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What can we learn from twin studies of pain and analgesia?
| Content Provider | Semantic Scholar |
|---|---|
| Author | Nielsen, Christopher S. |
| Copyright Year | 2012 |
| Abstract | Twin studies serve several functions, but the most common is estimating heritability. As progress is made towards identifying genetic variants that are associated with complex phenotypes, heritability estimates are gaining increasing importance. These analyses tell us how much variance can be explained by genetic factors and consequently form a benchmark to gauge our progress. Typically single nucleotide polymorphisms identified in large genome-wide association studies account for a small fraction of the heritability, but exceptions exist – most notably in age-related macular degeneration, where five single nucleotide polymorphisms explain 50% of the heritability [3]. It is too early to say whether pain and analgesia follow the typical or the atypical pattern, but knowing the heritability of our pain phenotypes will be an essential roadmap as research progresses. Twin studies of pain have almost exclusively been restricted to studies of clinical conditions, mainly based on questionnaire data. This is unfortunate because one of the comparative advantages of pain research is the availability of experimental pain models that form a bridge to animal research. To date only three twin studies have published heritability estimates for experimental pain [2,4,5], despite the growing use of these models as endophenotypes in genetic association studies. In addition to experimental models, pain research benefits from the availability of drugs that target specific pain modulating mechanisms. Genetic studies of the efficacy of analgesic drugs are important because they can help explain variation in drug response, but it is also likely that they will be informative with respect to endogenous pain modulation. Though considerable research effort is invested in molecular genetic studies of analgesics, there are as yet no twin studies addressing this topic, and consequently we do not know how important genetic predisposition is for the efficacy of these drugs. It is therefore highly welcome that in this issue of Pain, Angst and colleagues [1] report results from a twin study of opioid analgesia. Using a placebo controlled cross-over design and a sample of 81 monozygotic and 33 dizygotic twin pairs, they studied the effect of alfentanil, a highly potent, short acting opioid analgesic, on three experimental pain measures: heat pain threshold, cold-pressor pain threshold (time to pain) and cold-pressor tolerance (time to withdrawal). Results showed that 60% of the variance in the analgesic effect on cold-pressor pain threshold was explained by genetic factors. Significant familial aggregation was also found for alfentanil’s analgesic effect on cold-pressor tolerance (30%), but the sample size did not permit separating shared environmental from additive genetic effects. Results for heat pain threshold were not significant. The authors also report heritability estimates for baseline pain sensitivity. They found significant heritability for cold-pressor tolerance (49%), whereas estimates for cold-pressor pain threshold (17%) and heat pain threshold (20%) were not signif- |
| Starting Page | 1346 |
| Ending Page | 1347 |
| Page Count | 2 |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/j.pain.2012.03.014 |
| PubMed reference number | 22463823 |
| Journal | Medline |
| Volume Number | 153 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/S0304395912001674 |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/S0304395912001674?dgcid=api_sd_search-api-endpoint |
| Alternate Webpage(s) | https://doi.org/10.1016/j.pain.2012.03.014 |
| Journal | PAIN |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
