Below is a collection of previously answered membership questions.  For best results, use your browser's find feature (CTRL+F) to search for the terms or subject you are curious about.

MARCoNS in dogs

What is the procedure for testing and treatment of dogs owned by patients with recurrent MARCoNS? 

Note there are two main reservoirs of MARCoNS in the environment. One is the interior environment of water-damaged buildings and the other is deep nasal spaces in dogs.  There may be others that I don’t know about. For people who don’t have close contact with dogs, presence of this organism in a dog’s nose is not significant.  For people with close contact with dogs who have the same organism found in their noses as what dogs have, there are several issues. The first is hand washing; this simple procedure is the most critical element in prevention of droplet transmission of infectious diseases. Just like hand washing prevents diarrhea in day care children and transmissions of infections in the hospitals, it also helps prevent transmission of this organism from a dog to people. Pet the dog, wash your hands.  Scratch the dog’s tummy and ears, wash your hands.  I am reminded of the line from the famous cartoon strip Peanuts when Lucy says, “Ooh, I have been licked by a dog.” This form of affection, like nuzzling your dog’s face, isn’t a good idea if you are low MSH and have harbored a MARCoNS. 

Any kind of diagnosis or treatment of a dog should be made after a consultation with a veterinarian.  A veterinarian can do a deep nasal culture for a dog, using the same technique as for people, with the culturette inserted as deeply as possible into the nose. The culture is run by Diagnostic Laboratory Medicine using as the same API-STAPH (or similar method) culture technique to avoid overgrowth (false negative) with a non-biofilm forming organism. 

If the culture is positive and the organism is the same in the dog as it is in the low MSH person then the same BEG spray has been used by veterinarians with excellent success with the dog.  Physicians may not diagnose or treat dogs. 

As an aside, I am still unable to tell you why the positive-culture rate is so low in children. I don’t even culture children under age 15 any more.

Corticosteroids

I have been told that I will need to have injections of steroids into the areas around my hip due to a progressive deterioration of the joint. I have low MSH. Should I not have the injection?

My concern about use of injectable steroids goes beyond the problems with fungal infections that we saw coming from contaminated preparations of long acting steroid medications. For those with low MSH, regulation of ACTH (a hormone that stimulates the adrenal to produce glucocorticoids) is complicated by use of oral steroid preparations like Cortef, hydrocortisone or prednisone; or by intramuscular or intravenous dosing with those same steroids.  Topical steroid creams and injections into joint spaces do not have the same complications as shown by 15 years of clinical experience. We have clinical trials to confirm safety of inhaled preparations (nasal and pulmonary) that contain steroids.

If the injection is into the hip joint I think you will safely avoid suppression of ACTH. If the injection is into the soft tissue around the hip, I would suggest strongly that you measure ACTH and cortisol before the injection and then 2 weeks after, followed by 6 weeks after to show whether or not impairment of the ACTH production pathway has occurred.  If the steroid injection provides significant pain relief and improves quality of life then it is worth the risk.

Genomics

Do you think we will see a genetic cure for chronic inflammatory response syndromes and mold illness in the next 25 years?

We are close to publishing our paper showing the genomic fingerprint seen with mold illness.  We see the effects of mycotoxins and beta glucans on gene activation together with the effects of C4a, TGF beta-1, VIP and MARCoNS upon gene activation as well. This field shows such remarkable promise that I think it will be within 5 years that we will see particular treatments for differential gene activation including MicroRNA and antagomir therapies.

CIRS, the first stages.

How long does exposure to water-damaged buildings have to occur before an individual develops CIRS?

This question remains one of the most important in all of this field of medicine.  We know that people with HLA susceptibility and CIRS following exposure to water-damaged buildings have that HLA from birth.  What accounts for them developing a CIRS illness, say in their 20’s but not in their teens and not in their early childhood?

We have attempted to answer this question by following people prospectively with known susceptible HLA haplotypes but no illness.  What we have seen repeatedly is that an antecedent inflammatory illness, such as mononucleosis, Lyme disease, Coxsackie of ECHO virus infections, intense inflammatory lung responses and unusual conditions such as Kawasaki disease invariably occurs.  These inflammatory responses predispose an individual to have a change in antigen presentation such that an HLA that is “doing well,” protecting an individual against a moldy building, no longer does so.

Please take a look at some of the HLA questions on this list to see further discussion of HLA structure and antigen presentation.

The bottom line is that it makes sense for people to have an idea of what is their HLA, what is their baseline C4a and TGF beta-1 are and to monitor MSH levels before and after significant illnesses if the HLA is mold susceptible. Knowledge here is power.  If no illness develops then having the HLA becomes of no benefit. But if HLA is mold susceptible and an intense illness occurs, follow MSH.  When MSH falls, the HLA is likely to be “primed,” increasing risk of acquisition of uncontrolled inflammatory illness. If we have a CIRS in the early stage, and using the above approach makes detection easy, the illness is far easier to treat early in the course then later.

Avoidance of re-exposure

How do I avoid re-exposure after treatment?

This question is tied to the basic theme of Surviving Mold. Once you have developed a CIRS (with or without genetic susceptibility of HLA haplotype), and invariably with presence of low MSH, you are at risk to suffer another harmful inflammatory response if you are exposed to the interior environment of water-damaged buildings for as little time as 10 minutes.

