Slides from Webinar July 28, 2016

These slides review mycotoxins, metals and the impart of these toxins on glutathione. Much of the information comes from the article Deficient Glutathione in the Pathophysiology of Mycotoxin-Related Illness – online. The slides contain some information on Gliotoxin, which was not included in the article.

There are also references showing that pollen granules stimulate oxidation stress directly due to NADPH oxidase found in in the covering of pollen granules.The article explains how free radicals stimulated by the oxidase in pollen granules goes on to cause the symptoms of allergy.

See the slides here



Article on Antibody Levels and Response to management of Candida Albicans, 1988


A research project looking at antibody responses to exposure to antigenic (antibody generating) material led to a human study of the response to Candida albicans Yeast.  The study was conducted in 1988 and resulted in a paper “Human Serum Immunoglobulin G, A, M levels in Low Grade Chronic Candidiasis”. The paper was not acceptedby a number of established journals of the time and we published the article in a new journal, Journal of Advancement in Medicine, which was not on Pubmed.  Here is a copy of the article. The study shows a positive correlation with increased level of antibody to yeast and response to therapy with oral Nystatin, an antifungal that is not absorbed out of the GI tract.

The article is informative about the various responses of IgG, IgA and IgM to a common antigen. A number of conditions are now identified by using antibody responses to a immune challenge. For example, a response to an immunization with Strep pneumonia is is a commonly used test of immune function.

Guilford 1988 Candida Antibodies


Slide Presentation for AAEM Fall 2014Conference

On October 23-26 I visited Albuquerque with a great view of the city and the hot air balloons dotting the horizon early in the morning.  I presented information about mold toxins and how they decrease the function of the enzymes that make glutathione resulting in a decrease in glutathione. These toxins are fat soluble, so they find their way into cells to cause problems. The basis of the information  I presented comes from an article published in 2014 titled “Deficient Glutathione in the Pathophysiology of Mycotoxin-Related Illness” and is available online, just click the link. The history of finding out how the loss of these enzymes was found is reviewed in the paper and is interesting as presence of the mold toxins should increase glutathione, but a deficit was found.

This is a very important topic because the loss of expression of the glutamate-cysteine ligase (GCL) has been found in other conditions including chronic astham and HIV disease. The loss of the enzymes controlling GCL (called the modifier unit or GCLM) is discussed in the paper “Glutathione supplementation improves macrophage functions in HIV“. The abstract for this article is on line. Contact me for information about the whole article. The article discusses the pathways depicted in the presentation slides. You can find out more about the role of glutathione in the innate immune cells ( antigen presenting cells and neutrophils) in the following articles, which are available online: “Characterization of Dendritic Cell and Regulatory T Cell Functions against Mycobacterium tuberculosis Infection” and “An Elucidation of Neutrophil Functions against Mycobacterium tuberculosis Infection“.

The slide presentation: Glutathione depletion by mold toxins and other causes  AAEM Fall 2014 Mycotoxin