The National Institute of Health reports that nearly 50 million adults in the U.S. have significant chronic pain. More specific data from the National Health Interview Survey estimates that within any three-month period, 25 million adults experience daily chronic pain, while an additional 23 million experience severe acute pain. Yet, the available treatment options have changed little in 60 years—that is, the use of opioid-based analgesics. Until recently the differential diagnosis of pain focused on a linear model to identify specific bodily trauma or injury, post-surgical complication, or an illness known to generate moderate to severe pain. Once the pain generator was established, a treatment regimen of physical therapy plus oral or infused analgesic medication or a variation of this modality was universally accepted. Non-responders with low back or severe joint pain were referred to a surgeon or put on disability. Idiopathic pain syndromes, including conditions such as fibromyalgia, and other neuropathic pain syndromes are increasing, but our understanding of this phenomenon is very limited.
What Do We Know?
How we experience pain is a highly variable and subjective phenomenon. The variance in experience transcends most traditional etiological and pathophysiological models and differ to some degree between gender, race, age and ethnicity. Attempts to codify or generalize known pain generators (illness or injury) have not produced reliable benchmarks of predictability or diagnosis.
What we often called idiopathic is more likely a dynamic variance in genetic expression that underlies the somatic experience of pain. Our understanding that pain, or more precisely the vulnerability to pain, is highly heritable is primarily the result of monozygotic twin studies, most recently reported by Vehof and colleagues in 2014. Using twin modeling analysis, their research suggests a common pathway model to explain the pattern of correlation of vulnerability among twins, with estimated heritability of 66%—suggesting shared genetic factors underlie the conditions that result in chronic pain.
Data estimates of the general population reveal that heritability of specific pain conditions or pain perception resulting in persistent or chronic pain is between 25% and 60%.
Environmental mechanisms underpinning pain variability are nearly impossible to estimate. Depression and chronic pain are bi-directionally correlated, and numerous medical conditions are associated with both depression and chronic pain. Yet phenotypical paradigms demonstrate that environmental stressors and genetic expression account for a plethora of risk factors that contribute to pain perception and vulnerability. The specific mechanisms by which an individual’s genetic variance and environmental factors produce vulnerability are not known.
Why Does This Matter?
Chronic and intractable pain is a debilitating condition responsible for unfathomable suffering. The economic implication of 50 million ageing Americans with chronic pain is staggering and unsustainable.
We desperately need a large commitment of resources and expertise fully focused and invested in translational pain-research, medical education and new treatment modalities.