Many patients will elect to use low dose cholestyramine or Welchol before venturing forth from their safe “bubble” that is their residence.  Obviously, where you live needs to have adequate fungal DNA testing.  Don’t forget that ongoing rigorous cleaning needs to be taking place including use of HEPA air filtration.  You need to avoid bringing new possessions into your home that might be crossed contaminated from their prior location.  Some patients are so sensitive to low dose exposures that even materials on clothes of children or loved ones can make them ill.  If that is the case, and it rarely is, then some sort of changing room needs to be made available so people can enter the bubble without contaminating the safe environment.  Fortunately, with use of drugs like VIP this extreme reactivity has mostly become a thing of the past.

As far as exposure to environments outside of your home, a certain caution needs to be introduced to your day to day life.  Places that are high risk for water-damage or growth of microbes, such as antique stores and old book stores are not even worth considering visiting. Restaurants, movie theaters, grocery stores and other commercial buildings must be assumed to be moldy until proven otherwise.

If you are going to have lunch in a new restaurant I would suggest that you have either cholestyramine or Welchol on board for at least two hours before you go into the new building.  When you enter, look around for evidence of water intrusion.  Are their stained ceiling tiles? Does the floor show buckling, or does the wallpaper show wrinkling?  If so, simply leave. If not, and you have no evidence of musty smells, simply sit at your table, order a glass of water (to avoid running up a bill), look at the menu and wait 10 minutes.  Look carefully at yourself for development of symptoms.  If no symptoms appear after 10 minutes then I think it is safe to have lunch and enjoy the day.  Continue on Welchol or cholestyramine for another 24 hours waiting to see if new symptoms appear.  If not, then it is possible that the restaurant is safe for you.

If you do develop symptoms, and those symptoms will appear in a stereotyped manner, be sure to notice if you feel nauseated, have a headache, have shortness of breath or cough, feel “queasy” or have sore throat or just plain don’t feel well, write down those symptoms for future reference.  If they appear, leave the restaurant and take cholestyramine and Welchol for a week monitoring changes in symptoms.  If your symptoms are due to exposure, then the same group of symptoms will appear if you are exposed to another moldy environment in the future.  This similar clustering of symptoms really is reproducibly reliable.  You will recognize it quickly in the future.

If you remain ill beyond one week of treatment then it is time to involve your physician and obtain labs to document where you are.

Re-exposure symptoms

I know that symptoms from a “mold hit” appear in as little as ten minutes.  My concern is that now I seem to be getting stronger symptoms with re-exposure then what I did before. Please help me with my concerns.

Here you must be very certain that ERMI or HERTSMI-2 in your residence is normal.  The most common reason for worsening after treatment is re-exposure in the home environment. ERMI testing costs $300.  While I use Mycometrics more than any mycology lab (and there is no conflict of interest here), it is even less expensive to use HERTSMI-2 which only costs $125. Once you are assured that the home is safe, now is the time that you absolutely must have your labs done looking at treatable aspects of “sicker, quicker.” We see this phenomenon commonly, particularly in people with HLA haplotypes of 4-3-53 and 11-3-52B but can occur with any haplotype.  What happens is that the enzyme that makes C4a (MASP2) is one of the few (some say the only) enzymes that auto-activates. Trivial exposure will cause an exponential rise of C4a, with TGF beta-1 following as a result that in turn makes people much worse.

VIP has shown spectacular benefit in reducing this “sicker, quicker” part of surviving mold. If you haven’t discussed VIP with your physician, please do so. I encourage you to read the paper that was published in Health 3/13 ( accessed by this link) to look to see what you can expect from this safe and effective medication.

Corticosteroids

I have been told that I will need to have injections of steroids into the areas around my hip due to a progressive deterioration of the joint. I have low MSH. Should I not have the injection?

My concern about use of injectable steroids goes beyond the problems with fungal infections that we saw coming from contaminated preparations of long acting steroid medications. For those with low MSH, regulation of ACTH (a hormone that stimulates the adrenal to produce glucocorticoids) is complicated by use of oral steroid preparations like Cortef, hydrocortisone or prednisone; or by intramuscular or intravenous dosing with those same steroids.  Topical steroid creams and injections into joint spaces do not have the same complications as shown by 15 years of clinical experience. We have clinical trials to confirm safety of inhaled preparations (nasal and pulmonary) that contain steroids.

If the injection is into the hip joint I think you will safely avoid suppression of ACTH. If the injection is into the soft tissue around the hip, I would suggest strongly that you measure ACTH and cortisol before the injection and then 2 weeks after, followed by 6 weeks after to show whether or not impairment of the ACTH production pathway has occurred.  If the steroid injection provides significant pain relief and improves quality of life then it is worth the risk.

Genomics
Do you think we will see a genetic cure for chronic inflammatory response syndromes and mold illness in the next 25 years?

We are close to publishing our paper showing the genomic fingerprint seen with mold illness.  We see the effects of mycotoxins and beta glucans on gene activation together with the effects of C4a, TGF beta-1, VIP and MARCoNS upon gene activation as well. This field shows such remarkable promise that I think it will be within 5 years that we will see particular treatments for differential gene activation including MicroRNA and antagomir therapies.

CIRS, the first stages.

How long does exposure to water-damaged buildings have to occur before an individual develops CIRS?

This question remains one of the most important in all of this field of medicine.  We know that people with HLA susceptibility and CIRS following exposure to water-damaged buildings have that HLA from birth.  What accounts for them developing a CIRS illness, say in their 20’s but not in their teens and not in their early childhood?

