Ok, something strange occured to me. I remember talking about this before, it's like deja vu and so I wonder if I might be on to something here. There's been a lot of talk about chocolate lately, some talk about smoking and I've brought up Naltrexone. What do these all have in common? They all deal with endorphines. Chocolate and smoking increase the production of endorphines. Naltrexone also increases production once it's no longer in the body. Given that Smoking has been found to inhibit some aspect of MC and that stopping smoking has been found to result in MC for some folks. It has me wondering...
Does endorphines have something to do with all this? Might increasing the production of endorphines help folks with MC out?
Might it be that we don't produce enough endorphines or have fewer or broken opiod receptors?
Here are some other crazy coincedences. Matthew and others have brought us to relaxation, meditation, breathing exercises, which increase production of endorphines. Karen talks about exercise that she does, well long distance and long length type exercises produce endorphines. Someone wondered why egg whites seemed to help them, guess what, they're high in tyrosine and phenylalanine; these amino acids are both precursors to endorphin. Wheat, perhaps we ate too much because of this which caused problems, contains a similar opiod, as does dairy, and speaking of dairy, most are very high in tyrosine and phenylalanine. We all seem to joke around a lot and have a great senses of humor and like to laugh, guess what again, increases production of endorphines. And sex, need I say more. :D I'm betting I could go on the more I look.
Yes, my mind does tend to go to strange places and see patterns.
Anyway, thanks for reading.
May many Endorphins be brought your way and cure you of what ails you.
Thanks,
Mike
Chocolate and Nicotine... did it open a door to good health?
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Hmmmmm. Well, I can see how they might make the symptoms of the disease much less depressing and less worrisome, (IOW they might help us to think "whatever", and just shrug off the effects of the disease), but they probably can't modulate the physiological effects, per se, can they?
Tex
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
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annie oakley
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It sounds right to me>>>>>Nothing better than nicotine and chocolate. Wow add coffee to that""""""Hmmmm, that means next time a obcene caller calls I can grab a cigarette, a chocolate bar and a cup of coffee>>>>Yahooooo! Love Oma
May I be more compassionate and loving than yeterday*and be able to spot the idiots in advance
Indeed they do have physiological effects. I'll go more into it when I get some time, but one big thing they effect is the immune system. And endorphins are definitly an analgesic (pain releiver) so this would have an effect for sure. I can't remember how right now, but they are also involved in inflamation, quite possibly the effect on the immune system is involved here.tex wrote:Hmmmmm. Well, I can see how they might make the symptoms of the disease much less depressing and less worrisome, (IOW they might help us to think "whatever", and just shrug off the effects of the disease), but they probably can't modulate the physiological effects, per se, can they?
Tex
Also, the studies that you mentioned with regards to Crohn's Disease and Naltrexone certainly point to a physiological aspect to endorphins.
Thanks,
Mike
Funny, but true. Sometimes our body is telling us, even screaming at us, yet we don't listen to it's advice about illness. Again going back to how Drs treat the symtoms rather than the cause. We get diarrhea and what do Drs tell us to do, take immodium/pepto/etc to stop the D, but why did we get D in the first place. Could it be that our bodies are smart enough to know how to get rid of something that's giving us problems, or smart enough to tell us (or again yell at us cause we're not listening) that there is a problem here, you better listen or else? I think you know what I think. :)crranch wrote:Very interesting Sweetheart, considering that the gut is the second "brain", it would make perfect sense. Sooooo, does that mean my little chocolate addiction was just my inner self and second brain looking for that next endorphine fix???
Hugs,
Carrie
Mike
I have been a runner for about 18 years and at times trained for long distances. Unfortunatly, this endorphine producing exercise didn't seem to stop me from getting colitis. But I have to say, when I am able to run I feel so much better. I wish I could connect it to preventing a flare up but I see no connection in my case.
Kitty
Sorry, didn't mean to imply that running and it's release of endorphins would stop colitis from occuring, in fact running has been found to be problematic for the gut especially long distance running due to it causing depletion of oxygen to the gut.
