Mold Sickness on Valentine’s Day

February 25, 2011

Imagine the scene on Valentine’s Day. One spouse is chronically ill and the other isn’t. “Let’s go out for a nice romantic dinner,” isn’t going to be a winning suggestion when one person is dead on the couch by 7 PM. The healthy spouse might say, “What is wrong with you all the time? Surely, you can spend a little time with me, just for once, like in the old days.” While the affected spouse might mount a super effort to grab a glimpse of a pre-mold life, he/she will pay for that glimpse for several days afterwards. Just like he/she pays for the trip to the high school play Friday and Saturday night to see the daughter sing or the trip (“Just for a short visit”) to Grandma’s moldy home on her birthday. You can fill in the list of the extra efforts that mold patients pay for that non-mold patients feel is just a routine part of life.

There almost is a sense of jealousy, certainly of loss, when someone bounds up the high school stairs, like the mold patient once did, without becoming short of breath or having aching, crampy pains in legs, hips and back. Or when someone can go into a school and stay there, learning like we all want him to, not sickened by whatever bioaerosols are torturing one’s nose.

It really isn’t fair, you know.

Valentine’s Day surely is emotionally and physically better if your loved one knows what is wrong that makes the other’s illness never leave. If one knows what is wrong, the Valentine’s night date still might not occur (substituting a romantic pizza delivery happens more often than one might think), but the possible rift in the marriage might not be so pronounced. The “Spouse’s Tale,” when combined with awareness of objective parameters that show the reason one can’t just bound up stairs like a teenager, often becomes one of solidarity and support, leaving behind the predictable doubt, suspicion and mistrust. This change is not a small measure when no hope for cure is on the horizon.

To date, our data provide that assurance of presence of abnormalities. The labs our docs use give a reliable answer to the question, “Is something actually wrong with me?” Indeed so. Moreover, Surviving Mold describes (1) the 11-step sequential protocol I use to correct those lab abnormalities and (2) why the protocol must be sequential. Docs who use the protocol (from all 50 states and 31 foreign countries) already know: don’t skip steps. If someone does skip a step for some unfounded reason, the result of the protocol often will be like a recipe that leaves out a vital ingredient. The final product just doesn’t make it.

So how do I know that a given set of labs means something? Simple, we record them and compare cases to controls. We monitor changes in labs with sequential therapies. Please note that some of the labs I use are called “research use only (RUO),” or “lab developed tests (LDT).” Does that make them less valuable or reliable? Actually, no. They are tests that are all CLIA-approved and are eligible for insurance coverage/reimbursement.

Our office (and so many others) records data sets just about compulsively. The data pile up over time. Don’t listen when some Nay-Sayer (read uninformed person or if in litigation, a deliberate confabulator) says the tests aren’t FDA-approved. Such an argument is not only unfounded in fact; it is just plain silly. The FDA has nothing to do with CLIA or the actual practice of lab medicine. As an aside, about 40% of the tests for sale in the LabCorp and Quest manuals are not FDA-approved.

If one person is ill and the labs that show he is ill are sitting out alone on a limb of unreliable test results, not many people will accept such information as true medical fact. But when the lab results are all CLIA approved and insurance companies recognize them as reliable and the labs are internally consistent, then we need to look more closely at lab results in one person. So called “anecdotal data,” or “N=1 studies,” the lab numbers applying to one person, starts to reach statistical significance when the “one person-data” becomes thousands of patients-data. Our data show the abnormal physiology of patients affected by exposure to the interior environment of water-damaged buildings (WDB). Black and white. No argument about normal or not. The statisticians can help us: are these results statistically significant to a p < 0.0001? You bet. Such statistical data helps deal with the so-called null hypothesis, one that says no test result is important and no treatment makes any difference.

The GAO report of 9/08 tells us that cases of “mold illness” will have symptoms similar to those patients who are described in published literature and that the same patients will have the same lab findings as those in experimental animals and humans. We can therefore show that a given patient is a case using the commonality of symptoms, visual contrast sensitivity (VCS) and labs. We need to show that a patient improves with therapy too. As an aside, the newest and best VCS test (called APTitude)is now running on this site (see section on VCS).

Take a look at the paper from Kundi to read a bit about establishing the commonality of findings at baseline. This basic concept is called “causality.”

Don’t forget that the labs found to be abnormal in mold illness are ones that a lot of docs haven’t used before. We need to change that under-utilization, as the labs are all from accredited, high level, CLIA-approved facilities. So many people with exposure and illness are not given adequate respect for their multisystem, multisymptom illness because the objective data isn’t recorded. Physical exam isn’t remarkable for a lot of abnormalities; how many of WDB-illness patients are told that “they look so normal that nothing could be wrong.” Unless, of course, the doc assumes that there is a psychiatric problem present. That bogus assumption usually is quickly followed by another bogus assumption that the patient is making up the illness.

