Important Mold Announcements

August 17, 2012

Announcement 1: Patented Mold Diagnostic Procedure

I am delighted to tell you that after five years of planning, research and yes, hoping, Surviving Mold will now have access to a newly patented diagnostic procedure that uses analysis of over 22,000 genes called genomics (it uses assessment of mRNA and microRNA), combined with assessment of proteins in blood (the blood tests you are used to seeing), called proteomics, to identify mold patients accurately when compared to control patients and others with chronic inflammatory illnesses like the Post-Lyme syndrome and ciguatera. The combination of history, differential diagnosis, VCS, proteomics and genomics demonstrates the proteogenomics of these illnesses. The provisional patent, number 61/680,613, Methods for Diagnosing and Treating Chronic Inflammatory Response Syndrome, was issued 8/7/2012 to Proteogenomics, LLC. This company will have its own website ( up soon. will link to this site once it is ready for public viewing.

For patients who have visited my office in Pocomoke, Maryland for evaluation since 2007, it is more likely than not that the special tube of blood, called a PAXgene tube, was drawn with the other diagnostic tests and saved in our deep freezer. I hoped that there would be a day when the tube of blood would be of benefit in case analysis. That day is now here. While there still is much work to do to bring this test to the commercial market, having the patent will allow Proteogenomics to bring some remarkable findings to patient care. The genomics tests are done using FDA-approved procedures and strict quality control.

Over the next month as the new lab is prepped for opening, Surviving Mold will have more information about using the PAXgene tube in assessment of individual cases. Within six weeks, we will have a fact sheet available for patients interested in having the PAXgene mRNA and microRNA testing done. What the genomics show is that the differential gene activation and (interestingly) suppression that occurs in mold illness is affected by colonization with the HLA DR, biofilm-forming MARCoNS, C4a, TGF beta-1 and VIP (among others!). Also we are seeing curious patterns of gene activation in those with (1) chronic pain; and (2) demyelination (43% of patients have such demyelination on brain MRI) as part of the illness. If you have chronic pain or evidence of “gliosis” or scarring on MRI, stay tuned for these potentially blockbuster findings.

To suggest that these new data will revolutionize medicine is actually not a stretch. As the data will be showing you, the future of genomics is here. As I sit here now, I can’t imagine pursuing patient interventions without knowing about levels of microRNA 23a or microRNA let7b for example. This new approach will be especially interesting to patients using ongoing antibiotics for Lyme disease, as we are finishing the data analysis to confirm completion of our preliminary diagnostic fingerprint for Lyme before and after antibiotics and after correction of the chronic inflammatory concomitants of that illness. Remember, differential gene activation is paramount in defining the host inflammatory responses. By defining the gene activity, we believe we can define the actual inflammatory basis of this controversial illness.

In any event, the days of diagnosis of chronic fatiguing illnesses by symptoms alone or by speculation are over.

I am aware that some of these genomic terms might be new to some readers. Take a quick look at the PowerPoint talk (hosted on the Surviving Mold site) given by Dr. James Ryan to a Lyme audience in Tampa in January 2012 for an overview of what he will be teaching all of us soon. I will be writing to you soon on my understanding on what microRNA are, what they do and what relevance they have in regulating both translation of the genetic message and mRNA survival.

Want to know what would happen if we could just turn off the excess suppression of “bad” genes or turn on activity of good genes? We are getting there with genes of greatest importance in CIRS. Stay tuned.

We will be seeking participation from other docs using our protocols to send samples from known cases and controls. If the physicians are interested in learning more about this cutting edge approach to complex illnesses they should contact us. We will be opening up use of this technology to members of the physicians section of the site.

What this means is that there is a unique genomic fingerprint for these illnesses. In reality, the genomics work has opened a door widely that shows just how primitive our efforts to provide complete diagnoses and treatments have been for so many illnesses. Readers of Surviving Mold will be the first to know where this new science will take us.

But the bigger picture here is that lack of regulation of important regulatory elements, whether they might be MSH, VIP, T reg cells of microRNA all must be assessed in chronic fatiguing illnesses.

The application of genomics can provide support (or not) for some commonly espoused theories on causation of illness and therapy. We took a preliminary look at 38 genes involved in methylation pathways per the suggestion of Rich van Konyenburg and didn’t see differences between cases and controls. Does that mean methylation is not involved? Of course not, but in order to look more carefully at Rich’s ideas we will need to find the samples and the funds to do so. Genomics testing isn’t cheap!

The key element for consideration here is what we see in the genomic data is that it is a system of lack of regulation that must be corrected and not just one isolated gene or a single nucleotide polymorphism.

This next year of research holds great promise. For mold patients, that promise is here.


Announcement 2: Pattie Schmidt Introduction

Beginning within a week or two, we will be introducing Patti Schmidt to Patti knows firsthand about the emotional and psychological complications that can arise from chronic fatiguing illnesses. At one time, Patti’s Lyme and then mold illness took away any quality of life or hope that she can be a skilled healer. Now that those illnesses are fixed and she is in graduate school, Patti will use her skills to help those in need of some discussion or counseling. I won’t pretend to speak for her but we welcome Patti! You can see her graduation picture on my exam room wall. Patti edited Mold Warriors and helped with Surviving Mold as well.

