Two Paths to Sensitivity?

 

(The following is an excerpt from my paper "Solving the Riddle of Chemical Sensitivity," which can be downloaded from the home page of this site.)

 

In 2001, Pamela Reed Gibson, author of Multiple Chemical Sensitivity, published the results of a survey of 917 people with self-reported MCS. In answer to the question about how the condition developed, 20 percent of those with MCS could identify a single chemical exposure event which triggered onset, while 58.5 percent said onset came on gradually, after a “series of low level exposures.”  (The rest didn’t know or blamed things such as stress).  Most everyone familiar with MCS acknowledges that there are two different “speeds” of onset, some quite sudden, some gradual. This was the first fact that made me wonder, could there be two “types” of MCS?

 

In reading other people’s accounts of their MCS experiences, I also noticed that a certain number of people complained about food intolerances (such as salicylate sensitivity), while others didn’t. While I I didn’t find a lot of curiosity about this common co-occurrence between the two conditions, I myself felt it had to be a key clue to the problem. 

 

Especially attention-getting to me was that so many people reported that going on a low salicylate diet actually exacerbated their MCS, which is exactly what happened to me. My sensitivity to scented products dramatically increased within a week of starting a low salicylate diet. Indeed, Anne Swain, the scientist who first established salicylate levels in food, almost casually acknowledged this in her book, Allergy Friendly Food.  In one small warning paragraph, she wrote that going on a low food chemical diet makes many people suddenly “more sensitive to smells.”

   

Why the fact that a low salicylate diet could actually induce a higher stage of multiple chemical sensitivity wasn’t being highlighted and hotly debated in MCS circles puzzled me. The usual explanation of MCS being the result only of chemical injury or chemical exposure was clearly not true; for at least some sufferers it was impacted by diet.  Here again, I saw evidence for two different paths types of, or paths toward, MCS.

 

Another striking difference in people’s experience of chemical sensitivity was their responsiveness to the brain rewiring techniques of Ashok Gupta and Annie Hopper.  Many people with even the most long-standing MCS had apparently been able to dramatically and completely recover from the condition in a fairly short time with limbic system or amygdala retraining techniques. But many others, like me, had been unable to fully recover from the condition through even the most persistent effort at brain retraining.  Again I wondered, was this because there are actually two types of MCS?

 

It was while researching TRP channels that I came across a paper published in a pain journal which talked about different types of hyperalgesia, or the experience of pain in response to innocuous or low level stimuli (an apt description of MCS).  This paper described two different paths in the development of hypersensitivity to stimuli:

 

“Hyperalgesia arises either from peripheral and/or central sensitizationPeripheral sensitization occurs by enhanced excitability [due to TRP channel activity] of nociceptive C-fibres in sensory neurons.”  Meanwhile, central sensitization results from “in an increase in nociceptor synaptic efficacy and enhanced responsiveness of neurons.”  In other words, peripheral hypersensitivity is a phenomenon that happens at the local cell level, while central hypersensitivity develops throughout the nervous system and, because of our brain’s plasticity, it becomes “wired” into the brain.  

 

This same paper also pointed out that sensitivity that develops gradually over the long-term is often due to “expression and/or silencing of specific genes,” whereas more sudden and short-term sensitivity is likely due to “covalent modification of the receptor,” meaning something has happened to change (or injure) the TRP channels on the surface of the cell.

 

Reading this, I found confirmation that there must indeed be two different paths to developing MCS:  1)  the sudden onset from a chemical exposure and/or injury which set in motion the process of central sensitization;  and 2) the more gradual result of ongoing cell-level peripheral sensitization which could just as easily be the result of genetic susceptibility as the result of chemical exposures.  

 

If correct, a “two path” theory would explain why only some, and not all, of MCS sufferers could be cured through brain retraining techniques. For those who experienced a chemical exposure leading to temporarily malfunctioning TRP channels, that cell-level injury would heal over time, and normal cell-level TRP channel functioning would eventually return. However, because the brain had been so quick to rewire itself through central sensitization, one would be left “stuck” in the trauma loop of MCS, even when there was no longer a reason for it at the cell level. Those ‘sudden onset’ sufferers would therefore be the people most likely to completely recover through brain retraining.

 

On the other hand, ‘gradual onset’ MCS sufferers (nearly 60 percent of us, remember) were more likely to be afflicted with a cell-level problem -- such as a genetic tendency to overexpress TRP proteins -- resulting in ongoing peripheral sensitivity that simply could not be ‘healed’ over time.  While central sensitization almost certainly played an exacerbating role in this second path to MCS, no amount of brain retraining would lead to full recovery as long as that ongoing cell-level peripheral sensitivity was an issue. 

 

Next:  Sensitive TRP Channels

By Teena Booth