We have attempted to answer this question by following people prospectively with known susceptible HLA haplotypes but no illness.  What we have seen repeatedly is that an antecedent inflammatory illness, such as mononucleosis, Lyme disease, Coxsackie of ECHO virus infections, intense inflammatory lung responses and unusual conditions such as Kawasaki disease invariably occurs.  These inflammatory responses predispose an individual to have a change in antigen presentation such that an HLA that is “doing well,” protecting an individual against a moldy building, no longer does so.

Please take a look at some of the HLA questions on this list to see further discussion of HLA structure and antigen presentation.

The bottom line is that it makes sense for people to have an idea of what is their HLA, what is their baseline C4a and TGF beta-1 are and to monitor MSH levels before and after significant illnesses if the HLA is mold susceptible. Knowledge here is power.  If no illness develops then having the HLA becomes of no benefit. But if HLA is mold susceptible and an intense illness occurs, follow MSH.  When MSH falls, the HLA is likely to be “primed,” increasing risk of acquisition of uncontrolled inflammatory illness. If we have a CIRS in the early stage, and using the above approach makes detection easy, the illness is far easier to treat early in the course then later.

Relapse after re-exposure

I took Welchol for one month. Do I need to continue taking that medication?

Both cholestyramine and Welchol are continued beyond one month if (1) the VCS is still positive (2) the patient is still symptomatic; (3) exposure is ongoing to buildings which could possibly be water-damaged; (4) susceptibility is confirmed.

Once the susceptibility to illness is unveiled, and it seems likely from the rest of your question that you did have a confirmed illness before, usually with MSH falling below 35 and having HLA susceptibility, to date the only therapy that we have seen that reverses susceptibility is use of VIP at fairly substantial doses for at least 6 months. 

If you are (i) out of exposure; (ii) VCS is normal; and (iii) maximum improvement has been noted, then cholestyramine or Welchol will be used only if you venture forth out of your safe bubble but while in the bubble you do not need to take those medications.

VIP dosing

Is there benefit in using VIP even though the measured level is in normal range?

As of November 9, 2011 LabCorp changed their VIP kit and changed the normal range to the detriment of clinical medicine.  I do not recommend using LabCorp to test for VIP.  If a Quest measure of VIP is normal then we need to look at the risk/benefit of dosing VIP in face of normal VIP levels. 

Fortunately, over-dosage of VIP has not been reported to date even though some patients have used as much as 36 sprays a day.  VIP levels in the body are such that the total amount of VIP presented in the body can not be estimated from a blood test alone. The bulk of VIP is bound to receptors on cells. The good news is that free VIP (not bound to receptors) is broken down quickly by enzymes in the blood. Use of VIP despite a normal plasma level will simply guarantee that receptor sites are saturated thus assuring adequate benefits.

The best approach to dosing VIP involves repeating measurement of changes of pulmonary artery pressure in exercise.  These data are obtained by doing a stress echocardiogram with measurement of the tricuspid regurgitant (TR) velocity at baseline and then at maximum exercise.  For the treadmill aspects of the exercise testing employed, we usually suggest obtaining a heart rate of 95% of predicted and not 85% of predicted.  Please remember that echo technicians are used to looking (“interrogating”) at left ventricular and aortic valvular function in exercise.  They must be reminded that we are concerned with right ventricular (RV) pressures.  They need to take an extra 30 seconds recording the RV and TR pressures to ensure that the information we are looking for has been recorded precisely.

VIP treatment protocol

Can you discuss VIP treatment protocol including test dose, typical length of treatment and end point criteria.

VIP is added as a last step of the 11 step protocol.  Don’t start VIP until its time has arrived.  Remember, you must not have an ongoing exposure to ERMI > 2; positive nasal culture or positive VCS. Use of cholestyramine and Welchol will continue as long as there is the potential for exposure to a water-damaged building. 

The test dose of VIP involves giving 50 micrograms by nasal spray after a baseline blood test is done and observing the patient for 15 minutes.  During this time the patient is asked to discuss any possible changes in shortness of breath, pain/stiffness and cognition.  Asking people to describe whether their brain is working better or not requires some careful questioning!

At the end of 15 minutes a repeat blood test is done looking to see what changes occurred.  At baseline we look at MSH and VIP together with ACTH and cortisol; ADH and osmolality, C4a, MMP-9, TGF beta-1; VEGF, testosterone, estradiol; vitamin D3 and then of course, lipase.  The post-test labs look at TGF beta-1, C4a, MMP-9 and lipase.  Any rise of TGF beta-1 greater or equal to 5,000 is alarming.  It usually means that there is ongoing exposure to a water-damaged environment.

Once the test dose is safely accomplished and the patient is confirmed to be stable, a prescription for VIP begins with one spray (50 micrograms) a total of four times a day.  One can alternate sides of the nose used if desired but that is not necessary.  At the end of one month of low dose VIP repeat testing is done with lipase, C4a, TGF beta-1, MMP-9, testosterone, estradiol, ADH and osmolality and VEGF done together with Vitamin D3 to look for salutary effects of VIP.  At the end of one month, depending on symptoms, the dose can be increased or decreased as the patient and the physician agree.

Paralysis, full but temporary.

I have been diagnosed with a mold toxin illness and have been treated with cholestyramine and antifungals.  I seem to be deteriorating, getting weaker and with more fatigue.  I have had episodes of paralysis lasting more than 12 hours. Could the paralysis be connected to mold illness or treatment?