Look for her new section of

Announcement 3: Mold Bibliographies on Newsletters

I have asked the webmaster to start sending selected bibliographies to those on our email list. I hope you will save them, as they contain references I have used to answer questions that are relevant to medical issues impacting on mold illness. Our first “blast” earlier this week featured background on the pediatric speech delays I see commonly in children conceived in moldy buildings. The concept here is that there must be clear evidence of academic support for what I see every day in practice. I cannot let such clinical observations simply pass by without documentation in the medical and scientific literature. When there is a data base of peer reviewed published papers then those papers will become part of the backbone of science that leads us to insist that the rights of those people affected by water-damaged buildings cannot be tossed aside based on biased opinions of paid naysayers. What those people don’t have is data: we have it. What they don’t have is academic support: we have it. What they do have are backers with lots of money to be used to suppress the truth about mold illness.

The data will show us the way.


1. The first time (in 1999) I saw gastroparesis in a mold patient I was surprised. This condition of delayed emptying of the stomach basically occurs in older diabetics with a history of poor control of their metabolic abnormalities. To find this problem in any non-diabetics was bizarre. But finding one made me look for another. After finding another ten the question came, “How many others have I missed?”

My initial finding is what we call an N=1 study. No more than an anecdote, it is something interesting but who knows what significance the finding might bring. If other docs around the country were collaborating to collect and share data, maybe my N=1 gastroparesis finding wouldn’t be unusual at all. If so, let’s write a paper, right?

Actually, that ideal collaboration is starting to show benefits. Docs who take the time (and they aren’t paid to do so) to collect and collate data are making a difference in mold illness.

Back then there was no group of people linked by published peer reviewed data and there was no So I just kept recording the “oddities” I was seeing against the time in the future that those observations would reach statistical significance. Now in 2012 that I have a data base on gastroparesis showing that about 10% of non-diabetic mold patients suffer from this condition, compared to less than 0.1% of non-moldy, non-diabetics, I can ask are there others for whom this diagnosis is missed?

I suspect a lot of people are walking around with a diagnosis of irritable bowel syndrome because of their bloating, abdominal pain and feeling of fullness. Maybe they are taking reflux meds and not doing well because the problem is not gastric acid related but instead caused by the stomach being a big, floppy bag that doesn’t contract very well.

Maybe the problem is bile acid reflux instead, another incredibly common problem in my patients. I won’t be discussing this problem today so much as to say it is real, easily fixed and almost universally misdiagnosed

2. The first time I saw abnormal levels of von Willebrand’s profile in mold patients I was surprised. What did the inflammatory response I saw every day in mold patients do to create clotting problems? Sure enough, the various factors in the profile can be acute phase reactants, meaning that when things are going wrong with innate immunity, there will be problems with both clotting and bleeding as well. But when I kept on seeing patients with chronic illness having these acute phase reactants being abnormal and staying abnormal over time, how can the coagulation problems be a problem in acute phase only? And then, what is the reason that I wouldn’t see coagulation problems in systemic inflammatory response syndromes? What a surprise? Nope!

At first the scientific problem was compounded by the really odd results I received from LabCorp in the von Willebrand’s profile (vWF). When I switched to using the Quest Diagnostics assay the really odd variances in individual results disappeared. Using Quest routinely, and never LabCorp for vWF, what I have documented in vWF testing now in over 3000 patients is the clear delineation of a complexity of abnormalities in coagulation with respect to von Willebrand’s seen in all patients with biotoxin illnesses and not just those with mold illness.

LabCorp isn’t bad in everything: just don’t use their assays for VIP, C3a, and C4a, vWF or CD4 + CD25+. And remember the normal range for MSH is 35-81 and the normal range for MMP9 is less than 332.

3. The first time I saw problems in levels of T regulatory cells (T regs) was after reading that such a problem occurred in Post Lyme patients. And yes, I was surprised but by then not all that much. What was surprising was the finding that the literature on T regs had absolutely nothing on sequential changes in T regs with illness onset and resolution. By the time I had measured T regs in just 100 patients sorted by illness category I had the world’s largest series of findings on changes in T reg by steps in inflammatory illness. So who knows more about the changes in T regs with illness onset, treatment, relapse and re-treatment than my patients? No one. Now that we have data on over 1000 patients, I guess it is time to write up the results. The relationship of T regs to TGF beta-1 is incredibly tight. A later “blast” will show you a wealth of references on this subject.

4. As I move forward with the docs on our physicians’ section, our goal is to create a certification test. What that test would mean is that there would be objective data that would support referral from the site to physicians from a list of those who passed a comprehensive test. Without confirmation of the ability to pass a certification exam, I’m not sure how we can provide referrals with confidence. Of course, we need to make sure that those who received referrals are using the published protocols for diagnosis and treatment of biotoxin illnesses.

I wish you health. Please don’t forget to insist on data collection supporting what you do in diagnosis and treatment; verify that the process of logic is always employed; always seek for guidance in published literature; and don’t accept guesses as proven fact.

Ritchie C. Shoemaker MD