Not dead yet!
Well-Known Member
I discovered a new supplement company I trust and they have some odd choices. Keter Wellness, Cissus and L-dopa, and there's a third that didn't grab me as much, and that's all. I'm always fascinated by these small businesses who "know something" and share it. Another one I support is O24 - my grandmother swore by camphor I think she was right.
Anyway, I'm taking Cissus because I've never had "belly fat" before I was ill. After I developed ME/CFS, my belly girth started to sag and fold over my hips. That didn't happen before. I might have been "pudgy" before but it was well distributed until the ME/CFS really took hold and I started being unable to move much.
The Cissus is supposed to lower cortisol levels, helping me sleep and hopefully redistributing this fat into a more healthy form. I'm also experimenting with a lower protein, higher vegetable diet to reduce wear and tear on my liver.
To make a long story short, I ended up on an article about GABA and how it lowers autoimmune inflammation. I had a lighbulb moment because I'd been taking exactly what they talked about, baclofen and topiramate. It made me wonder about other neurotransmitters. In retrospect it should be obvious that neurotransmitters have a role to play in directing the immune system. But for some reason it was never something I thought about directly, until here:
http://content.iospress.com/articles/advances-in-neuroimmune-biology/nib012044
"Abstract
There is a well-defined influence of dopamine (DA) within the immune system. It can be synthesized not only in neurons, but also in immune cells, especially in T cells. In addition, these cell are bearing an active uptake mechanism, which could serve another source of DA. Therefore, it is highly likely that a functional DA-erg autocrine/paracrine regulatory loop exists, where lymphocytes-derived DA acting through its own receptors, also expressed on the same cells, can have an influence on its own function. However, the possibility that immune cell derived DA may act in accordance with DA secreted by other sources, i.e. from sympathetic terminals, cannot be ruled out. In harmony with these observations have provided evidences for the existence of a functional DA-erg system in the thymus, indicating that DA may have also a role in the maturation and selection of a certain subpopulation of lymphocytes as well. Based upon all of this information and evidences, for being able to summarize this topic, a much broader survey, including all direct and indirect immune-modulatory role of DA is required. Therefore, in this review we are going to discuss the most relevant aspects of this regulatory function. Facts and theories based upon experimental (pre-clinical) data are extended with the evidences accumulated by clinical observations."
If I"m not mistaken, "dopamine" is a class of neurotransmitters, not one distinct chemical, and that the distinguishing feature is the use of L-dopa amino acid as the basis for the specific dopamine in use locally. I also think that opiate painkillers attach themselves to the same receptors as some dopamines in use by the body. That the differences between opiates is which receptors they specifically attach to. So pain control can be seen as a manipulation of the immune system. Or am I off the mark on that one?
It might explain other things like the therapeutic action of THC in chronic pain control.
It would also fit with my experience I've expressed to pain doctors: that what happens when I take an opiate pain drug isn't ecstasy, it's the quieting of the raw nerve that keeps announcing that I"m sick, in pain and not well. Pain drugs stop that alarm. One of the reasons I can't take antidepressants is they make that "alarm" feeling much worse until I can't sleep, and eventually can't even think, I can become catatonic on some of them.
All the same, if this theory I just floated is true and stays afloat on its own, it's a valid reason for me to stop taking opiates. I trust my body to know what it needs to communicate and why. I think that if this is true, then the system can only become more out of whack by me messing with it. Because it means my body has to communicate over the static I just introduced into the system. And it's not a "side effect" - instead it looks like this is the mechanism by which the pain is stopped, maybe.
I've always defended pain control and I still do. People should be able to find their own solutions that work for them. But now I have a reason to consider seriously not taking these drugs anymore, assuming I'm not way out in left field.
In case you're interested, this was the article on Cissus that mentioned GABA: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249909/
Anyway, I'm taking Cissus because I've never had "belly fat" before I was ill. After I developed ME/CFS, my belly girth started to sag and fold over my hips. That didn't happen before. I might have been "pudgy" before but it was well distributed until the ME/CFS really took hold and I started being unable to move much.
The Cissus is supposed to lower cortisol levels, helping me sleep and hopefully redistributing this fat into a more healthy form. I'm also experimenting with a lower protein, higher vegetable diet to reduce wear and tear on my liver.
To make a long story short, I ended up on an article about GABA and how it lowers autoimmune inflammation. I had a lighbulb moment because I'd been taking exactly what they talked about, baclofen and topiramate. It made me wonder about other neurotransmitters. In retrospect it should be obvious that neurotransmitters have a role to play in directing the immune system. But for some reason it was never something I thought about directly, until here:
http://content.iospress.com/articles/advances-in-neuroimmune-biology/nib012044
"Abstract
There is a well-defined influence of dopamine (DA) within the immune system. It can be synthesized not only in neurons, but also in immune cells, especially in T cells. In addition, these cell are bearing an active uptake mechanism, which could serve another source of DA. Therefore, it is highly likely that a functional DA-erg autocrine/paracrine regulatory loop exists, where lymphocytes-derived DA acting through its own receptors, also expressed on the same cells, can have an influence on its own function. However, the possibility that immune cell derived DA may act in accordance with DA secreted by other sources, i.e. from sympathetic terminals, cannot be ruled out. In harmony with these observations have provided evidences for the existence of a functional DA-erg system in the thymus, indicating that DA may have also a role in the maturation and selection of a certain subpopulation of lymphocytes as well. Based upon all of this information and evidences, for being able to summarize this topic, a much broader survey, including all direct and indirect immune-modulatory role of DA is required. Therefore, in this review we are going to discuss the most relevant aspects of this regulatory function. Facts and theories based upon experimental (pre-clinical) data are extended with the evidences accumulated by clinical observations."
If I"m not mistaken, "dopamine" is a class of neurotransmitters, not one distinct chemical, and that the distinguishing feature is the use of L-dopa amino acid as the basis for the specific dopamine in use locally. I also think that opiate painkillers attach themselves to the same receptors as some dopamines in use by the body. That the differences between opiates is which receptors they specifically attach to. So pain control can be seen as a manipulation of the immune system. Or am I off the mark on that one?
It might explain other things like the therapeutic action of THC in chronic pain control.
It would also fit with my experience I've expressed to pain doctors: that what happens when I take an opiate pain drug isn't ecstasy, it's the quieting of the raw nerve that keeps announcing that I"m sick, in pain and not well. Pain drugs stop that alarm. One of the reasons I can't take antidepressants is they make that "alarm" feeling much worse until I can't sleep, and eventually can't even think, I can become catatonic on some of them.
All the same, if this theory I just floated is true and stays afloat on its own, it's a valid reason for me to stop taking opiates. I trust my body to know what it needs to communicate and why. I think that if this is true, then the system can only become more out of whack by me messing with it. Because it means my body has to communicate over the static I just introduced into the system. And it's not a "side effect" - instead it looks like this is the mechanism by which the pain is stopped, maybe.
I've always defended pain control and I still do. People should be able to find their own solutions that work for them. But now I have a reason to consider seriously not taking these drugs anymore, assuming I'm not way out in left field.
In case you're interested, this was the article on Cissus that mentioned GABA: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249909/
![ME/CFS lecture | Dr Nancy Klimas | 2011 [Chronic Fatigue Syndrome / SEID / New Zealand] - YouTube](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