There are several issues with the scenario.  In the absence of culture positive confirmation of fungal infection I find that antifungals are not needed.  Your physician is the best source for this information. Improvement of laboratory parameters but presence of progressive neurologic deficits suggest an alternative process going on in addition to your inflammatory response syndrome.

The presence of paralysis, while not defining your question, sounds truly alarming.  I would recommend that you discuss your neurologic deterioration with your physician and revisit the differential diagnosis in that with improvement of labs biotoxin patients do not go on to develop paralysis.

Pediatric mold

My grandson has been exposed to black mold. He is being treated for asthma only.  I am his caregiver and I am upset to see him doing poorly. What should I do?

Children with CIRS can be diagnosed and treated. I would suggest you take a look on this site at the Pediatric Mold paper that was published in April 2009, in the Bulletin of the International Association of Chronic Fatigue Syndrome. Results of labs on over 160 patients and 50 controls are reviewed. The labs we use in kids include HLA, MSH, C4a, TGF beta-1, anticardiolipin antibodies and antigliadin antibodies. If you were able to have the Quest T-regulatory cells panel (60336 Quest Baltimore) that would be very useful. But the issue that I see in this case is that you as a grandmother certainly are a valuable member of the healthcare team, but I would suggest that the parents have the ultimate decision-making responsibility for what medical intervention the child would have. If the parents agree to have testing done, then proceed to have the blood drawn.

As an aside, it has not been a happy experience in the past every time I have had a sick child caught between parents who were not in agreement on what to do. Unless there is mutual agreement of both parents I do not intervene with the children.  I would suggest that you find a middle road to be the advocate for the child together with being the parent of a parent.

Hydrocortisone replacement

For a patient who takes hydrocortisone, is there a time during treatment when weaning off the drug can begin?

For those patients with MSH deficiency, the role of ACTH, another melanocortin like MSH, is often overlooked.  In my experience some physicians have found benefit in giving supplemental Cortef or hydrocortisone or other adrenal glucocorticoids in the thought that it would benefit the inflammatory response syndrome and/or chronic fatigue patients have.  My concern here is that over 60% of our patients with MSH deficiency will have impairment of normal responses of ACTH and cortisol.  These two hormones are intricately tied such that rising cortisol will suppress ACTH production and falling cortisol with stimulate ACTH production. ACTH then will stimulate release of cortisol from the adrenal cortex. That is the normal function.

When MSH is deficient however, this relationship of ACTH/cortisol becomes perturbed.  Blind use of supplemental steroids can permanently adversely affect (and suppression of ACTH production is by far the most common result) ACTH/cortisol relationships. This disastrous outcome is not rare. For patients who are being asked to consider taking adrenal steroidal preparations by their attending physician, I suggest measuring MSH first.

What happens for those people who have a biotoxin illness as the source of low MSH is that the ACTH/cortisol relationship begins being repaired as the innate immune inflammatory response diminishes.  While MSH may not necessarily increase, the demand for extra cortisol, and therefore extra ACTH, is lessened.  What this means is that any supplemental cortisol that is being used before inflammation was reduced will now potentially become even more hazardous to ongoing integrity of ACTH production. Weaning must start here!

I suggest that patients follow ACTH levels for those people who are on cortisol supplementation. As inflammation improves, there should be a reduction of cortisol without change of ACTH.  Similarly if there is an additional fall of ACTH for the same given measure of cortisol (measured simultaneously) then it is time to begin tapering the cortisol supplement.

Tapering is agonizingly slow. Sometimes as such a slow rate as 1 mg per month is all people will tolerate but nonetheless needs to be mapped out, charted and followed carefully.

How does reduction of hydrocortisone supplementation affect treatment over all?

Once the effect of supplemental cortisol on ACTH has been identified in an MSH deficient patient there will be a reduction in need for supplemental cortisol if inflammation is corrected.

Beta glucans

Are orally administered beta glucan supplements a useful treatment for Lyme disease as I am told beta glucans stimulate the immune system?

Beta glucans are diverse group of sugar-based substances.  They are key components of fungal cell walls as well as being in so many different organisms. The beta-glucan structure of greatest interest is called (1, 3)-beta-D-glucans. Of note is that other similar structures are included in the overall class of compounds called beta glucans but the structural differences are critical to their function. Organisms as diverse as lichens, algae, fungi and monocotyledonous plants are known to make beta glucans. This is not a complete list.

Without knowing which beta glucan you are consuming, (and I really am not an expert in the structural chemistry of beta glucans) I would be cautious in suggesting its use in nutritional aid. As far as treating Lyme disease goes I do not know of any literature that would support such a use. 

In water-damaged buildings, exposure to fungal cell fragments will activate innate immune receptors called dectin-1 and dectin-2 receptors that in turn activate an inflammatory response. I am not familiar with literature that would show that fragments of one kind of fungus will be more activating that another. Seems to me that this field could use some light!

The vital role of beta glucans made by fungi in water-damaged buildings is under represented in the world’s literature.  From what I see I think that as time goes by data will clearly show that beta glucans are far more important then other compounds such as mycotoxins.

Saunas

Do saunas help remove mycotoxins from the body? If so, what is the duration of time and frequency per week? 

