I was checking something about thyroid hormones in the brain, and found this paper interesting: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978256/
Thyroid hormones are definitely important for proper adult brain function, but it's certainly not as simple as "a normal level of T4 in serum = everything is okay". There are several feedback loops in the brain to keep the levels of T4 and T3 at appropriate levels. "Additionally, untreated hypothyroidism in the adult is associated with severe intellectual defects, abnormal balance and defects in fine motor skills, spasticity, and deafness"
Astrocytes are important for converting T4 from serum to T3 in the brain. Since astrocyte function might be affected by immune system activation, it's possible that this will affect T3 levels in the brain.
"Thyroid hormones mediate CNS effects primarily through thyroid hormone receptors (TRs), members of the nuclear hormone receptor family (4, 7, 8). TRs bind to the DNA regulatory regions of target genes to activate or repress transcription through interactions with accessory proteins known as coregulators." I think this is at least a possibility for having genes play a role in predisposition to ME. The paper (falsely) considered T2 to be inactive, but my experiences with supplemental T2 convince me that it too is important in transcription. A boost to T2 seemed to produce something that lasted a consistent 21 days before abruptly failing.
The paper introduced me to another new (to me) brain cell: tanycytes. "Deiodinase 2 <converts T4 to t3> is only expressed in selected cell types within the CNS: astrocytes and tanycytes." Tanycytes are specific to the hypothalamus. Here's a paper on them:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605593/
"Abstract
Tanycytes, glial-like cells that line the third ventricle, are emerging as components of the hypothalamic networks that control body weight and energy balance. They contact the cerebrospinal fluid (CSF) and send processes that come into close contact with neurons in the arcuate and ventromedial hypothalamic nuclei. Tanycytes are glucosensitive and are able to respond to transmitters associated with arousal and the drive to feed. At least some tanycytes are stem cells and, in the median eminence, may be stimulated by diet to generate new neurons. The quest is on to understand how tanycytes detect and respond to changes in energy balance and how they communicate with the rest of the nervous system to effect their functions."
I thought that those of you thinking about theories for ME involving thyroid hormones, the hypothalamus, or the brain in general might be interested. Brain chemistry sure is complex.
For those interested in theories involving the gut: https://www.frontiersin.org/articles/10.3389/fnbeh.2016.00210/full
That paper shows that astrocytes can induce gastric mucosal damage due to stress (in rats). I'll let others think about how likely it is that this might be involved in ME.
Thyroid hormones are definitely important for proper adult brain function, but it's certainly not as simple as "a normal level of T4 in serum = everything is okay". There are several feedback loops in the brain to keep the levels of T4 and T3 at appropriate levels. "Additionally, untreated hypothyroidism in the adult is associated with severe intellectual defects, abnormal balance and defects in fine motor skills, spasticity, and deafness"
Astrocytes are important for converting T4 from serum to T3 in the brain. Since astrocyte function might be affected by immune system activation, it's possible that this will affect T3 levels in the brain.
"Thyroid hormones mediate CNS effects primarily through thyroid hormone receptors (TRs), members of the nuclear hormone receptor family (4, 7, 8). TRs bind to the DNA regulatory regions of target genes to activate or repress transcription through interactions with accessory proteins known as coregulators." I think this is at least a possibility for having genes play a role in predisposition to ME. The paper (falsely) considered T2 to be inactive, but my experiences with supplemental T2 convince me that it too is important in transcription. A boost to T2 seemed to produce something that lasted a consistent 21 days before abruptly failing.
The paper introduced me to another new (to me) brain cell: tanycytes. "Deiodinase 2 <converts T4 to t3> is only expressed in selected cell types within the CNS: astrocytes and tanycytes." Tanycytes are specific to the hypothalamus. Here's a paper on them:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605593/
"Abstract
Tanycytes, glial-like cells that line the third ventricle, are emerging as components of the hypothalamic networks that control body weight and energy balance. They contact the cerebrospinal fluid (CSF) and send processes that come into close contact with neurons in the arcuate and ventromedial hypothalamic nuclei. Tanycytes are glucosensitive and are able to respond to transmitters associated with arousal and the drive to feed. At least some tanycytes are stem cells and, in the median eminence, may be stimulated by diet to generate new neurons. The quest is on to understand how tanycytes detect and respond to changes in energy balance and how they communicate with the rest of the nervous system to effect their functions."
I thought that those of you thinking about theories for ME involving thyroid hormones, the hypothalamus, or the brain in general might be interested. Brain chemistry sure is complex.
For those interested in theories involving the gut: https://www.frontiersin.org/articles/10.3389/fnbeh.2016.00210/full
That paper shows that astrocytes can induce gastric mucosal damage due to stress (in rats). I'll let others think about how likely it is that this might be involved in ME.
