It is clear that our ability to experience pain is inherited from our parents. Some are more susceptible to pain than others and this is directly related to our genes. This fact is being exploited for the development of treatments for pain. It is helpful for both new drug discovery and target identification. This explains variability in response to therapy. Not everyone has the same genetic makeup, so not everyone will respond in the same way to a given treatment. Using this information, we will be better able to target responders to particular treatments, including surgery and other invasive treatments.
Most painful diseases and disorders do not follow Mendelian genetics. They appear to be induced by diverse environmental exposure and genetic factors. Penetrance is variable and is dependent in part on genetic code. Probably several genes interact to alter penetrance. In other words, we are not just the product of our genetics. Not everyone with genes that make them susceptible to pain, or likely to develop painful conditions such as Fibromyalgia or CRPS actually go on to suffer from these conditions.
It is likely that about 25-60% of pain response is probably genetic. Phenotypes can sometimes be linked. That is, the characteristic of blond hair and the propensity to sunburn are linked phenotypes. Phenotypes that are often linked together are the development of anxiety and depression and the development of chronic pain. It is likely that the phenotype of high degree of psychological stress is associated with genes that are also associated with heightened experience of pain. By understanding this linking of phenotypes, it is possible to develop treatments that are more effective for these specific characteristics. It is also possible to develop treatment protocols that can be implemented early in the course of an illness to reduce the likelihood of developing other linked conditions. As an example, if I treat my patient who is suffering with pain for anxiety and depression as well, I may get a better result than if I treat them for pain alone.
Pain sensitivity is associated with high sympathetic tone as well. High sympathetic tone is associated with low heart rate variability. Recall that a decrease in heart rate variability is associated with low vagal tone and is also associated with the presence of, or the risk of developing pain from a chronic inflammatory condition.
As you can see, it is possible to see pain in a variety of different ways. We know that the risk of developing chronic pain is inherited. It is linked to the genes you get from your parents. We also know that the risk of developing chronic pain is linked to the risk of developing anxiety and depression. The genes that carry the risk for pain and the genes that carry the risk for depression and anxiety probably reside very close together in our chromosomes. The more conditions we can link to the pain genes, the more likely we are to be able to identify these genes. If we can identify them, we will be able to develop treatments aimed specifically at these genes. The hope is to identify clusters of genetics that will be targets for treatments for specific syndromes. Genes for Fibromyalgia, Tempo= Mandibular Joint disease, Irritable Bowel Syndrome, etc will eventually be identified and we will be able to manufacture treatments aimed at turning these genes off, or blocking them so they never turn on and result in the condition at all.
In the mean time, we can to simple things to check to see if you are more likely to develop chronic pain. One is to look at your heart rate variability. If you have little or no heart rate variability, you may be at risk for developing chronic pain, or you may already be suffering from chronic pain. If you have low heart rate variability, there are things you can do. Get on a strict regimen of diet and exercise, learn things like meditation and yoga. Change your life, before it gets the better of you.
