Earlier this month, a group of Australian researchers has published a new theory of CFS – a disease of the hypothalamic paraventricular nucleus (PVN).
This might be an exciting breakthrough for medical CFS community but it’s old news for me. I’ve been betting my chips on hypothalamic dysfunction – or more broadly limbic system dysfunction – ever since I read Jay Goldstein’s book in the summer of 2015.

“A disorder of sensory gating”
“A disorder of sensory gating”. This was the phrase that Jay Goldstein won me over with back in 2015.
Prior to that day, I was struggling to explain what was going on with me. I would choose specialists based on my own hypothesis and they were happy to oblige me with a diagnosis I was seeking to confirm.
When I thought I had a mental problem, I went to see a psychiatrist who diagnosed me with ADHD and depression, and also PTSD for good measure. When I believed I had adrenal fatigue, I called an adrenal fatigue specialist who agreed that I have stage V adrenal fatigue. When I believed that I had POTS, I went to see POTS specialist who after a lot of (mostly unnecessary) testing confirmed that I indeed had POTS due to Ehlers Danlos symptom. When I went to see CFS specialist she was unequivocally sure that I had a textbook case of CFS with the highest viral titers she ha ever seen.
In a way none of these people were wrong but they were all presenting me with the partial and rather superficial bits of my clinical picture. But I wanted to know to understand what was the main underlying disruption in my nervous system that made me feel so unbearable? I could correct my pulse with medications, I could take stimulants to boost my energy but none of that was really getting at the root of the ineffable that was going on inside my brain. But Goldstein made me realize that the intense discomfort inside me was not caused by any of those specific conditions but by my loss of ability to properly process incoming external and internal stimuli.
Everything’s the same and yet completely different…
Although I looked and acted normal on the outside, because of the abnormal sensory gating, I was not living in the same “reality” as other people.
The reason this issue in CFS is so difficult to capture in words and to communicate is because we do not have the right kind of vocabulary for these subtle changes in neurologic function. A writer or a poet might be able to capture the feeling but it is bound to elude a medical doctor especially a non-psychiatrist. As a result, most doctors who treat patients like me still assume that they are treating physical fatigue or irregular heartbeat but this is not at all what true CFS or dysautonomia is about, at least in my experience.
What it feels like is that if your brain were a city and all the traffic lights within it suddenly lost electrical power. And now there are all these cars crawling around and crashing into each other… in a total sense of helpless panic… until everything comes to a complete, paralyzed stall…
It’s a terrible and extremely torturous feeling which at its worst can only be described as absolute and sheer agony.
By calling it a disorder of sensory gating, Goldstein pinned down the nature of my suffering just right. I knew that he was talking about applied to me and having read that, I perhaps for the first time after a torturous year was able to grasp inside my mind what my real problem was. Underneath my fatigue, underneath my pain, underneath my brain fog – it was the same underlying glitch in my “sensory processing software”.
I’m not talking about specific sensory abnormality (such as altered sense of taste or smell or blurry vision), which can also occur in these conditions. It’s also not a flagrant distortion of reality as you would observe in psychosis or delirium. It is a very odd, very subtle change in the perceptual processing of external and internal reality.
To become aware of these changes one needs to be very mindful, very observant. A lot of times the internal reality is so uncomfortable and the change of external perception is so subtle and elusive, that less perceptive people may be completely unaware that they have shifted from one perceptual state into another and they explain their suffering entirely in physical terms. For others, the shift is so sudden and jarring – often going as far as complete derealization or depersonalization – that it often becomes the primary concern, pushing aside whatever physical issues they might have.
Having breached the subject with other patients, I know that most of those who’ve had the disease for a while, who’ve learned to navigate in and out of certain states, are very aware of these perceptual change of interfacing or being better attuned with the “outer world”.
The change can be as

One has to come out of CFS states – and not just brain fog – to appreciate the difference in processing that occurs when the metabolic and neurochemical changes are restored to normal. Some people only palliate their physical symptoms and do not notice the perceptual aspect of the disease. But if you focus on treating the perceptual aspect, the physical symptoms often disappear on their own
Limbic system and the “double hit” theory
Let’s go back to the hypothalamic paraventricular nucleus and see how it’s involved in all of this.
In CFS there is central hypothyroidism associated with either excessive or blunted secretion of Cortisol Releasing Factor (CRF, also known as Cortisol Releasing Hormone or CRH). It is not just Hashimoto’s thyroiditis with normal TSH. The overwhelming majority of people with Hashimoto’s does not have CFS. A vast majority of people with subclinical hypothyroidism does not develop CFS. Even though Addison’s disease shares some of the features with the CFS/
The fact that the colloquial term of “adrenal fatigue” is an outdated explanation for a well-described hypothalamic-pituitary-adrenal dysfunction that also exists in other neurologic illness such as fibromyalgia, depression, dysautonomia, and PTSD is pretty obvious to anyone studies both adrenal fatigue and basic neuroscience.
But CFS associated with dysautonomia and improper sensory processing is also not the same disorder as depression. The mechanism might be similar but there is, more metabolic and hormonal disturbance in CFS. The parts of the limbic system involved in CFS probably involve parts of the limbic system closely involved in autonomic regulation, including control of immunity. In depression, the parts of the limbic system that are involved are more involved in emotional regulation. However, there can be significant overlap. The limbic system is
The question of whether hypothalamic dysfunction is the cause or consequence of CFS has been an ongoing debate. Previous studies suggested that it’s more likely to be the consequence but the Australian study offers a different perspective. My personal view is that it is a more broad disorder of the

Conclusion
The greatest problem with CFS, in my opinion, is that people who study it focus on external rather than internal truths about this condition. This has been leading the researches in the direction of chasing secondary manifestations rather than a root cause. The new Australian study gives me hope that the science will finally start catching up on the primary neurological nature of this illness, which Jay Goldstein, a brilliant rogue family practitioner
Correction on mistyped word that would be issues with Mitrocondria Complement Factors. This was found in the study done by Drs. Light in Utah. It was a study between families and those if us with multiple family members having CFS, FMS, POTS etc. Even though my sister and I share similar genes, the function of mine was much lower. Meaning I had much more dysfunctional expression, at that moment, than she did. I was told I was in lowest 20% of function of all CFS patients in the study. So trying to tweak this and see if there is a way around the apparent lack of energy in the powerhouses of the cells – mitrochondria.