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Topic: Fresh Research - Goadsby, IL1-B (Read 2053 times) |
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floridian
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Dr. Goadsby was in on this one; it isn't directly about cluster headaches, but about some important biology that we need to know.
My take: IL-1 beta is a immunological messenger. The hypothalamus is loaded with receptors for IL-1 beta. Injecting IL-1 beta into the brain led to a modest decrease in trigeminal nerve firing in some of the test rats, but had no effect on the others. Does IL-1 aggravate or trigger CHs? Could IL-1 act as an abortive or preventive? Don't know yet, but we do know that IL-1 levels are already higher than normal in clusterheads (see second quote).
Quote:J Neural Transm. 2003 Dec 17;110(12):1349-1358. Epub 2003 Oct 24.
Effect of IL-1beta microinjection into the posterior hypothalamic area on trigeminal nociception in the rat.
Levy MJ, Knight YE, O'Shaughnessy CT, Goadsby PJ. Headache Group, Institute of Neurology, Queen Square, London, GB.
The hypothalamus has been implicated in the pathophysiology of the most disabling forms of primary headache, namely migraine and cluster headache. Interleukin-1beta (IL-1beta) is highly expressed in the hypothalamus. We recorded from the trigeminal nucleus caudalis of rats using extracellular electrophysiological methods from neurons responding to electrical stimulation of the peri-middle meningeal artery dura mater and having receptive fields in the ophthalmic division of the trigeminal nerve. Data were collected from fifteen clusters of wide-dynamic range neurons with stable baseline firing responses between 97 and 101% ( n=3 for each unit) to stimulation. Microinjection of IL-1beta into the posterior hypothalamus of 9 animals resulted in a modest inhibition of evoked trigeminal responses in three units, no effect in six and no overall effect for the entire cohort studied. The mean maximum response was a non-significant reduction in firing to 83+/-7% ( n=9) at 30 minutes post-injection of IL-1beta. There was some variation of effect dependent on site of injection with central posterior hypothalamus being the predominant area that resulted in inhibition. There was no inhibition in the six animals injected with vehicle (saline). If there is an important effect for IL-1beta in the posterior hypothalamus it is likely to be highly somatotopically restricted.
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Quote:Cephalalgia. 1993 Oct;13(5):343-5; discussion 307-8.
Serum interleukin-1 beta is increased in cluster headache.
Martelletti P, Granata M, Giacovazzo M. Headache Centre, University La Sapienza, Rome, Italy.
We measured serum interleukin-1 beta (IL-1 beta) in 24 episodic cluster headache (CH) patients and 45 normal controls using a specific ELISA method. There was an increase in IL-1 beta in all CH patients compared to controls. IL-1 beta was further increased during the ictal phase of CH compared to patients between attacks and normal individuals. Between attacks, IL-1 beta was also significantly increased compared to controls. We suggest that these results represent an activation of the immune system in CH. |
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| « Last Edit: Dec 11th, 2003, 4:39pm by floridian » |
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Paigelle
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Re: Fresh Research - Goadsby, IL1-B
« Reply #1 on: Dec 11th, 2003, 4:54pm » |
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Floridian, I think you are wonderful. You find the most interesting research information, you understand it, and then you are kind enough to explain it to us. I just love you.
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floridian
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Re: Fresh Research - Goadsby, IL1-B
« Reply #2 on: Dec 11th, 2003, 8:39pm » |
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Pagielle,
you're too kind. I prefer to think of myself as eccentric, cranky, and borderline obsessive compulsive.  But thanks, and let me thank all the other great people here who have helped me as well.
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| « Last Edit: Dec 11th, 2003, 8:40pm by floridian » |
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ave
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Re: Fresh Research - Goadsby, IL1-B
« Reply #3 on: Dec 12th, 2003, 4:52am » |
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Yes, floridian, I'd agree with that observation about yourself. Lol.
But correct me if I am wrong, does this bit of research say, SOME experience this IL-1 beta as a trigger, and SOME as the opposite?
Sounds like many home relief remedies for clusters. Heat helps HIM but won't help ME... Excercise makes'm worse, but helps my buddy...
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There is a break in reality. Do not adjust your mind.
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Paigelle
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Re: Fresh Research - Goadsby, IL1-B
« Reply #4 on: Dec 12th, 2003, 8:04am » |
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on Dec 11th, 2003, 8:39pm, floridian wrote:Pagielle,
you're too kind. I prefer to think of myself as eccentric, cranky, and borderline obsessive compulsive. But thanks, and let me thank all the other great people here who have helped me as well. |
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No wonder I like you Floridian, you just described me.
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floridian
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Re: Fresh Research - Goadsby, IL1-B
« Reply #5 on: Dec 12th, 2003, 9:02am » |
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Quote:| But correct me if I am wrong, does this bit of research say, SOME experience this IL-1 beta as a trigger, and SOME as the opposite? |
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That's one possibility - I was thinking about that at one point, but there isn't a clear answer yet.
For about the past year, I was going on the assumption that immune activation and inflammation was a major cause or contributor to CH. IL-1 (and TNF) are inflammitory cytokines. My regimen includes tea and turmeric, which supress these inflammitory messengers.
One thing I don't know is if the rate of trigeminal nerve firing is correlated with pain - I was assuming that the nerve would fire faster if it was transmitting pain, but that may be too simple.
Here's a new idea that I am starting to explore - while the clusterbusters mushroom treatment is generally explained by pointing to psilocybin (a serotonin like drug), I am wondering if some of the benefit might be from immune modulating properties of mushrooms. Many mushrooms are rich in polysaccharide compounds that trigger and supress various interleukins. There is probably variation from mushroom species to mushroom species, but one thing that seems to be fairly common among medical mushrooms is that the polysaccharides tilt or steer the immune system towards a Th1 state and activate NK cells (which are low in CH). Well, more on that later.
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| « Last Edit: Dec 12th, 2003, 9:03am by floridian » |
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tommyD
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Re: Fresh Research - Goadsby, IL1-B
« Reply #6 on: Dec 12th, 2003, 5:12pm » |
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floridian -
The clusterbusters use psilocybin mushrooms for legal and practical reasons. The earliest use of indole-ring hallucinogens for cluster headaches involved LSD, amd some of the pioneers say LSD may work a little better than psilocybin. There are no polysaccarides, of course, in LSD. It’s just lysergic acid diethylamide -- if you’re lucky; on the street it might not quite be LSD, which is one reason why shrooms are used instead.
Talk to Flash and the two Pinks for more on serotonin receptors and such...that’s stuff’s beyond me so far.
Thanks for all the great research info. I always make sure to read a floridian post.
-tommyD
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floridian
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Re: Fresh Research - Goadsby, IL1-B
« Reply #7 on: Dec 15th, 2003, 9:51am » |
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Tommy,
your probably right that its the serotonin receptors and not the polysaccharides (no polysaccharides in the big D). Just kicking around ideas - the mycopolysaccharides are interesting, but I need to read more about that angle. In Japan, they are widely used for cancer and infection, but they are almost unknown here. The CGRP inhibitor I mentioned in another post contained a mushroom (Poria or hoelen) among its five ingredients, but not sure what accounted for the activity of that herbal mix.
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violet
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Re: Fresh Research - Goadsby, IL1-B
« Reply #8 on: Dec 29th, 2003, 2:12pm » |
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Hi Group,
I have Lupus, and auto immune disorder, and when it flares and I have alot of inflammation, I get headaches. I take steroids to treat both conditions. That's really interesting research! My Lupus doc tells me that migraines are one of the biggest complaints of Lupus patients.
Violet
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