In many cases, the cause of RLS remains unknown. I conducted a long study and found the cause of RLS in my case. It's unlikely that my case is unique—though it's hard for me to judge how common it is, as one case can hardly be considered representative :). So, I’m sharing my findings here, hoping they might help someone.
In my case, the cause of RLS was directly related to the so-called Pharyngeal Pituitary (PP). This peculiar gland is located in the nasopharynx and is considered a part of the ordinary Pituitary Gland, which regulates the human hormonal system. During embryonic development, the PP separates from the Pituitary Gland and remains in the nasopharynx, while the Pituitary continues to develop near the brain.
For some reason, the scientific community has largely ignored the PP—most researchers consider it hormonally inactive, an "unnecessary" body part :). However, there are studies suggesting otherwise. For instance, in cases of Pituitary removal for patients with Acromegaly, hormones were still found in the blood, leading to the conclusion that they were produced by the PP.
Another study suggested that the PP plays a compensatory role when the Pituitary is underperforming or malfunctioning. This study also mentioned that the PP is regulated by the same Hypothalamic hormones as the regular Pituitary Gland.
In short, there is enough evidence to believe that the PP does participate in hormone production, though in healthy individuals, its role is minimal or nonexistent because the Pituitary handles everything on its own.
The PP is located directly in the nasopharynx and releases a significant portion of its hormones there. These hormones then partially end up in the mucus of the nasopharynx, and some reach the lungs and stomach. There is a condition likely linked to the PP called Burning Mouth Syndrome. It occurs when a person experiences a sudden hormonal imbalance, such as when taking hormone-based medications. This represents the PP’s compensatory role: it tries to restore the previous hormonal balance by releasing hormones into the nasopharynx. As a result, the mucous membranes of the mouth are "burned" by the high concentration of Pituitary hormones. This is just my hypothesis, as science does not yet know the exact cause of Burning Mouth Syndrome.
Another consequence of excessive PP activity is RLS. I will describe how this mechanism works in my case.
When I lie down to sleep, I feel my pulse speed up after a few minutes—this is one of the effects of PP hormones, which the scientific community seems unaware of. The simplistic explanation given by scientists is that you are afraid of dying in your sleep, and that’s why your heart races. Sure, but it passes after five minutes—maybe I realize I’m an idiot and stop being afraid. And this happens every evening. I don’t feel any fear myself, without the scientists' explanation—it’s complete nonsense :).
I figured out that this pulse acceleration is linked to hormones. If you experience similar pulse acceleration while lying down, you may notice the same effect if you hold your head tilted forward for a long time or breathe in through your mouth and out through your nose for several minutes, among other methods—like rinsing your nose with saline, for example. By using a combination of these techniques, I managed to double my testosterone levels in half an hour! — confirmed by lab results. Science knows nothing about these methods. However, they only work for those who have the issues I’ve described.
All these methods share one thing in common: they influence the absorption of hormones from the mucus in the nasopharynx. The nasopharynx always contains a decent amount of mucus, and if it contains PP hormones, they get absorbed more intensively in all these cases. When you lie down, gravity pushes the mucus against the inner surface of the nasopharynx, making hormone absorption faster. This is what happens as people like me with RLS are falling asleep.
What happens next: the suddenly absorbed Pituitary hormones create significant chaos in the hormonal system. Among other effects, adrenaline levels rise, speeding up the heart rate. But it’s not only hormones that increase—as a result of hormonal spikes, neurotransmitter levels, like dopamine, also rise. For some, this is good—dopamine facilitates a pleasant transition into sleep, and they experience no negative effects. But for people who already have high dopamine levels (or whose neurons are too sensitive to dopamine), this leads to dopamine neurotoxicity—in simple terms, brain neurons get damaged by excess dopamine. It’s known that the brain can sharply block the Hypothalamus-Pituitary axis to reduce neurotoxicity. And that’s what it does.
So here’s what we get: we lie down to sleep, and this position change triggers a surge of dopamine in the brain. Then, dopamine production is blocked to protect the neurons, and after a while, we have a dopamine deficit instead of an excess. Official science considers dopamine deficiency the main cause of RLS. So, here we have the complete mechanism of the syndrome's development.
It’s understandable why science is unaware of this: the PP is still under-researched and considered an unnecessary body part. But, as with appendicitis, an “unnecessary” part can seriously disrupt the main system's function.
Now, about how I deal with this problem.
The main strategy here is to reduce the dopamine spike when transitioning to sleep by stretching out this transition over time and then, later at night after the spike, to compensate for the dopamine deficiency. This way, the brain won’t need to protect itself from dopamine neurotoxicity by blocking dopamine production. I am currently testing the following method: I use a reclining chair and gradually lower the backrest into a lying position over the course of 20 minutes. But I also need to sleep on my back for the first few hours after that; otherwise, all this “preparation” doesn’t work :).
This reduces a bit RLS symptoms but doesn’t solve the problem entirely: after some time at rest, hormone absorption from the nasopharynx stops, and dopamine levels in the brain decrease—though less than without these steps. I still need a way to boost dopamine at that time.
If dopamine is increased before this (as is done with Levodopa), instead of a therapeutic effect, we get a toxic effect—the body fights off the toxic excess of dopamine by reducing D1 receptor numbers and other methods. We all know the consequences: Levodopa has a terrible number of side effects and eventually stops working, but it becomes impossible to stop taking it.
I figured out the correct way to use Levodopa. The right approach is to take Levodopa only after going to bed and experiencing strong RLS symptoms—never earlier. Additionally, after taking Levodopa, it’s best to avoid sudden changes in position. Using Levodopa this way (50 mg) is currently working for me—I’ll continue testing it. Previously, with the usual method, even 100 mg stopped working after 3–4 days, and the side effects were terrible.
As a stronger measure, I also tested 1/8 of a tablet of Pipamperone 10-15 minutes before starting all the above routines. Pipamperone temporarily lowers dopamine levels and, together with the preparation routine, reduces the dopamine surge even further. However, Pipamperone is a serious medication, so consulting a doctor is necessary. Given that official science is unaware of this whole mess, it’s unlikely that anything will work out for you. So, I don’t recommend trying my Pipamperone tricks at home :).
If you’ve not only read this far (which I highly doubt) but also tried my method (which I doubt even more), and, unbelievably, it even helped you—I'd be very grateful if you wrote to me about it via the Chat icon. (Email address deleted for your own security - Kaarina). Then, I’d feel my effort in describing this deeply subjective experience wasn’t in vain :).
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