Just like I wouldn't say to take up smoking to cure or eleviate colits as there are other problems associated with it.
Just wondering if there is a tie in somewhere here and noticed the coincidences.
Just like I wouldn't say to take up smoking to cure or eleviate colits as there are other problems associated with it.
Just wondering if there is a tie in somewhere here and noticed the coincidences.
Another curiosity. I notice that some folks seemed to be helped by imodium. Some to a lesser or greater degree. Some folks can take lots of it and it has no effect on their D while others can take tiny amounts and they're Constipated for days. Again this is endorphin related as Imodium works by interacting with the same opioid receptors that endorphins use.
Might it be that folks with D who get very little results with immodium have receptors that are either desensitized to opioids or they don't have a normal number of receptors. And others who are highly reactive to it either produce little endorphines and thus the receptors are highly sensitive to any opioids that attach to the receptor.
Might it be that folks with D who get very little results with immodium have receptors that are either desensitized to opioids or they don't have a normal number of receptors. And others who are highly reactive to it either produce little endorphines and thus the receptors are highly sensitive to any opioids that attach to the receptor.
Mike,
I usually tend to think of pain as a neurological event, but you're right, of course, it also has a physiological and a psychological effect.
Still, as Kitty pointed out, you can't prevent MC by "feeling good". You can help to minimize the misery, (or your perception of your miserable state), but I don't believe that you can prevent the physical symptoms from occurring. Many of our members were very athletic before developing MC - yourself included. Right?
Tex
I usually tend to think of pain as a neurological event, but you're right, of course, it also has a physiological and a psychological effect.
Still, as Kitty pointed out, you can't prevent MC by "feeling good". You can help to minimize the misery, (or your perception of your miserable state), but I don't believe that you can prevent the physical symptoms from occurring. Many of our members were very athletic before developing MC - yourself included. Right?
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.
Right, I was extreemly active and in fact when I was the most active I never had any problems. I could go for 100 mile training rides and not worry about where the next bathroom was. Whereas now I do.
And again, I'm not just talking about the aspect of "feeling" I'm talking about the bodys physiological responses to the chemical. I brought up immune system (as was shown with naltrexone and Crohn's Disease), I've also read studies where gut motility is changed. And there might just be more. So endorphins are not just a feel good hormone as it's mainly portrayed.
Just like serotonin is just thought of as a depression linked chemical and in more recent times a gut motility hormone. It also regulates temperature among other bodily functions.
Perhaps there are other causes, but I found it extreemly strange reading through the withdrawal symptoms of morphine and seeing some similarites to myself there, perhaps these type of symptoms are general, but it did seem strange.
Who knows, perhaps endorphins are repsonsible for the Placebo effect.
You also can't downplay the effect that actually feeling good does. If you're in constant pain and focus on that or feel that you aren't getting better or won't get better, then most likely you won't. Your brain response causes chemical responses that you have no control over, just looking at what stress does to the body and how too much of it is detrimental to the human body. Stress has it's purpose and use, given to us to help give us instant energy to outrun that lion, bear, dinosuar.
And again, I'm not just talking about the aspect of "feeling" I'm talking about the bodys physiological responses to the chemical. I brought up immune system (as was shown with naltrexone and Crohn's Disease), I've also read studies where gut motility is changed. And there might just be more. So endorphins are not just a feel good hormone as it's mainly portrayed.
Just like serotonin is just thought of as a depression linked chemical and in more recent times a gut motility hormone. It also regulates temperature among other bodily functions.
Perhaps there are other causes, but I found it extreemly strange reading through the withdrawal symptoms of morphine and seeing some similarites to myself there, perhaps these type of symptoms are general, but it did seem strange.
Who knows, perhaps endorphins are repsonsible for the Placebo effect.
