All in the Family: Why Chronic but not Acute Back Pain may be Heritable

If your mother, father, sister or brother suffers from chronic back pain and you do as well, this may not be a coincidence. Researchers are discovering that certain genetic variants may predispose individuals to developing chronic back pain due to changes in bone and cartilage structure, pain processing and pain signaling in the brain (Tegeder & Lotsch, 2009). In addition, genetic changes will affect the way persons who live with chronic back pain respond to various types of drug therapy, particularly opioids.

Genomic studies in the UK and Scandinavia revealed 355 single nucleotide polymorphisms (SNPs) that were significantly associated with chronic back pain (Borstov, Parisen et al., 2022). SNPs, pronounced “snips,” are variations in DNA building blocks, called nucleotides (Medline Plus, n.d.). Nucleotides are organic molecules that serve as the basis for all life forms. Four nucleotides are found in DNA and RNA: adenine, thymine, guanine and cytosine. SNPs are generally found between genes and can help to predict a person’s response to various drugs and toxins. They can also help researchers study the heritability of certain pathological conditions, such as chronic pain.

Although the heritability of chronic back pain is relatively high at 30-45% of the population, this does not hold true for acute back pain (Tegeder & Lotsch, 2009). Researchers believe that the reason is that different biological mechanisms underlie to two conditions. While acute back pain, defined as pain resolving within about 3 months is often caused by traumatic injury to the bone or musculature, chronic back pain typically results from ongoing pathological conditions such as osteoporosis, certain types of arthritic conditions such as ankylosing spondylitis, and widespread pain syndromes (fibromyalgia). In each case, genetic predisposition plays a role in a person’s risk for developing the condition.

Genetic variations also play a role in an individual’s sensitivity to pain, and in pain signaling systems within certain parts of the brain. In some cases, genetic variations make a person less sensitive to pain, such as the “pain protective” haplotype found within about 16% of the Caucasian population (Tegeder & Lotsch, 2009). A very small percentage of the population have channelopathies which make them completely insensitive to pain. This Congenital Insensitivity to Pain (CIP) can be very dangerous, because afflicted individuals do not sense the warning signs of injury. On the other hand, genetic variations may also drive inflammatory processes via chemical messengers called cytokines. Once the ball gets rolling, such inflammatory conditions tend to become chronic, with ongoing pain.

A person’s genome also determines how well or poorly they may respond to drugs for controlling pain, by how well the individual metabolizes the drug. For example, about 7% of the Caucasian population lacks the enzyme for metabolizing morphine products resulting in inadequate analgesia, while others have too much of it, leading to dangerous side effects for what are considered normal dosages of these drugs. All of this speaks to the importance of personalized medicine: drug therapies designed specifically to work with a person’s genetic makeup. This is an active area of research that is slowly finding its way into clinical applications. It holds the promise of pain relief for millions of persons who currently suffer from chronic pain, for whom existing therapies are ineffective.


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