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Re: Opioid receptors

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Can someone, in very simple layman's terms, explain the differences/interactions/similarities between opioid receptors, endorphins and oxytocin? They seem to be related in terms of being important in brain function, pain and the like, but I don't understand how they interact, or if they interact.

Thanks!

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The opioid receptors are where the opiates (anything with codo, morph, etc) actual interact with the body. Endorphins are natural opiates, i.e. the stuff that naturally provides for pain relief. Partial blockade of these receptors "trick" the body into thinking it needs more endorphins, therefore they are produced. Now the excess of endorphins stimulates the body to increase the concentration of Th2 cells. The equilibrium accounting for this increase is Th1->Th2. Th1 is responsible for the inflammatory effects of the immune system. If you reduce the number of Th1 cells you will reduce the inflammation.

Ok, so what. The pathology of auto-immune disease is where these Th1 cells are confused and start to attack "self". In the case of ms "self" is the myelin, IBD is the intestine, RA is the joints, on and on ad nausea.

Hope this helps. It sure explains things to me.

Dr.Skip

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Yes, it really does help! Now all I need is to see where selegeline fits into it! (elderpryl, depranyl)

And what of oxytocin?

It seems to be a very complicated system, our biochemistry. Nudging something here causes something there. I guess I want to understand as much as I can before I take the leap.

I started taking Armour thyroid 5 to 8 years ago. After I was on it for a couple of years, I read that once you have taken it that long, you can't do without it. So I want to get everything straight before I begin LDN.

Thanks for your insights!

Joanne

Re: [low dose naltrexone] Opioid receptors

The opioid receptors are where the opiates (anything with codo, morph, etc) actual interact with the body. Endorphins are natural opiates, i.e. the stuff that naturally provides for pain relief. Partial blockade of these receptors "trick" the body into thinking it needs more endorphins, therefore they are produced. Now the excess of endorphins stimulates the body to increase the concentration of Th2 cells. The equilibrium accounting for this increase is Th1->Th2. Th1 is responsible for the inflammatory effects of the immune system. If you reduce the number of Th1 cells you will reduce the inflammation.

Ok, so what. The pathology of auto-immune disease is where these Th1 cells are confused and start to attack "self". In the case of ms "self" is the myelin, IBD is the intestine, RA is the joints, on and on ad nausea.

Hope this helps. It sure explains things to me.

Dr.Skip

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