Saunas are widely recommended by a variety of physicians involved with treatment of illness acquired by exposure to the interior environment of water-damaged buildings. I personally enjoy taking saunas; indeed a sauna is the first structure I usually build upon moving to a new home.  Other practitioners anecdotally suggest use of infrared saunas with exposures of up to 3 hours of day recommended for affected patients.

Most of my patients do feel better after taking a sauna provided dehydration is prevented.  There are no data published that I have seen that would suggest any objective measurements taken before and after exposure to support use of saunas.

I am aware that several environmental medicine practitioners rely on use of saunas and I have asked them personally to obtain data looking at inflammatory parameters before and after such therapies that would support ongoing use.  To date, no data have been ever shown to change by taking saunas up to two hours. 

There are so many variables with this one kind of therapy I think you can see the methodological problems that advocacy for using saunas would create. Is this an infrared sauna? Is it a near infrared sauna? Is it a sauna that uses rocks? Is it a sauna that uses other compounds to transmit heat? Are there frequent episodes of pouring water onto the rocks or other materials to create steam? How often is that done? What is the maximum temperature as recorded by a thermometer in the sauna room? Is the individual lying down? Is the individual sitting on an upper level shelf…?

Because of the lack of data I can not recommend saunas as an effective anti-inflammatory protocol for patients.  It seems easy enough to collect data to support such use. 

This modality of treatment brings up the conflict between anecdotal data which is not supported by evidence based practitioners and scientific data that is.  If we have no opportunity to collect lab data then so be it. We just can’t assume that something that makes us feel good is going to provide significant or lasting benefit in inflammatory responses. But after a busy afternoon working outside, I can tell you that my old arthritic body will be cooking in a sauna for 15-20 minutes before supper for sure.

IV Ig

I have a very complex patient with Lyme, Epstein Barr Virus, likely mold, evidence of exposure to strep, low levels of gammaglobulin and deficiencies of lymphocytes. I have obtained many of the labs recommended on Surviving Mold and would appreciate some guidance.  I use IV Ig for therapy.

I am happy to review labs and critical material as the request of any physician.  I have had a small number of patients who have received IV Ig who have gone through sequential testing to look to see what happens to them after IV gammaglobulin therapy. Surprisingly we did not see a fall of TGF beta-1 with such therapy. What was amazing to me was the rather impressive fall in levels of acquired T-regulatory cells (CD4+CD25++) but not the thymus derived T-regulatory cells which are (CD4+CD25++ CD127 lo/-). This drop of T-regs was a consistently observed finding.  As you are in an ideal situation to evaluate anti-inflammatory affects of pooled gammaglobulin, I hope you will collect some of the laboratory data with your patient’s pre and post gammaglobulin blood draws.

I am uncertain how the diagnosis of active EBV or active Lyme was made in this case.  Those data would be important to share.  The first element in confirming exposure to mold would be inspection of a building looking for water intrusion followed by environmental mold testing using QCPR either with the HERTSMI-2 or ERMI testing. Visual contrast sensitivity testing is incredibly important in assisting you in sorting out these different diagnoses though a deficit would not separate mold from Lyme. It would separate EBV and strep.  Look also for the presence of an elevated C3a as indicative of Lyme and strep exposure.  If there is absence of a bacterial membrane in blood or tissue, C3a will not be elevated. 

If the patient is actively infected with a strep organism, obviously antibiotics are indicated even though such antibiotics create more cell wall deficient forms (L-forms). Confirming active Lyme can be quite difficult.  There are several questions regarding Lyme included in this section of the website.

I would very much look forward to having the opportunity to speak with you about your case in person.

Non-mycotoxin Formers

Can molds that do not produce mycotoxins set off biotoxin inflammatory cascade?

This appears to be a loaded question that can be restated as “What do we know about specific causation? If we have a water-damaged building and compulsive search using mask spectroscopy and liquid chromatography, mycotoxins will be found. If a species of a fungal organism that doesn’t make mycotoxins is found, say Aureobasidium pullulans, does this organism create a health risk? 

We know that fragments of cell walls are associated with potential for creating adverse health affects.  These cell wall fragments would not necessarily include mycotoxins.  If there is an inflammatory response seen in the patient, can we say that A. pullulans did the damage? The difficulty is being assured that an observed inflammatory response could only come from one specific element found within a mixture inside of a building. As the inflammatory responses will be activated non-specifically by a variety of different initiators, finding the inflammatory response does not  tell us what initiated the pathway. One can make an analogy to a famous scene in one of my favorite movies, Blazing Saddles, where cowboys are sitting around the camp fire eating beans. When one fellow passes gas followed by another and then another, how do we know which bean created the flatulence?  Of course, we do know that poor Mongo is but a pawn in the game of life, but that doesn’t translate to causation of inflammatory illness by non-mycotoxin formers.

The answer is that we can not ascribe causation to a single bean or a single element found in water-damaged building to causation of illness. Perhaps in the future there will be some sort of elegant science that enables us to do so but not now.

Cholestyramine

What type of food and drinks can we take with cholestyramine to help those who have a hard time getting cholestyramine down?

Cholestyramine should not be taken with food as the food will be bound by cholestyramine. Any liquids can be used to assist digestion, prevent reflux and help prevent constipation.  For years we have given cholestyramine mixed in apple sauce to children but the cholestyramine will be bound to some of the particulates in the apple sauce material. Similarly the dosing of CSM with ice cream reduces its efficacy understanding that no tolerance of CSM really knocks out its efficacy. Mixing CSM with Gator-Ade and processing that mixture in a blender has helped a lot of people.