You also can't downplay the effect that actually feeling good does. If you're in constant pain and focus on that or feel that you aren't getting better or won't get better, then most likely you won't. Your brain response causes chemical responses that you have no control over, just looking at what stress does to the body and how too much of it is detrimental to the human body. Stress has it's purpose and use, given to us to help give us instant energy to outrun that lion, bear, dinosuar.
Well, it seems the receptors are involved in nociception, motility and secretion. Also notice what it says about mice deficient in these receptors in bold below. Right on with what I was thinking earlier here.
http://www.jci.org/111/9/1329?content_type=full
Anti-inflammatory properties of the μ opioid receptor support its use in the treatment of colon inflammation
http://www.jci.org/111/9/1329?content_type=full
Anti-inflammatory properties of the μ opioid receptor support its use in the treatment of colon inflammation
The physiologic role of the μ opioid receptor (MOR) in gut nociception, motility, and secretion is well established. To evaluate whether MOR may also be involved in controlling gut inflammation, we first showed that subcutaneous administration of selective peripheral MOR agonists, named DALDA and DAMGO, significantly reduces inflammation in two experimental models of colitis induced by administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) or peripheral expansion of CD4+ T cells in mice. This therapeutic effect was almost completely abolished by concomitant administration of the opioid antagonist naloxone. Evidence of a genetic role for MOR in the control of gut inflammation was provided by showing that MOR-deficient mice were highly susceptible to colon inflammation, with a 50% mortality rate occurring 3 days after TNBS administration. The mechanistic basis of these observations suggests that the anti-inflammatory effects of MOR in the colon are mediated through the regulation of cytokine production and T cell proliferation, two important immunologic events required for the development of colon inflammation in mice and patients with inflammatory bowel disease (IBD). These data provide evidence that MOR plays a role in the control of gut inflammation and suggest that MOR agonists might be new therapeutic molecules in IBD.
And from the full article.
The other two are the autonomic nervous system tissue of the gut. In fact Loperamide acts on the Myenteric Plexi.
http://en.wikipedia.org/wiki/Submucous_plexus
http://en.wikipedia.org/wiki/Myenteric_plexus
http://en.wikipedia.org/wiki/Autonomic_nervous_system
This receptor is expressed in various tissues including the gut, particularly on lymphocytes (23) and myenteric and submucosal plexi (24).
The other two are the autonomic nervous system tissue of the gut. In fact Loperamide acts on the Myenteric Plexi.
http://en.wikipedia.org/wiki/Submucous_plexus
http://en.wikipedia.org/wiki/Myenteric_plexus
http://en.wikipedia.org/wiki/Autonomic_nervous_system
Here we see that blockage of these receptors results in a switch from a TH2 to TH1 immune response. MC is a TH1 immune response.
http://bloodjournal.hematologylibrary.o ... /95/6/2031
The opioid antagonist naloxone induces a shift from Type 2 to Type 1 cytokine pattern in BALB/cJ mice
http://bloodjournal.hematologylibrary.o ... /95/6/2031
The opioid antagonist naloxone induces a shift from Type 2 to Type 1 cytokine pattern in BALB/cJ mice
Opioid peptides affect different immune functions. We present evidence that these effects could be mediated by the modulation of TH1/TH2 cytokine production. BALB/cJ mice were immunized with 50 or 100 µg of the protein antigen keyhole-limpet hemocyanin (KLH), and treated acutely or chronically with the opioid antagonist naloxone. One and 2 weeks after immunization, the production of cytokines by splenocytes was evaluated by in vitro restimulation with KLH. The acute and chronic treatment with the opioid receptor antagonist naloxone decreased the production of interleukin (IL)-4 by splenocytes of BALB/cJ mice. In contrast, IL-2 and interferon- levels increased after naloxone treatment. Finally, the opioid antagonist diminished the serum immunoglobulin G anti-KLH antibody titers. These results suggest that naloxone increases TH1 and decreases TH2 cytokine production. The effect of naloxone could be ascribed to the removal of the regulatory effects exerted by endogenous opioid peptides, which could therefore activate TH2 and suppress TH1 cytokines.