Childhood traumatization is associated with differences in TRPA1 promoter methylation in [..] multisomatoform disorder [..], 2019, Achenbach et al

[Andy]

Full title: Childhood traumatization is associated with differences in TRPA1 promoter methylation in female patients with multisomatoform disorder with pain as the leading bodily symptom

Background
The construct of multisomatoform disorder (MSD) is a common point of reference for patients in different somatic and psychosomatic specialties and therefore useful in studying large well-characterized cohorts of a prototype of a somatoform disorder and in parallel as a functional somatic syndrome (FSS). This disorder is characterized by distressing and functionally disabling somatic symptoms with chronic pain as the most frequent and clinically relevant complaint. Pain is perceived by nociceptive nerve fibers and transferred through the generation of action potentials by different receptor molecules known to determine pain sensitivity in pathophysiological processes. Previous studies have shown that for the transient receptor potential ankyrin 1 (TRPA1), receptor methylation of a particular CpG dinucleotide in the promoter region is inversely associated with both heat pain and pressure pain thresholds. In this study, we hypothesized that TRPA1 promoter methylation regulates pain sensitivity of patients with multisomatoform disorder (MSD). A cohort of 151 patients with MSD and 149 matched healthy volunteers were evaluated using quantitative sensory testing, clinical and psychometric assessment, and methylation analysis using DNA isolated from whole blood.

Results
We found CpG -628 to be correlated with mechanical pain threshold and CpG -411 to be correlated with mechanical pain threshold in female volunteers, i.e., higher methylation levels lead to higher pain thresholds. A novel finding is that methylation levels were significantly different between patients with no and severe levels of childhood trauma. CpG methylation also correlated with psychometric assessment of pain and pain levels rated on a visual analog scale.

Conclusion
Our findings support the hypothesis that epigenetic regulation of TRPA1 plays a role in mechanical pain sensitivities in healthy volunteers. They further provide evidence for the possible influence of childhood traumatic experiences on the epigenetic regulation of TRPA1 in patients with MSD.

Open access at https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-019-0731-0

 

[Saz94]

Can someone translate this into simple language please?

 

[Midnattsol]

Can someone translate this into simple language please?

Haven't read the study properly, but the abstract says something like this (not sure if I managed the "simple", though):

Basicly they looked at methylation at certain CpG islands found in the promoter area of TRPA1. They found that an increase in methylation at CpG -628 and -411 led to a higher tolerance for for pain. Methylation is the process of adding a methyl group to something, in this case a certain part of the DNA called a CpG island. They found that the more methylation a person has at site -628 and -411 the higher their tolerance for pain is.

They then looked at methylation patterns and compared them to levels of childhood trauma. In controls the levels of methylation didn't differ between people with and without trauma, but in patients of MSD they found that those who had experienced trauma had lower levels of methylation.

So in healthy people childhood trauma did not cause a decrease in methylation (didn't make them more likely to experience pain?) but they suggest that this might be the case with people who receive a MSD diagnosis.

 

[Mithriel]

So childhood trauma does not lead to more pain sensitivity but being ill does. Yet they have manage to bend these results to say that childhood trauma leads to functional somatic syndromes!

 

[rvallee]

Can someone translate this into simple language please?

"We found correlation and argue that it means causation"

This table shows clear problems with any correlation with trauma, a very subjective self-assessment, since there are variations in chronic pain patients with no trauma compared to controls. The hypothesis should mean no difference and yet there is, likely down to the imprecise nature of assessing whatever people may mean by trauma. This is just fishing for some way to rationalize a predetermined belief that trauma is a significant causative factor in chronic pain.

Basically they found nothing of significance but argue they did because they want to do more research and reporting null results does not favor that. Should be referred to remedial science 101. Instead this will likely lead to more funding. Typical.

 

[alktipping]

if you cannot dress garbage in twenty dollar words then you have no future in psychology . or baffling people with imprecise language can be great for your bank account . all this tripe just makes me ill .

 

[Jonathan Edwards]

The abstract does not even say which cells the methylation was in. I doubt they checked brain cells.

 

[James Morris-Lent]

The abstract does not even say which cells the methylation was in. I doubt they checked brain cells.

A cohort of 151 patients with MSD and 149 matched healthy volunteers were evaluated using quantitative sensory testing, clinical and psychometric assessment, and methylation analysis using DNA isolated from whole blood.

I don't suppose that there would be any reason to think nucleated blood cells and whatever else is floating around tell us much about relevant nervous functioning in this case.