Cross contamination 

We have had professional inspectors identify conditions in our rental home that are typical of a water-damaged building. We have multiple questions on what to do including remediation, avoidance of cross contamination and access to treatment.

There are several sections on the Surviving Mold website devoted to remediation issues.  We have many questions that have been asked about remediation that are answered in Frequently Asked Questions, Volume I.  I suggest that you take a quick review of both the site and the FAQ to help you out.  In addition, there are several chapters in both Mold Warriors and Surviving Mold dedicated to these questions. 

The important issue in avoidance of cross contamination is to recognize that the particulates from the air of the water-damaged building that you transfer on your possessions will make you sick in the new building just like they can make you sick in the old building. As such, removal of these particulates before the move is mandatory.

Porous materials such as textiles and fabric used in upholstery and curtains as well as carpeting has never been confirmed to be successfully cleaned by any technique. No one will say save the sofa or the rug without creating the risk of cross contamination. Literature on this vitally important topic is scanty at best but you should be prepared to reupholster furniture or to sell porous materials.

Non-porous materials can be HEPA vacuumed after having been wiped down outside of the old residence. Then the item can be moved successfully. Any cellulose materials including photographs and books are problematic.  Discarding some of these possessions is painful for most of us. 

The vast bulk of cleaning possessions is something I personally think anyone can do provided time is available. I personally feel that if you want a job done right, do it yourself, as opposed to paying someone thousands of dollars when they don’t have the same vested interest as keeping you healthy as you might. 

Cleaning shoes 

I have to move out of my moldy apartment to a new location. I am prepared to discard porous materials but my shoes and I are old friends and I am not sure what I can do to save them. 

Leather is problematic in terms of cleaning to avoid cross contamination. Suede substances or “fuzzy leather” in my experience are no different from upholstered sofas. I can not recommend attempting to clean irregular surfaces such as those.  Other leathers that have a finish on them can be remediated.  I would suggest using a quaternary  ammonium compound (409, Windex, Fantastic, Clorox [NB: Clorox spray is not bleach!]) to test those sprays on the leather surface. After the cleaner has been shown to be safe on the surface I would HEPA vacuum the shoes inside and out. HEPA vacuum a second time and then place the shoes in plastic and then transfer to the next living situation. I understand that caring for shoes this way is time intensive but at approximately one minute per shoe a collection of 500 pairs of shoes would take 1000 minutes.  I don’t think this is too much time to spend in saving precious possessions.

Pediatric mold 

How do I treat my one and three year olds for their mold illness?

In order to meet the case definition for pediatric mold illness there must be presence of exposure combined with a subsequent development of a multi-symptom, multi-system illness.  If your children do not have multiple health symptoms then I think observation is reasonable. If they do have multiple health symptoms we unfortunately can not use visual contrast sensitivity to aid in diagnosis as children under eight are too young. 

I would suggest that you would review the paper our group published in 2009 on pediatric mold illness in the Bulletin of the International Association of Chronic Fatigue Syndrome. This paper is available as a free download on Surviving Mold. The laboratory studies we use in diagnosing children are all included in that paper.

You told me your physician did not think that children needed to be treated.  That may be true if they don’t meet the case definition.  However, if your children are symptomatic, then the physician needs to confirm absence of lab abnormalities.

Pets

Since I have moved out of moldy house, two of my four cats have died for unrelated reasons.  One had congestive heart failure and the other had liver damage according to the attending veterinarian.

We have not published any work on veterinary illnesses but it is not unusual that this question is raised.  I would suggest that you take the paper published in Health in March of 2013 that is available as a free download on Surviving Mold to your veterinarian.  While we can’t do visual contrast sensitivity on the two remaining cats, he would be able to look at presence of inflammatory parameters such as C4a and TGF beta-1. I would be happy to discuss those results with your veterinarian understanding that we do not have a control data set used to compare the result to.

Cholestyramine, short duration of Rx not helpful

I have been taking cholestyramine now for two weeks and I feel no relief. What does this mean for me?

We have had a number of people over the years improve dramatically in two weeks or less. The real driving force however behind development of the 11 step treatment protocol is that many people will have additional problems documented with baseline laboratory studies and nasal culture that create barriers to “instantaneous” benefit. Simply stated, when people in the past didn’t get better with CSM alone, it was time to look for what I was missing.  Then when I found something, like the biofilm-forming staphs, for example, it was time to see what would happen if the staph were eradicated first.  Applying this trial and error method has resulted in the current protocols, though much of the protocol has been in place since 2004.

By far the most common reason for lack of benefit in short course cholestyramine usage is not enough time on treatment. This may be applicable to you.  Second, there may be some problems with how you are taking cholestyramine dose.  The powder should be dissolved in liquid and be dissolved on an empty stomach waiting 30 minutes to let the liquid clear the stomach and get into the duodenum before eating or taking any medications. Taking cholestyramine 4x a day is the recommended dose. 3x a day is not as good. 2x a day is a maintenance dose and 1x a day is a dose to help your irritable bowel syndrome and very little else. 

Taking cholestyramine alone will not overcome the adverse affects derived from spending time in water-damaged buildings.  I routinely rely on DNA measurements of fungi using settled house dust as the medium for analysis.  Both ERMI and HERTSMI-2 are available at a low cost from Mycometrics with excellent levels of detection (www.mycometrics.com).  You need to know that I have no conflicts of interest to reveal regarding Mycometrics.  If there is an elevated ERMI (>2) or an elevated HERTSMI-2 (>10) I strongly recommend that cleaning and remediation be initiated to speed your resolution.

