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Genetics and Pain 

Genetics and Pain
Genetics and Pain
Pain: Dynamics and Complexities

Daniel M. Doleys


This section provides a background for the study of genetics in the area of pain by highlighting the vast amount of individual differences in the expression of pain, even given an identical stimulus. It notes how extremely small differences in the genome may result in large differences in phenotypes. The consequences of genetically based insensitivity to pain are noted. Animal and human studies examine the importance of COMT, OPRM1, GCH1, nerve growth factor. Data from studies using experimental induced pain EIP) involving various modalities, suggests the potential involvement of COMT, and two SNPs of TRPV1 and OPRD1 and MC1R. At this point in time, genetics appear to account for about 50% of the variability in EIP. COMT, OPRM1, GCH1, TRPV1, and OPRD1 are among the most commonly considered candidate genes linked to variability in individual experience with EIP. Congenital insensitivity to pain (CIP) and hereditary sensory and autonomic neuropathies (HSAN) are marked by the absence of primary sensory and autonomic neurons necessary to the perception of pain. The role of genetics in aabsorption, distribution, metabolism and excretion of various analgetic agents is summarized. The cytochrome P450 system, A118 MOR ‘major’ allele of the A118G SNP, and its variant, G118 MOR are reviewed. Data suggesting the G118 MOR to have some type of ‘protective’ function against chronic pain and to modify the patient’s responsiveness to opioids is discussed. The OPRM1 118G allele was associated with decreased opioid requirements and/or decreased opioid effectiveness

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