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Studies have shown that the manner in which an individual experiences pain and the magnitude of the response to a given pain stimulus may reflect a genetic "set point" in pain sensitivity, irrespective of the degree of tissue damage or inflammation. It may very well not be the case that a given individual can deal with pain better because he or she is "tougher"; it may just mean we have one more thing for which we can lay the blame on genetics.
For example, fibromyalgia, that chronic pain syndrome characterized by widespread pain in the absence of inflammation or damage in the tissues that can explain the extent and severity of the pain symptoms, has among its sufferers individuals whose experience of pain may be genetically determined and result from differences in the expressions of genes for important receptors and signaling pathways. Potential genes might be those responsible for catechol-O-methyltransferase (COMT), GTP cyclohydrolase 1, and the voltage-gated sodium channel Nav1.9, which can have significant effects on the control of pain perception in humans.
There has been data published showing the relevance of COMT to human pain perception, the genetic expression related to this substance playing a role in influencing differential pain sensitivity, working perhaps in conjunction with the mu-opioid system. Of note, some of these same gene expressions have also been associated with psychiatric disorders. Genetic analyses have shown individuals can be grouped into three subsets, depending on nucleotide configurations:
1. Low pain-sensitive.
2. High pain-sensitive.
3. Average pain-sensitive.
These subgroups are extremely predictive of pain sensitivity on a variety of different experimental pain tasks. In addition, the development of temporomandibular joint disorder was three times as likely in high pain-sensitive individuals as in the other groups.
Animal studies have given further evidence for the influence of COMT on pain. It was found that rats with the low pain-sensitive genetic configuration produced much higher levels of COMT activity when compared with the average pain-sensitive or the high pain-sensitive genetic configurations. Inhibition of COMT in these animals causes a marked increase in pain sensitivity.
But rats are not alone in being affected by the COMT genes. It was found that humans with a particular COMT genetic variant had an approximately three-fold increase in the risk for hip pain among osteoarthritis patients. Female carriers of the genetic variant were more likely to suffer pain. This sex difference is of interest, as the expression of COMT can be induced by estrogen, and it is well known that the chronic pain syndrome, fibromyalgia, has a much higher incidence in the female population.
And so science continues to break genetic codes that confirm we are not alone in our suffering. Our chromosomes are crying right along with us, for better or worse, as whipping boys of blame, and as explanations of what is and what is not sane.