When people look at the physicians’ order sheet found on this website, very often the first question is “Are all these tests necessary?” If you are one of the “two-weekers” the testing is not all necessary.  If you are still symptomatic after two months then we go back and say “Why weren’t the tests done as instructed to begin this program?”  The reason here is that each one of these tests does contribute to analysis of where people are at a given time.

CIRS is an extraordinary complicated illness.  It is not one in which you can take a few doses of penicillin or doxycycline and magically walk around feeling fine.  This is a case of not only correcting dense inflammatory response systems that are interacting.

Cholestyramine, short duration of Rx not helpful

I have been taking cholestyramine now for two weeks and I feel no relief. What does this mean for me?

We have had a number of people over the years improve dramatically in two weeks or less. The real driving force however behind development of the 11 step treatment protocol is that many people will have additional problems documented with baseline laboratory studies and nasal culture that create barriers to “instantaneous” benefit. Simply stated, when people in the past didn’t get better with CSM alone, it was time to look for what I was missing.  Then when I found something, like the biofilm-forming staphs, for example, it was time to see what would happen if the staph were eradicated first.  Applying this trial and error method has resulted in the current protocols, though much of the protocol has been in place since 2004.

By far the most common reason for lack of benefit in short course cholestyramine usage is not enough time on treatment. This may be applicable to you.  Second, there may be some problems with how you are taking cholestyramine dose.  The powder should be dissolved in liquid and be dissolved on an empty stomach waiting 30 minutes to let the liquid clear the stomach and get into the duodenum before eating or taking any medications. Taking cholestyramine 4x a day is the recommended dose. 3x a day is not as good. 2x a day is a maintenance dose and 1x a day is a dose to help your irritable bowel syndrome and very little else. 

Taking cholestyramine alone will not overcome the adverse affects derived from spending time in water-damaged buildings.  I routinely rely on DNA measurements of fungi using settled house dust as the medium for analysis.  Both ERMI and HERTSMI-2 are available at a low cost from Mycometrics with excellent levels of detection (www.mycometrics.com).  You need to know that I have no conflicts of interest to reveal regarding Mycometrics.  If there is an elevated ERMI (>2) or an elevated HERTSMI-2 (>10) I strongly recommend that cleaning and remediation be initiated to speed your resolution.

When people look at the physicians’ order sheet found on this website, very often the first question is “Are all these tests necessary?” If you are one of the “two-weekers” the testing is not all necessary.  If you are still symptomatic after two months then we go back and say “Why weren’t the tests done as instructed to begin this program?”  The reason here is that each one of these tests does contribute to analysis of where people are at a given time.

The CIRS is an extraordinary complicated illness.  It is not one in which you can take a few doses of penicillin or doxycycline and magically walk around feeling fine.  This is a case of not only correcting dense inflammatory response systems that are interacting adversely but also correcting differential gene activation/suppression that is the basis of this illness. 

If you have not completed your database, this would be a good time to do that. Skipping steps just won’t cut it for the complex patients.  Monitoring each step along the way, including doing VCS, confirms that you are making progress with each sequential intervention as shown by objective testing that is admissible in courts of law across the country. 

IgA Nephropathy

Any information that you could offer (in layman’s terms) that might be helpful to this young man would be greatly appreciated.

One of the students in my current Mold Remediation Technician class is 39 years old and has recently been diagnosed with Berger’s Disease – a non-curable kidney problem.  The symptoms and diagnosis follow several years of work for a former employer who conducted mold remediation with the appropriate engineering controls to protect the occupants (they did most of their work in hospitals so they had to follow ICRA procedures), but with no suits or respiratory protection for their workers handling the moldy materials.  He just had a sense that those unprotected activities and his disease onset are somehow connected even though the doctors tell him it is “genetic”.  The one thing that he recalls from the discussion with his physician is that the doctor said he had an “IgA NEPHROPATHY"

I worked up one other person with IgA nephropathy last fall.  Here is the literature search I did to support the finding that it is TGF beta-1 that is the driving force in this unusual kidney disease. The elevated TGF beta-1 was driven by his mold exposure.  Fixing the TGF beta-1 stops the progression of renal failure but doesn’t reverse the injury sustained before Rx.  Hope this helps:

