses and pain sensitivity.
Key genes studied in relation to Chronic Pain
The following genes have been studied in relation to Chronic Pain and Pain Sensitisation. These genes span the biological pathways most commonly discussed in this area of research.
35 genes total studied in relation to Chronic Pain across the ChronicDNA dataset.
Genetic variants commonly discussed
The following genetic variants (SNPs) are found in genes that have been studied in relation to Chronic Pain. Each variant represents a position in the genome where individuals may carry different alleles.
60 variants total across genes studied in relation to Chronic Pain.
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 Chronic Pain.
This is not a diagnostic service. Genetic variants do not determine whether you have Chronic Pain, 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
Chronic Pain shares biological pathways and genetic associations with the following related conditions and areas of research.
Frequently asked questions
Is chronic pain genetic?
Genetic factors influence pain sensitivity, pain processing, and susceptibility to central sensitisation. Variants in ion channels, neurotransmitter genes, and inflammatory mediators may contribute — but chronic pain results from complex interactions between genetics, environment, and neuroplasticity.
What is central sensitisation?
Central sensitisation is a state of amplified pain processing in the central nervous system, where neurons become hyper-responsive and generate pain signals without proportionate peripheral injury. It is proposed as a key mechanism in fibromyalgia, ME/CFS, and Long COVID-related pain.
Which genes are studied in relation to chronic pain?
Key genes include COMT, OPRM1, TRPV1, TRPA1, SCN9A, BDNF, and P2RX3. These cover catecholamine metabolism, opioid signalling, ion channels, and neurotrophic factors relevant to pain sensitivity.
How may pain genetics relate to Long COVID?
Musculoskeletal pain, headache, and neuropathic symptoms are common in Long COVID. Genetic predisposition to central sensitisation or neuroinflammation may contribute to why some individuals experience more severe or persistent pain following COVID-19 infection.
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 Chronic Pain and connected biological pathways.
Get Your Personalised DNA ReportInformational and educational only · Not a diagnostic tool · GDPR compliant
35 genes · 60 variants analysed in relation to Chronic Pain