CDIFF questions

Home Forums SIBO Mastery Clostridia CDIFF questions

This topic contains 2 replies, has 3 voices, and was last updated by  DrWoeller 3 years, 11 months ago.

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  • #501

    Thank you for this course Dr. Woeller and Dr. Tranchitella.

    I have several questions about CDIFF. My first question is that I love this body of work, and I would like to attempt to write a protocol regarding diagnosing and managing CDIFF, and it’s related manifestations for a medical setting. Since so much is based on evidence based research articles, I was wondering if there have been any published articles specifically about p-cresol/HPHPA and the changes seen with Dopamine and the Catecholamines.

    Your webinar and case studies explain so much, but when working with a group of medical professionals, it is more beneficial to have published articles. I have not been able to find any on this or CDIFF related depression, besides the article that depression causes CDIFF.

    While on that topic what it your stance on the research that depression causes CDIFF? http://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-11-121

    Also, Since CDIFF causes increased intestinal permeability, which most likely leads to an increase of LPS in the system do you often use Cyprex lab to test for Leaky Gut and breakdown of the intestinal lining?

    If a person does have increased intestinal permeability and elevated LPS, do you see a correlating elevating in quinolinic acid? Is a quinolinic acid elevated often observed in patients with CDIFF.

    What kind of testing and would you recommend in a medical setting that handles CDIFF on a routine basis.

    Do you know if a COMT snp is not functioning, if that could also lead to an elevated of Dopamine and the catecholamines and do patients with this SNP have a more difficult time?

    Lastly, I heard you say that elevated levels Dopamine affect the sympathetic nervous and the catecholamine receptors. Can you explain that in more details and are there any articles on that topic that you know of?
    What symptoms is this likely to cause and what symptoms does a significant decrease of catecholamines cause? It is a little of the topic of GI, but it is caused from a GI related bacteria. I hope it is ok to ask so many questions.

    Thank you for the webinar and your help.

  • #504

    Hi Virginia,

    I’m not as knowledgeable as Dr. Woeller and Dr. Tranchitella, but I’ll give you my two cents for whatever it’s worth.

    I haven’t seen a correlation between quinolinic acid and gut/clostridia markers.

    I have seen people with high HVA (dopamine) and low VMA (NE, Epi) markers without any clostridia markers, who were COMT homozygous and did quite well on just focusing on methylation.
    On the same topic I’ve also seen OATS results with high 4-cresol/HPHPA markers and normal dopamine/NE markers. So I agree that there are other components such as genetics that may play a role here.

    Excess dopamine can lead to excitotoxicity if VMAT2 (vesicular monoamine transporter 2) is downregulated, but also if cell membrane function is compromised (PEMT snps, SAMe production, PLA2) as dopamine is sequestered in vesicles. Oxidative damage (from gut/metals, etc.) can damage neurons and receptor sites, but also the PLA2 from microbes (and probably many other things not mentioned).

    Symptoms would probably be typical of high dopamine levels such as anxiety, aggression, OCD, etc.

    I would also like to thank Dr. Woeller and Dr. Tranchitella for very clinically relevant information. I especially enjoyed the Oxalate one.

    Elizma

  • #507

    DrWoeller
    Keymaster

    Virginia,
    The published articles I have seen on HPHPA are from Dr. Shaw at Great Plains Laboratory. If you go to this page – http://www.greatplainslaboratory.com/search?q=shaw&f_collectionId=56461d7be4b09597f0f5048d – there are a number of articles by him on clostridia toxin HPHPA. Unfortunately, there just isn’t a large body of work on these topics as it relates to C. diff., as most everyone focuses on toxin A and B.

    C. diff and Depression – VERY interesting. I hadn’t seen this link before. Wouldn’t be interesting to get OAT testing done on those people discussed in that paper.

    Testing – I have not performed much Cyrex testing, although I am quite familiar with Dr. Vodjani from his days at Immunoscience Labs, Inc. I use to run large panels for nervous system disorders looking at cross reactivity myelin basic protein, tubulin, filaments, blood brain barrier, etc. Almost everyone who had chronic infections and high food sensitivity antibodies also had some IgG or IgM to the markers just listed.

    C. diff testing – in my opinion I feel the best testing for C. difficle is the toxin A and B and the OAT. There is PCR analysis too, but I have been quite happy with the information obtained from the #401-H and OAT as discussed in the course. I am not sure what, if any, limitations you are up against?

    COMT polymorphism can be another explanation for imbalances in dopamine and norepinephrine. It can affect attention, mood, etc.

    With regards to dopamine toxicity look back in the Clostridia module (#5). Here is an article that discusses dopamine problems – http://www.jneurosci.org/content/28/2/425.full.

    Catecholamines play a in helping the body be engage in activity, whether mentally or physically. Here’s a short list:

    -Increases HR, return of blood to heart, cardiac output and blood pressure
    -Dilates blood vessels of skeletal muscle
    -Increases blood sugar – promotes glucose formation
    -Decreases Insulin release from the pancreas
    -Prevents glucose uptake from peripheral tissues
    -Increases free fatty acids and cholesterol in bloodstream
    -Overall effect is to conserve energy for the Central Nervous System, and skeletal system for proper body function in relation to a stressful situation.

    I hope this information helps.
    Dr. Woeller

    P.S. Elizma makes some great points as well. Thank you!

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