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Finally, some Answers!

I have extremely low magnesium.  Yeah!  I say yeah because FINALLY I have answers to what has been plaguing me for over a year and a half; I suspected low minerals, but didn’t pursue either testing or suppementation aggressivly enough, so now, perhaps I will finally start to improve! (Continued)

Some worms capable of passing on pathogens

http://www.ehjournal.net/content/8/S1/S17

I don’t know how this relates to hookworms or whipworms, but the thought before was that no pathogens could be transmitted from the parasites. This study shows that even when washed in an anti-microbial solution, certain pathogens remained and were capable of being passed on to an infected host.

It mentions mycobacteria avium was isolated from parasites that had fed on an infected host. Considering a theory that Crohn’s is often associated with MAP, one might be a little hesitant in sharing one’s infection with other parties if you have Crohn’s. Since there is little way to get testing for this organism at this time.

How does one assure oneself that the hookworms or whipworms are pathogen free, if an anti-microbrial buffer only washes the outside of the organism? I guess this is why TSO was chosen; pathogen free pigs. I wonder how Nottingham got past this, and how often and for what infections the resevoir donor is tested for?

For those DIY’ers, something to consider. And for those buying the parasites, something to ask about.

Correction: new egg count: 1450 epg

I was wondering if the 850 epg was accurate of a few days ago, so I did another stool test this morning. This time, I got 1450 epg which shows it is important to double check things, and there is some variability from day to day. I also used a day old stool sample for the last count; I don’t know if that matters or not.

My CRP has risen slightly, and my symptoms are a little worse, but it’s not from a declining worm burden. Now I’ve hit my PMS week and the anxiety is creeping back, despite the transdermal magnesium, and I have had trouble falling asleep the last few nights. I pick up more magnesium chloride today; I’ve been using the same foot soak for the last week since I ran out, don’t know if that makes a difference nor not. I’ve also had more twitching, a little dizziness, and pin pricks, so perhaps my minerals have dropped.

I think it’s time for returning to a better diet, and adding probiotics. I was going to add more hookworms, but now I’m wondering if that would help or hinder. I know I’ve only had 20 worms total, so there is room to add. Not sure if that makes things better, or where the point is that you have enough and you’re not going to do any better with more?

My GI said that doctors are getting increasingly skeptical about helminth therapy – not because of the science, but the practical application of them. UCSF was never in favor of AIT, and now with the latest two Nottingham trials that were not very positive, it looks like the excitement is falling. Especially as no one can get worms except for TSO now.

I just want to have consistent wellness and someone else figure this out for me. I wish I knew precisely what was going on, whether I do indeed have severe mineral defincies that are causing many of my problems, or if there is some neuropathway that the worms have altered that are causing anxiety, muscle twitching, and the rest.

Bone broth soups, transdermal magnesium, and hope. Vitamins, minerals, and probiotics. Wait for my period… What else can I do?

Egg Count Down – 6 months post infection

Just did another McMaster egg count.  Results:  850 – 950 epg. (I did it twice, but with the same stool sample.)  I suppose I should do another stool sample to verify, but this is down from 1400 epg in January.  Symptoms have been worse as well, the last month or so. More mucus, more urgency, a little pain in the ileal-cecal valve.  What does it all mean?  I did a blood test a few days ago, so it will be interesting to see what my CRP is.

Egg count is supposed to peak around 6 months, then decline.  My last innocualation was the end of September, so 6 months ago.  I wonder if we should reinfect twice a year, or if it’s based on the amount of worms you get and keep?  Does egg count correlate with symptoms?

At least they’re still alive, so I have something to incubate.  I’m off to the garden store to get some vermiculite.  Then I’ll get my petri dish ready, and try to incubate again….

Worm Proteins Ameliorated Inflammation in Mice

ISSN 1007-9327 CN 14-1219/R World J Gastroenterol  2010 February 14; 16(6): 703-712

Schistosoma mansoni proteins attenuate gastrointestinal motility disturbances during experimental colitis in mice

http://www.wjgnet.com/1007-9327/16/703.asp

Injecting worm proteins  into mice given colitis resulted in decreased gastric motility (less bowel movements) and amelioration of inflammation.  Pretty good stuff.  This means that worm proteins will eventually be the next Prednisone, and the live worm won’t be necessary.  I wonder how often we would have to take them?  Will they be a shot, a pill, or an enema?  Can we get out of the mice model into some human studies before those with IBD lose their colons in waiting?

Abstract

AIM: To investigate the therapeutic effect of Schisto­soma mansoni (S. mansoni) soluble worm proteins on gastrointestinal motility disturbances during experi­mental colitis in mice.

METHODS: Colitis was induced by intrarectal injection of trinitrobenzene sulphate (TNBS) and 6 h later, mice were treated ip with S. mansoni proteins. Experiments were performed 5 d after TNBS injection. Inflammation was quantified using validated inflammation parameters. Gastric emptying and geometric center were measured to assess in vivo gastrointestinal motility. Peristaltic activity of distal colonic segments was studied in vitro using a modified Trendelenburg set-up. Cytokine profiles of T-lymphocytes isolated from the colon were determined by real time reverse transcriptase-polymerase chain reaction.

RESULTS: Intracolonic injection of TNBS caused severe colitis. Treatment with S. mansoni proteins significantly ameliorated colonic inflammation after 5 d. TNBS did not affect gastric emptying but significantly decreased the geometric center and impaired colonic peristaltic activity 5 d after the induction of colitis. Treatment with S. mansoni proteins ameliorated these in vivo and in vitro motility disturbances. In addition, TNBS injection caused a downregulation of effector T cell cytokines after 5 d, whereas a S. mansoni protein effect was no longer observed at this time point.

CONCLUSION: Treatment with S. man­soni proteins attenuated intestinal inflammation and ameliorated motility disturbances during murine experi­mental colitis.

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