It’s the best time to be alive, when almost everything you thought you knew is wrong.

— Tom Stoppard

As you can see – or hopefully as you will see later on while I explain it more, the trace amine theory begins with the old fashioned assumption that ME/CFS is somehow linked to EBV virus. I called it Herpesviridae family to which EBV virus belongs rather than EBV virus because it is not technically proven that it is the only virus involved. There could be some other herpes virus such as HTLV-1 or HHV-6. The fact that antiviral therapy has been of little help in the treatment of ME/CFS would support EBV virus since unlike Herpes virus it has not shown much response to antiviral therapies, such as acyclovir.

Virtually everyone has been exposed to EBV virus by the time they finish college, although there is some evidence to believe that those who have been exposed to it later in life are more likely to develop problems later on. It lives inside of us in what is described as “latent infection” – the virus chooses to co-exist with its host peacefully as long as the immune system keeps it in check.

In my case, it is very likely that I have contracted a pretty vicious strain of EBV during my sophomore year in college. My boyfriend at the time came down with a severe case of mononucleosis. I don’t remember getting very sick but shortly thereafter I began to have chronic throats, enlarged lymph nodes and white exudates on my tonsils. My solution to that was to get rid of my tonsils. I remember that hurt as hell but I have recovered quickly and ten days later went on adventure tour to Canadian Rockies, which was my college graduation gift. Thinking back to it, I can’t help but wonder what role getting rid of my tonsils in adult age – which serve as an immune system point and was probably given to me by nature for a reason – has had on the spread of EBV virus later in my life. It did temporarily get rid of my sore throats in the short term but very likely contributed to my problems with thyroid gland infection, throat are neuropathy and future lifelong struggle with ME/CFS/fibromyalgia. Not the best trade off but who knew, right?

Throughout my 20s, during the periods of increased physical or emotional stress (and life has provided me with plenty of that), my immune system has dropped the ball on more than one occasion, allowing the EBV virus to migrate through lymphoiod tissue from my oropharynx and invade the surrounding territories, with their most strategic conquest being a small yet extremely crucial organ called the thyroid glad (The link between thyroid autoimmunity and EBV virus is not just my idea, you can read about it here.

I would have never known that I had a thyroid problem since my thyroid values have always remained stone cold within the normal range. Most regular physicians will not check the thyroid antibodies if your TSH and thyroid hormones are normal. Moreover, the thyroid antibodies, in my opinion, have little to do with the actual disease in my case which is caused by viral infection and not the autoimmunity itself, therefore it is probably possible to have EBV thyroid infection with normal thyroid antibody levels if there is no Th2 immune system shift, e.g the immune system is not cranking out antibodies at higher than normal rate).

The only reason I found out that there was a big trouble with my thyroid – other than from mild, “non-significant” elevation of antibodies, is because I had thyroid ultrasound which showed several large nodules that appeared consistent with areas of inflammation. Thyroiditis is a common problem that tends to occur in women after pregnancy. This is because during pregnancy the immune system becomes suppressed which allows the virus to proliferate and then once post-partum it bounces back, leading to a “double-whammy” of both viral and autoimmune attack.

This is why around six months post-partum after I gave birth to my son, for the first time in my life I found myself laying on the couch, feeling completely unable to get up. (Of course back then I just choked it up to sleepless nights and changing hormones). Yep, without a doubt, things did go down the drain for me after each pregnancy.

Never-the-less, I do not think that viral thyroiditis alone is enough to explain ME/CFS and POTS phenomenon. There are literally millions of people out there who have thyroid problems. Yes, they do not enjoy the greatest health but they do not fall apart in the way that we do. There has to be something else. I’ve spent my years traveling the world of online communities and reading research publications on cellular biology and neurochemistry trying to figure out what that missing link might be. The people in thyroid fringe communities sounded in many ways similar to me, but the treatment that worked for them (large, progressively doses of natural dessicated thyroid) did not work for me, in fact I felt like it nearly killed me (!).

The clinical course of the illness described in adrenal fatigue books was eerily similar to mine but the science it relied on was clearly simplistic and outdated, and taking steroids only made me worse.

I don’t remember how exactly I came across the TAAR functions – I believe that it was while I was researching PEA – but once I began reading about tri-iodothyronamine (or T1AM for short- not that it is not at all the same as tri– idiothyronine which is essentially a fancy name for T3 or the most potent form of thyroid hormone). it felt like a true eureka moment. I finally found what I was searching for all this time – a plausible link that could connect everything I knew about myself and the nature of mysterious illness I was sharing with thousands of other people. It explained my paradoxical reactions to thyroid hormone, my extreme sensitivity to changes in neurotransmitter levels, my altered autoimmunity, my heightened sense of smell… Literally it explained pretty much everything and surely this could not be just a coincidence.

To sum up my current understanding of the nature and evolution of my disease: the Epstein-Barr (or similar) virus inserts itself infects oropharynx/nasopharynx and over time travels through nerve endings toward thyroid gland. The insertion of viral genome into human DNA leads to abnormalities of thyroid trace amine production which in turn leads to severe neuroimmunoendocrine function compromise in predisposed people with either inborn or acquired abnormalities of trace amine receptors, which have likely predisposed them to immune system dysfunction in the first place.

It is painfully obvious that the reason ME/CFS is so untreatable despite the efforts of traditional and alternative medical establishments – is because it’s a vicious cycle that most of the time is never truly broken. There is no good cure for chronic thyroiditis or chronic EBV virus so any effort to combat the disease in those two quadrants is likely to fail. One is more likely to succeed by manipulating the cycle at the point of neurological changes or immune system – which is essentially what everyone is doing with herbs and supplements and you name it – but because the underlying dysfunction that threw those systems out of balance is not being address, the success rate is usually modest.

Over ten yeas ago, I have set out on a quest to find a cure for my problem but what I found instead was an explanation.

While there is no cure for ME/CFS, I am feeling much optimism that we are on the brink of discovering one. To support my belief I want to use the example of Type I Diabetes. Here’s what the Wikipedia tells us about its history:

“Although diabetes has been recognized since antiquity, and treatments of various efficacy have been known in various regions since the Middle Ages, and in legend for much longer, pathogenesis of diabetes has only been understood experimentally since about 1900.[6] An effective treatment was only developed after the Canadians Frederick Banting and Charles Best first used insulin in 1921 and 1922″.

After invention of insulin people with T1DM were able to survive longer and suffer much less. Now almost a hundred years later, as the understanding and management of the disease have evolved, they are not just surviving, they are thriving, they can go on to become doctors and win the Amazing Race several years ago.

In other words, there was a twenty year lag between understanding the disease and finding the treatment, and that was a hundred years ago. While the diagnostic predecessor of ME/CFS (known back then as neurasthenia) has been described in the 19th century, trace amine receptors was first discovered in 2001, and it took another ten years for scientific community to realize their important role in the physiology of metabolism.

I believe that TAAR1 and T1AM are just about getting ready to make their breakthrough into the clinical scene, and when they do it’s going to be huge. There are already prototypes of TAAR agonists and antagonists that have shown promise in animal models, and once the importance of T1AM is realized it won’t take long to figure out how it is synthesized and regulated. These will provide new avenues for treatment of poorly understood conditions such as fibromyalgia, ME/CFS, multiple chemical sensitivity, POTS, dysautonomia, and atypical depression (since all of this conditions reflect dysfunction of autonomic nervous system, I will refer to them from now on for simplicity sake as “dysautonomic illness”. Also, please note that I’m choosing to use the form dysautonomia in a broader sense that is currently accepted by the traditional medical community where it mainly used to describe cardiovascular dysregulation).