Mold Treatment - Updated Legal, Disability, Genomics, Asthma and Lyme Prevention
May 25, 2011
Our monthly newsletter is a bit delayed for April in part due to too much happening all at once. Maybe the May newsletter will come out sooner.
Reviewers of Surviving Mold continue to write us some happy comments, though the absence of an index bothered more than one reviewer. Check the website for the reviews we have permission to post. As an aside, the index for Mold Warriors took many hours to create and never generated one single comment on how useful it was, despite being thorough. We will try to have a supplemental index for Surviving Mold available before too long for those who request it.
Otherwise, please let us know what you think about Surviving Mold. That is, besides telling us the book is too long. We know that any book that is nearly 800 pages is too long. “Mold and Peace” is a good nickname.
But we need to share more information on survival for those who have been changed by water-damaged buildings. In a way, developing a “safe-ness” for a given environment for people with prior mold illness is a basic requirement. A simple example is to say, “How can I tell if the new apartment I want to rent is safe?” ERMI testing is an obvious answer but waiting a week to find out the news and spending $300 can get tough when you have been in five prior moldy apartments. One approach we like is to take with you a handheld device that will tell you when nasties are in the air. Such an early detection system could tell us about harmful bioaerosols within minutes. Our crew at SM.com and affiliated labs are busting their tails to create a strip that will turn from red to blue color (for example) when exposed to endotoxins (from gram negative bacteria, a common colonizer in water-damaged buildings). When we have a good device, clinical trials will follow.
The big push in April was the Lee Daniels case in Florida. She is opposed by a defense outfit that isn’t afraid to create new information. I am trying to be kind by saying “create.” My counterpart on the expert witness side is Andrew Saxon MD, co-author of the ACOEM 2002 and AAAAI 2006 subterfuges. I am certain that any person who can read “ACOEM, ploys and lies” will not waste time deciding if Dr. Saxon has any clue about treating patients sickened by exposure to the interior environment of water-damaged buildings. He doesn’t.
The facts about ACOEM and AAAAI are clear: they are among the most reviled attempts to cover up science ever. Please review the “ACOEM, ploys and lies” (published on this site last month) and the recent commentary by the Institute of Medicine on Consensus Practice Guidelines that came out two weeks ago. The days of Tobacco Boys and their clones pushing people around in the mold world are over. Still, some judges are persuaded by the razzle and dazzle of the ACOEM-quoters. Sad, but truth falls to the wayside in those cases.
In my review of the motion of the defense to exclude my testimony (one of the sloppiest attempts at a legal document I have ever read) there was one consistent approach of the defense that was my theme in my rebuttal. See if you can see from my actual words in my rebuttal what I thought of the statements thrown up against the wall by defense: prevarication; confabulated; fabrication; distortion; plain untruths; deceptions we have come to expect from defense. There were more. Does anyone have any illusions about the games that defense attorneys must play when their medical back-up consists of plainly blatant malarkey?
One would hope that the opinions of the WHO, GAO, POA, CDC, EPA and thousands of academic papers would supersede the blather from a few cabalistic defense consultants. We would think that data from thousands of treated cases would triumph over intentional deception about ingestion of mycotoxins being the only way to create illness from exposure to the interior environment of water-damaged buildings. One would expect that definitive laboratory delineation of the illness would trump the Nay-Sayers. We will see.
A word to the wise here: Any plaintiff in a personal injury case had better be worried if they shade the truth. Such shading, or overt intentional deletion of information shared with their expert will haunt them and cause the loss of the case. Let the defense people lie: we all know they will. Don’t you try to alter records or alter your medical history. As soon as you lie, all your credibility and that of your consultants will disappear.
Also, the Bianca Jagger case is starting to heat up. New York had some very aberrant views about what WDB can do to people (see NY State recommendation and criticisms on this site) so the recent Frye decision in NY (Holland; case settled before trial after a Frye challenge) in my favor is heartening. The Jagger case will likely be postponed.
The Lanier Middle School case in Virginia will go to trial on June 20. Every school teacher affected by mold in the US should be watching this case. The approach used by the defense in this case is one that I see repeated in school districts across the US.
