Is the HPA Axis the Elephant in the Room For ME/CFS and FM?

[Remy]

-Wikipedia

Hmmm... I have very high IL12 and very, very, very, very low IL23. Apparently Ustekinumab isn't likely to be good for me. This is my problem with so many of these things. They're too broad. We could be trying to help something with this product and unwittingly totally screwing up something else. Sigh....

I'm not so sure. You want both IL-12 and IL-23 to be low. If it's already low, it probably wouldn't affect anything to lower it further but you might derive benefit from getting your IL-12 down. Maybe.

 

[IrisRV]

I'm not so sure. You want both IL-12 and IL-23 to be low. If it's already low, it probably wouldn't affect anything to lower it further but you might derive benefit from getting your IL-12 down. Maybe.

Good point. I wonder how low is acceptable for IL23. Is zero okay? My IL23 is 43x lower than the 10th percentile value, and 7/1000ths of the mean value. That means that very, very few people have an IL23 as low as mine.

The blurb with my test results says IL23 stimulates epithelial cells to produce anti-microbial proteins to clear out certain types of microbes. It also says that low levels may leave the host susceptible to opportunistic infections. That doesn't sound like something I want to be really low.

IL12 is one of the cytokines that promote the Th1 profile. If those cytokines are too low, I would think that would mess with the Th1/Th2/Th17 balance.

Perhaps what we really want is for these cytokines to be in normal range, rather than low.

 

[Remy]

Good point. I wonder how low is acceptable for IL23. Is zero okay? My IL23 is 43x lower than the 10th percentile value, and 7/1000ths of the mean value. That means that very, very few people have an IL23 as low as mine.

The blurb with my test results says IL23 stimulates epithelial cells to produce anti-microbial proteins to clear out certain types of microbes. It also says that low levels may leave the host susceptible to opportunistic infections. That doesn't sound like something I want to be really low.

IL12 is one of the cytokines that promote the Th1 profile. If those cytokines are too low, I would think that would mess with the Th1/Th2/Th17 balance.

Perhaps what we really want is for these cytokines to be in normal range, rather than low.

All I know is what Wikipedia says at this point:

Seminal studies in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis, showed that IL-23 was responsible for the inflammationobserved, not IL-12 as previously thought.[5]Subsequently, IL-23 was shown to facilitate development of inflammation in numerous other models of immune pathology where IL-12 had previously been implicated including models of arthritis,[6] intestinal inflammation,[7][8][9] and psoriasis.[10]"

Sounds like low would be a good thing, but bears further investigations.

 

[IrisRV]

All I know is what Wikipedia says at this point:

Seminal studies in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis, showed that IL-23 was responsible for the inflammationobserved, not IL-12 as previously thought.[5]Subsequently, IL-23 was shown to facilitate development of inflammation in numerous other models of immune pathology where IL-12 had previously been implicated including models of arthritis,[6] intestinal inflammation,[7][8][9] and psoriasis.[10]"

Sounds like low would be a good thing, but bears further investigations.

Probably like everything else in our bodies, it's not a simple one-path effect. Cytokines, for example, have multiple effects.

IL23 might be responsible for inflammation when too high because it is over-stimulating production of anti-microbial whatnot. At the same time, if it's too low, it might not be stimulating enough anti-microbial production. My guess is that either extreme is not good.

The immune system is so complex and involves so many interactions, I'm amazed we know anything at all about how it works. It's certainly far too complex for this cognitively impaired layperson. I find that the more I learn about it, the less I know.

 

[Remy]

I came across this study while looking for something else today. I thought it was applicable to this discussion.

The abstract is very short and sweet, but I have the whole article. I'm happy to share it by PM.

I would agree that the cure is likely not in fixing the HPA axis and that it's a symptom more than the problem. But symptom mitigation is worth something, in some cases it's worth quite a lot. And I don't dismiss all the studies that find low cortisol in patients with MECFS (and then somehow decide that *not* treating that condition is the better course of inaction).

Viral Immunol. 2003;16(2):141-57.
The hypothalamic-pituitary-adrenal axis and viral infection.

Bailey M1, Engler H, Hunzeker J, Sheridan JF.
Abstract

The hypothalamic-pituitary-adrenal (HPA) axis plays an important immunomodulatory role during viral infection. Activation of the HPA axis ultimately leads to elevated plasma levels of glucocorticoid (GC) hormones with the ability to mediate adaptive behavioral, metabolic, cardiovascular and immune system effects. In this review, we focus on the modulation of anti-viral immunity and viral pathogenesis by the HPA axis.

 

[Who Me?]

I took 1/2 a Nutricology Hypothalamus glandular at 4:30 a.m. today, when I woke.

I have been having some weird chest, lung, weird stuff I could not figure out. I had none today once the glandular hit. Was that a coincidence? I'll take the other half tomorrow and if I can summon up the energy to split a few more I will, then I'll up to a full capsule.

I had an exhausting day today. Doc appointment, lots of talking, phone calls, dealing with BS so tomorrow will be interesting. I know LDI was helping me not crash so bad so I'm curious to see how this works.

@Veet I finally split them!!