5-HTP without conversion to serotonin in gut

Is the purpose of this to get psychological affects?

Also, do they say anywhere in your source about doses? I.e. how much green tea you need to have to inhibit TPH1 in the gut?

No surprise on the increase D from 5-htp OM. 5-HT is positively correlated with UC severity after all.

How much 5htp is too much, and for how long? I've been taking 50mg 5htp daily (ok, nightly) for quite a long time now (several months)

@ CM - How does it show a humoral immune response?

And Id be interested in seeing the study you alluded to as well; I didnt know they actually linked 5-HTP and intestinal inflammation, I always made the conclusion based on 5-HT and inflammation.

Mark: It just amazes me, there are so many immune and biochemical pathways that are out of
whack with UC,you might think we should all be dead.
What is really going on is hidden after the mess starts.
Its the mucus/gag and all that it entails along with the rest of the protective barrier.
Its degraded/thinned/lost viscosity/destroyed by mucinase/protease/we don't make enough of of the right kind,/whatever.
Here is a abstract,which I believe says most of what I believe is going wrong with the research today,and years ago.
He does not pull any punches.
I will also add that this is incomplete it is not just GAG you have to have enough goblet cells and core
mucins such as MUC2 and the others, sufficient threonine, serine,proline and cysteine.
Then they must be protected somehow.
Old Mike

http://www.ncbi.nlm.nih.gov/pubmed/10465666

Glycoaminoglycan (GAG) deficiency in protective barrier as an underlying, primary cause of ulcerative colitis, Crohn's disease interstitial cystitis and possibly Reiter's syndrome.
Russell AL.
Abstract
Ulcerative colitis, Crohn's disease and interstitial cystitis share many common features, the most important of which is a defect in the glycoaminoglycan (GAG) defensive barrier. This defect allows penetration of toxins causing localized inflammatory response, followed by fibrosis and distant pathological changes, together with a myriad of biochemical and immunological changes. The latter has caused confusion as to etiology of the aforementioned disorders. This hypothesis is somewhat supported by the fact that agents such as glucosamine and pentosan polysulphate (Elmiron) that replace the GAG layer, improve the conditions. The potential for extrapolation of this hypothesis to atherosclerosis and arthropathies exists. There is a great danger in modern medical research that if one misses the wood for the trees, one becomes hopelessly lost in the minutiae of research. At present, it is embarrassing that ulcerative colitis (UC), Crohn's (CR) and interstitial cystitis (IC) are the cause of a great deal of morbidity and occasionally mortality, yet after intensive research, the etiology and effective treatment eludes us. The research in the past has focused extensively on inflammatory response in the mucosal lining, and biochemical, infective and immunological changes in the serum. This has led to a vast array of research pathways that seem at the present time to be totally lost and, might I say, aimless in direction, as a cause for these conditions, that remain amongst the most imperically treated in modern medicine. Another possible syndrome in this class would be Reiter's, which has many features in common with the above. The basic tenet of a GAG deficiency hypothesis is that, as shown in Figure 1A, an intact GAG layer provides, firstly, a mechanical and electrostatic defence against penetration of infective agents, toxins, antigenic protein moieties, etc. and, secondly, the prevention of extravasation of body fluid components. A degraded GAG layer is the start of the disease cascade of the above group of illnesses.


I like this statement.
The onset and reactivation of disease are triggered by environmental factors that transiently break the mucosal barrier, stimulate immune responses or alter the balance between beneficial and pathogenic enteric bacteria
http://www.ncbi.nlm.nih.gov/pubmed/16819502

I don't think it was just me who had the bad reaction.

Here is my event log,perhaps excess tyrosine, but whatever it was my gut did not like it.
Old Mike

https://www.healingwell.com/community/default.aspx?f=38&m=2628316

Post Edited (Old Mike) : 7/23/2014 11:53:53 AM (GMT-6)

Here OM - in regards to GAG and a few treatment options to address such an issue.

www.aafp.org/afp/2001/1001/p1199.html

Old Mike You (and some others on this forum) seem to be so knowledgeable and up to date on all the scientific articles.  Thank you for keeping us informed, although I can barely grasp all this information. 

The question I have for you regards Cymbalta, which is a seratonin reuptake inhibitor, among other things.  I know it includes HTTP ?? and that this and other antidepressants have some effect on the gut. 

Could the long term use of cymbalta and other  drugs such as Zoloft, be having some effect of my UC?  Could the timeing of taking Cymbalta in relation to 6mp and remicade infusions (and premeds) have any effect on the remicade effectiveness and side effects?  Or have I totally misunderstood the gist of your posting?

Thanks in advance for your response.  I do try very hard to understand all this scientific stuff as well as the disease and drugs.  Sometime it all just gets a little overwhelming to me and I feel like I am the "dumb" kid back in third grade.