The world of disability claims has been turned upside down in the past several weeks. Lee Ann Mason is still embroiled in her fight for her rights in Hawaii but she has kindly shared a series of files that all of us need to know (click here to visit the Disability section on SurvivingMold.com). Disability claims for mold illness and chronic inflammatory response syndromes (CIRS) are winners in an ever-increasing number of cases involving Social Security and the Federal Office Workers Compensation Program (OWCP) but commercial insurance carriers are still fighting CIRS. Their weapons? Surprise! Its ACOEM and AAAAI. The decision-makers? Internal consultants with absolutely no credentials in this field are produced as if they came from down after lunch at Olympus or Valhalla. Are they? Nope. They are just guys who happen to have MD after their name making a living attacking plaintiffs. One wonders who else sells their soul for a few bucks in this field.
Along this line of thinking, some day the fee structures for some of the defense consultants needs to be published: wouldn’t we all enjoy seeing defense people explain the basis for what they charge for making a telephone call or reading records.
We are considering the development of a repository for disability claims decisions. Opinions from Social Security are in the public domain. If you have an opinion about posting decisions (or not), let us know. Privacy is an issue here. The idea is that patients injured by exposure to WDB aren’t likely to be able to be their own best advocates.
There are some disability agents and attorneys with good track records. We want them to be featured here (if they agree). I guess such an appearance might look like advertising. But I don’t agree about the advertising argument; only those attorneys and agents who have done good work at reasonable prices will be invited to list their contact information. We will start to develop a roster of cases of pitifully absent attention to detail and outright rip-off as well, understanding that we are not in the slander business. When physicians sell telephone time for $180 per minute (no kidding, in court documents from one case from Vermont we found that the plaintiff was charged $1800 for 10 minutes) all credibility and respect disappears. When one’s financial life is in the hands of someone who will profit from your case and there is an outrageous crime against financial integrity, there is no room for being nice and polite.
We invite you to send us reports of who did good work and who did bad work. We will work on these cases to distill truth from hype, and reputation from performance. This idea won’t be finished tomorrow, but we will get started today. If you need help with short term or long term disability, Social Security and commercial insurance battles, we might be able to help you. We aren’t attorneys or agents, but we sure are interested in seeing everyone receive what they have earned (or paid for). Email us at firstname.lastname@example.org.
The basic approach to winning disability cases or any legal cases based on personal injury caused by exposure to the interior environment of WDB is defeating the idiocy of ACOEM and AAAAI. That defeat begins by learning what we have here for all to review.
Take a look at the eloquent court decision from Idaho way back in 1999 that punished State Farm to the tune of $9 million if you think that entrenched bureaucracies of financial institution don’t know just how serious disability claims are.
this section might apply better to the physicians and health care providers but all patients are welcome too in this new world of diagnosis. Simply stated, we can now assess the differential activation of nearly 40,000 human genes with one tube of blood. No kidding. It is true.
What our genomics team has done in the past with ciguatera and now with mold illness (and Post-Lyme) is to develop a series of assays using established genomic technologies that break down the huge number of genes that might be active (or not!) at any one time to approximately 500 that are shown to be critically different in cases compared to controls, understanding that there are gender differences that must be controlled.
At the recent IFM conference in Seattle (4/30/2011) I offered to all providers that if they sent us PAXgene tubes (email us to arrange for shipment of these tubes to your physician) from three control patients (we will need to know WHY a person is a control) we will run one case patient at no charge (normally a $500 fee). Our turn around time can be several weeks but these data are the cutting edge of a cutting edge approach to correction of human illness. PAXgenes tubes are expensive ($15 each); we can send some to you, billing at our cost. We will then credit the cost of the PAXgene tubes and shipping costs when we receive the four properly prepared specimens in the mail. We will have a complete list of instructions on handling the PAXgene tubes. It is really so simple, even a defense consultant could do it.
I wish we could just forward PAXgenes for free to anyone who asked for them. We can’t. The idea of reimbursement (like what we are using) works in cell phones and TVs, so maybe it will apply to PAXgene tubes.
Send us an email if you want more information about PAXgene tubes and genomics - email@example.com.
As simple example of how genomics helps comes from our work with T regulatory cells (see section of this newsletter below). I had never heard of butyrophilins, yet the sparse world’s literature says these compounds may be the players that convert beneficial T reg cells induced by high TGF beta-1 into pathogenic T cells that in turn make more TGF beta-1. Our genomics data told us that cases are way more likely to have high butyrophilin gene activation than controls. We have along way to go, of course, but the fundamental basis for cellular innate immunity created in tissues may have been revealed. Is this a big deal? We will find out.