Let’s see, how can any one diagnose a psychiatric illness, one with no laboratory parameters to support it, in the face of obvious inflammatory parameters?

Just do the labs. It is so simple. Like Barry Marshall, Nobel Prize winner who said that a bacteria, Helicobacter pylori caused stomach ulcers. No one agreed. He simply asked, “Will you do the labs?” Finally, enough people did and now Dr. Marshall is regarded as a great thinker of the 21st century.

I am not comparing the work of our group to that of Dr. Marshall’s group but I submit that the prevailing attitude of physicians is no way to measure advances in science. In Dr. Marshall’s case, there was an abundant existing literature to support his ideas that bacteria can disrupt normal stomach defenses to acid and therefore result in ulcers.

There is an abundant existing literature to support my contention that illness acquired following exposure to the interior environment of WDB creates a chronic inflammatory response syndrome (CIRS; ICD-9 995.93) in those with genetic susceptibility that results in predictable illness following exposure to the interior environment of WDB (see data sets from the 815 patient, 132 control study presented after peer review at the International Mycology Congress, 8/10). Chapter 4 of Surviving Mold has an overview of the labs that I use to help make the differential diagnosis process exacting and precise. For those who want to know what is wrong with them, that chapter (and Chapter 3 in Mold Warriors) is a good place to start.

New developments:


The search for data confirming cellular immunity involvement with CIRS-WDB has taken a rocket step upwards. T regulatory cell (T reg) function has been an attractive candidate for the final immunologic insult found in CIRS-WDB. We now have clear data that the role of TGF beta-1 in cellular immunity is crucial in how it interacts with T reg cells. Simply stated, if the T reg cells are too low (less than 9 CD4+CD25+ cells), bad things happen. Effective treatment raises T regs (mean 18.2 CD4+CD25+ cells) to match or exceed control levels (17.2 CD4+CD25+ cells). Re-exposure that brings relapse will cause the CD4+CD25+ cells to fall almost overnight to a mean of 5.1. Incredible. But as readers of Surviving Mold know, VIP treatment provides such spectacular help IF IT IS USED EXACTLY ACCORDING TO PROTOCOL. Is anyone surprised that the CD4+CD25+ cells reach to over 25 as an average in treated patients?

As time passes, I hope that we can learn more about CD4+CD25+ cells, particularly with regard to the nuclear replication factor FoxP3. There is a lot of alphabet soup going on…just wait until you start to learn about Akt-P1, 3K impact on FoxP0/FoxP3 fluxes. In this milieu I feel is the epicenter of the inflammatory illness that we call a chronic inflammatory response syndrome (CIRS).

Don’t be confused about all these cell determinants. We aren’t talking about CD4 or CD8 cells. We aren’t talking about CD57 cells.

If the jargon terms here are too much “acronymitis” to bear, believe me I am with you. Take some time and just remember that at one time MSH and HLA were unfamiliar terms too.

I mentioned that the APTitude Test is now available on this site. Early results show that this test is a marked improvement on the many other VCS tests available on the Internet compared to the actual hand held VCS test. Congratulations to Paul Taylor and Jodi Ashcraft for manufacturing something completely new for the survivingmold.com website. We look forward to seeing the confirmation of the validity of the test borne out over a longer period of time.

Legal News:

• Vermont is now on the list of states that will approach CIRS as a viable entity. In the case of Ross v. Irons, we will see if the defense pursues a Frye challenge. Despite the plaintiff attorney’s position that Vermont is laid back and not one for which challenges to expert testimony is accepted, I expect to be matched against Dr. Mike Phillips again. We have so much of his prior deposition and trial testimony that I suspect that he will be challenged for sure. Anyone who says that mold illness doesn’t exist except if people eat pounds of moldy hay just has no chance to be accepted in 2011.
• Dave Wise is bringing the case of the Lanier cohort closer to trial. This battle has been particularly absurd due to the involvement one particular person from NIOSH saying the building was just fine even though there was a sodden crawlspace under the whole affected part of the building and ERMI evidence of massive contamination throughout the affected areas. Despite attempts of the defense to say that no one is ill, there are 23 affected teachers who are classic cases. This case brings forward the first academic correlation of the paper from China showing markedly elevated levels of TGF beta-1 in cases of vocal polyps now reproduced by a repetitive exposure protocol of one of the teachers. If you see vocal polyps, nasal polyps and acrochordons, think TGF beta-1.

Upcoming:
 

• Our Roundtable discussion of water-damaged buildings is delayed; just too much to do.
• We are writing the VIP manuscript now that we have one-year follow-up showing safety and efficacy in some of the worst CIRS patients. Never a dull moment!