Genetics and Fibromyalgia

Can our genes affect our likelihood of getting FM?

There is some evidence for genetic markers in Fibromyalgia, however I think we should approach these results with caution.

Genetic markers for the COMP gene in a ‘met/met’ sequence have been found in Fibromyalgia patients. 

Human pain studies have shown that a low COMT gene activity is often associated with increased pain sensitivity. These studies were done using experimental pain models, and showed an increase in pre- and postoperative pain in acute clinical situations.

BUT, and this is the important part …..stress can actually change our genes so that genes are silenced, or even switched on. This means that even if we find that Fibromyalgia sufferers do have an active gene sequence that increases pain, we do not know if they were born with this gene, or it was altered and switched on due to environmental cues.

“DNA methylation – a molecular modification that alters gene expression without changing DNA sequence, can be modified by stressful and socio-environmental factors”

Stress can change our gene expression (what the gene does). 

The Human Genome project was started in 1990 and completed in 2003. It was supposed to give us all the blueprints for humanity, we believed that finally we would have all the code to make humans! We thought we would be able to alter genes, cure diseases and gain control of our destinies. However, as usual in the human body, things were a little more complicated!

There were two problems with the idea of a human ‘code’.

Firstly it turned out that the difference between us humans and a fruit fly was tiny, and between us and chimpanzees was even smaller, only 1.2%! People were amazed that such a tiny amount of code could change a chimpanzee into a human being.

Secondly, we found out that genes are not fixed. We found out that genes had sequence (what the code said) and expression (what that gene actually did). The sequence and the expression were not always the same.

This means that, the set of genes we are born with, may not give us the same functions later in life. It also means that if two people with the same genes (like identical twins) could have different body functions later in life if they live in different situations. 

Some genes remain silent our whole life, while others are switched on, and others get switched off. To explore this, a whole new brand of science called Epigenetics appeared, looking to try and understand the effects of our environment on our genes.

We have moved on at incredible speeds since 2003 and now use DNA sequencing to explore and screen for many diseases (such as Leukaemia).

Our genes hold many clues to understand how we age and why we develop disease but they are not a quick fix. 

. . . . .

References:

Tammimäki, A, & Männistö, P. T. (2012) Catechol-O-methyltransferase gene polymorphism and chronic human pain: a systematic review and meta-analysis. Pharmacogenetics and Genomics: September 2012 – Volume 22 – Issue 9 – p 673-691

Martínez‐Jauand, M., Sitges, C., Rodríguez, V., Picornell, A., Ramon, M., Buskila, D. and Montoya, P. (2013), COMT gene, pain sensitivity and Fibromyalgia. EJP, 17: 16-27. doi:10.1002/j.1532-2149.2012.00153.x

Peng, H., Zhu, Y., Strachan, E., Fowler, E., Bacus, T., Roy-Byrne, P., Goldberg, J., Vaccarino, V., & Zhao, J. (2018). Childhood Trauma, DNA Methylation of Stress-Related Genes, and Depression: Findings From Two Monozygotic Twin Studies. Psychosomatic medicine80(7), 599–608.

The Smithsonian National Museum of Natural History, link here

Abelson, S., Collord, G., Ng, S.W.K. et al. Prediction of acute myeloid leukaemia risk in healthy individuals. Nature 559, 400–404 (2018). https://doi.org/10.1038/s41586-018-0317-6