But even if this lead doesn’t pan out, we have 50 more that we didn’t have before the genomics data became available.
The day will come soon that we can show consistency of abnormalities in previously asymptomatic patients using simple genomic techniques and then using gene-targeted therapies to initiate new treatments.
The idea of cure will be symptoms equal to controls; VCS equal to controls; labs equal to controls; and genomics equal to controls.
for years I have been astonished by the bogus criteria that some docs use to diagnose asthma. Wheezing on one occasion just isn’t enough; neither is wheezing with a respiratory illness. We used to say that asthma was repeated reversible bronchospasm. That meant more than one episode. The episodes responded properly to standard asthma meds. We knew that asthma had an inflammatory basis, largely in allergy, so-called extrinsic asthma. Allergy was the big culprit here, with elevated IgE the standard test that supported the diagnosis of an allergic basis (see case/control IgE). A few people had intrinsic asthma (normal IgE) but just about all of the exploding asthma population in the US was extrinsic, the experts said.
So then the EPA (Fisk and Mudarri) announced in 2007 that 21% of all asthma in the US is due to exposure to the interior environment of water-damaged buildings. This illness from moldy buildings conservatively cost us over $4 billion (in 2007). Is the asthma due to extrinsic allergy? Intrinsic allergy? Or is it something else that we call asthma that really isn’t asthma?
Granted, I complain that docs can be sloppy about diagnosing asthma. What basis do I have? Simple: most abnormal pulmonary function testing results in patients with CIRS-WDB don’t show obstruction. They show restriction. And most (by far!) CIRS-WDB patients don’t have high IgE. To make it even worse for the asthma diagnosis, most mold patients don’t get better with inhaled beta-agonists, leukotriene antagonists or inhaled glucocorticoids taken singly or in combination.
What is going on here?
Let’s take another look. Do a quick literature search on asthma and what stands out? Remodeling. The airway itself is remodeled. What does that actually involve? Something in the airway has to change. What does the changing? One player is TGF beta-1. Do a search on TGF beta-1 and remodeling. Just look at all the tissues affected by high TGF beta-1, especially the lungs. Add to the mixture of concern about asthma the role of high TGF beta-1 in interstitial lung disease: it is causative! Remodeling indeed.
Let’s make the diagnosis of asthma even more suspect (at least in adults). About 98% of mold patients (OK, OK, I’ll call the illness its given name CIRS-WDB [see POA report]) are deficient in VIP. What does low VIP do to lungs and hearts? VIP prevents a significant rise in pulmonary artery systolic pressure (PASP) in exercise. Low VIP is marked physiologically by a rise in PASP in exercise that exceeds 8 mm Hg (mercury).
Follow along here. If we want to increase the output of blood from the left ventricle in exercise (we do) then that cardiac output is determined by two factors. One is pulse rated and the other is stroke volume. Stroke volume is determined by the ability of the left ventricle to eject blood and the return of blood from the lungs (venous return) to the left side of the heart. If the heart muscle itself is not injured then ejection fraction is not compromised. A rise in cardiac output can be accomplished by increasing stroke volume before pulse rate goes up.
But here is the kicker in VIP deficient patients. Their stroke volume doesn’t compensate for the needed rise in cardiac output because (1) they don’t increase the amount of blood sent to the lung from the right ventricle (2) due to a rise in the pressure in the pulmonary artery (3) that doesn’t fall in exercise like it should (note I am over-simplifying some physiology here on purpose). If (4) the extra blood needed by the left ventricle in exercise isn’t getting to the lung, the return to the left ventricle by the pulmonary veins will be reduced.
The heart still has to pump out the extra blood needed in exercise. It compensates by increasing pulse rate prematurely after the patient doesn’t receive adequate blood flow, especially in the lungs in exercise. The patient gets short of breath in exercise but really doesn’t wheeze. When he takes asthma meds, none of which affect the PASP, he doesn’t get better. When mold illness patients come here, they do get better because the inflammatory changes brought on by the illness that cause shortness of breath are directly impacted for the better.
Now let’s go back to my complaint about sloppy diagnosis of asthma. Exercise induced shortness of breath with tachycardia must be asthma based on clinical grounds, right?
Nope, that is simple low VIP. No wonder the standard lung meds don’t have a chance of helping VIP-deficient mold patients.
Don’t forget that measurement of PASP is tricky. You need a good stress test lab and a skilled echo technician. Stress echo testing must focus on the right ventricle and not the left. I can tell you that 99% of stress echos, if not more, are looking for abnormalities in left ventricle function. So a good echo tech is a valuable asset.
Add to that the stress test itself in which all attending will be monitoring the patient for ischemia. The pulse that is targeted for left ventricular function may be too low to show the maximal adverse effect of exercise on PASP. Finally, when the stress test is done, now an exhausted patient, probably sweaty and most assuredly short of breath must lie down immediately in his (her) left side to repeat the echo survey of the right ventricle, looking for the telltale “tricuspid jet.” Newer echo machines will calculate the PASP automatically but otherwise the cardiologist has to review the echo tapes and do the calculation manually.
Suffice to say, when we schedule a stress echo, we are looking for the facility, the tech and the cardiologist. When I hear a patient saying he/she gets short of breath going up five or six steps, I now wonder what is happening to the tricuspid jet. PASP problems happen that quickly.
Now, let’s throw in some VIP into those without the needed regulatory neuropeptide. What happens to venous return to the left ventricle? Back to normal. What happens to tachycardia? Gone. What happens to exercise–induced shortness of breath? Gone. What happens to the asthma diagnosis? Out the window it goes. What would happen to Dr. Fisk’s projection of $4 billion spent on mold-induced asthma? Maybe not gone, but just look at the people who would be helped.
And then we fix the epithelial to mesenchymal transformation (EMT) in the lung, the remodeling piece of this puzzle that is driven by VIP.
T regulatory cells (Tregs): Normally, our thymus derived (T cells) lymphocytes have varied roles. We have T killer cells, T helper cells and T regulatory cells too. Out of the bunch Tregs are probably the bosses and the other T cells are either “thugs or drones.” They do what they are told. The immunology here is so volatile: pick up a standard Immunology Reviews and there will be two papers on TGF beta-1 and at least one on Tregs every month.
What we know is that low levels of T regs are not good. Low levels are confirmed in a variety of illnesses, like Post-Lyme and untreated mold, among many others. We have two abstracts submitted on our work with T reg cells. I will keep you updated on those abstracts over the next several weeks.
Basically, what we are seeing is the cellular basis of innate immune response and not just the humeral (blood-borne) basis of innate immune responses.
many of our subscribers are Lyme patients. Many of those are affected by exposure to WDB and sickened by that exposure but they continue to think that Lyme is their problem. Sad, but true.
As we enter the months with the greatest incidence of tick bites and acute Lyme disease you will read a lot of verbiage about prevention of tick bites. Please discard most of what you hear as the ideas are not logical. For example, have you heard to use insect repellents like DEET? I use these products every day to reduce the number of mosquito bites I risk entering the forests and swamps of this area. But I never saw any reduction in tick bites. Why? Ticks are arachnids, like mites and spiders. Permethrin is an excellent tick repellent. The Army puts permethrin into the uniforms of soldiers stationed in tick endemic areas.
But the commercial permethrin-containing sprays were pulled from the market last year. Why? Ask the Feds. No logic touched that decision.
So after I was permethrin-less and had another beautiful ECM rash from a tick bite last spring, it was time to visit the farm store. There in the horse chemical section was 10% permethrin, used by horse people all the time on their animals. Simply put one ounce of the stock solution into a 32-ounce misting container, fill with water and spray your clothes. Good bye ticks.
While you are there, pick up some rotenone powder too. Take two ounces; dissolve in a gallon of water. Now take cotton balls, dunk them into the rotenone solution and use tongs to place the soaked cotton balls at the end of your gardens, plantings, trees and wildlife edges. I suggest you do this at dusk to try to make sure your dog or cat can’t play with the cotton balls. In the morning, take a look at where you cotton balls were. Just about all will be gone.
Mice (mousies, as they are known around here) love cotton balls. They take the cotton to line their globes (nests) quicker than anyone would believe. Now the rotenone soaked cotton kills the ticks on the mice as the mice sleep away. Keeping the ticks off mice will protect you far better than shooting neighborhood deer!