TGF Beta-1 IgA Nephropathy

11/12/12

1. Lepenies J, Eardley K, Kienitz T, Hewison M, Ihl T, Stewart P, Cockwell P, Quinkler M. Renal TLR4 mRNA expression correlates with inflammatory marker MCP-1 and profibrotic molecule TGF-b inpatients with chronic kidney disease. Nephron Clin Pract 2011; 2: c97-c104.
2. Brabcova I, Tesar V, Honsova E, Lodererova A, Novotna E, Maixnerova D, Merta M, Burgelova M, Hribova P, Skibova J, Zadrazil J, Maly J, Viklicky O. Association of advanced vasculopathy and transforming growth factor-beta 1 gene expression with immunoglobulin A nephropathy progression. Nephrol Diah Transplant 2011; 2: 573-9.
3. Brezzi B, Del Prete D, Lupo A, Magistroni R, Gomez-Lira M, Bernich P, Anglani F, Mezzabotta F, Turco A, Furci L, Ceol M, Antonucci F, Abaterusso C, Bonfante L, D’Angelo A, Albertazzi A, Gambaro G. Primary IgA nephropathy is more severe in TGF-beta1 high secretor patients. J Nephrol 2009; 6: 747-59.
4.  Li X, Feng J, Hu C, Chen Z. Does Arkadia contribute to TGF-B1-induced IgA expression through up-regulation of Smad signaling in IgA nephropathy? Int Urol Nephrol 2010; 3: 719-22
5.  Wang C, Liu X, Peng H, Tang Y, Chen Z, Lou T, Zhang H. Mesangial cells stimulated by immunoglobin A1 from IgA nephropathy upregulates transforming growth factor-beta1 synthesis in podocytes via renin-angiotensin system activation. Arch Med Res 2010; 4: 255-60
6. Ito Y, Goldschmeding R, Kasuga H, Claessen N, Nakayama M, Yuzawa Y, Sawai A, Matsuo S, Weening J, Aten J. Expression of connective tissue growth factor and of TGF-beta isoforms during glomerular injury recapitulate glomerulogenesis. Am J Physiol Renal Physiol 2010; 3: F545-58.
7. Wang F, Xie X, Fan J, Wang L, Guo D, Yang L, Ma X, Zhang L, Li Z. Expression of P311, a transforming growth factor beta latency-associated protein-binding protein, in human kidneys with IgA nephropathy. Int Urol Nephrol 2010; 3: 811-9.
8.  Wu W, Jiang X, Zhang Q, Mo Y, Sun L, Chen S. Expression and significance of TGF-beta1/Smad signaling pathway in children with IgA nephropathy. World J Pediatr 2009; 3: 211-5.
9. Vuong M, Lundberg S, Gunnarsson I, Wrammer L, Seddighzadeh M, Hahn-Zoric M, Fernstrom A, Hanson L, Do L, Jacobson S, Padyukov L. Genetic variation in the transforming growth factor-beta1 gene is associated with susceptibility to IgA nephropathy. Ann Acad Med Singapore 2000; 3: 364-9.
10.  Silva G, Costa R, Ravinal R, dos Reis M, Dantas M, Coimbra T. Mast cells, TGF-beta1 and alpha-SMA expression in IgA nephropathy. Dis Markers 2008; 3: 181-90.
11. Nonaka Takahashi S, Fujita T, Wade Y, Fuke Y, Satomura A, Matsumoto K. TGF-beta1 and CTGF mRNAs are correlated with urinary protein level in IgA nephropathy. J Nephrol 2008; 1: 53-63.
12.  Ihm C, Jeong K, Lee S, Lee T, Park J. Effects of therapeutic agents on the inflammatory and fibrogenic factors in IgA nephropathy. Effects of therapeutic agents on the inflammatory and fibrogenic factors in IgA nephropathy. Nephrology 2007; 3: S25-6.
13. Chihara Y, Ono H, Ishimitsu T, Ono Y, Ishikawa K, Rakugi H, Ogihara T, Matsuoka H. Roles of TGF-beta1 and apoptosis in the progression of glomerulosclerosis in human IgA nephropathy. Clin Nephrol 2006; 6: 385-92.
14. Yang C, Hsueh S, Wu M, Lai P, Huang J, Wu C, Hu S, Chen J, Huang C. Glomerular transforming growth factor-beta1 mRNA as a marker of glomerulosclerosis-application in renal biopsies. Nephron 1997; 3: 290-7.
15.  Syrjanen J, Hurme M, Lehtimaki T, Mustonen J, Pasternack A. Polymorphism of the cytokine genes and IgA nephropathy. Polymorphism of the cytokine genes and IgA nephropathy. Pub Med 2002; 1
16. Lim C, Yoon H, Kim Y, Ahn C, Han J, Kim S, Lee J, Lee H, Chae D. Clinicopathological correlation of intrarenal cytokines and chemokines in IgA nephropathy. PubMed 2003;
17. Woo, S, Bhattacharya S, Derby G, Taylor I, Myers B. A serum cytokine network in immunoglobulin A nephropathy 2012;
18. Walker N. Is IgA nephropathy the commonest primary glomerulopathy among young adults in the USA? Kidney Int 2006; 8: 1455-8.
19. Castegnaro M, Canadas D, Vrabcheva T. Balkan endemic nephropathy: role of ochratoxins A through biomarkers. Mol Nutr Food Res 2006; 6: 519-29.
20.  Tipping P, Holdsworth S. T cells in crescentic glomerulonephritis. J Am Soc Nephrol 2006; 5: 1253-63.
21.  Roos A, Rastaldi M, Calvaresi N. Glomerular activation of the lectin pathway of complement in IgA nephropathy is associated with more severe renal disease. J Am Soc Nephrol 2006; 6: 1724-34.

Swiffer testing

How will amount of dust on a Swiffer cloth affect the result?

The Swiffer cloth is used to swipe over the tops of ten surfaces in a given room or building when there is not a carpet present to use for a vacuum sample.  The goal is to collect 5 mg of dust.  The results are reported out as a ratio of spore equivalents per gram of dust.  As long as there is a diversity of surfaces sampled and the minimum amount of dust is present, the amount that you submit of the dust will not affect the results. 

Swiffer testing 2

How do I know if I have sent enough dust to the lab?

The lab will report out the sample as QNS or quantity not sufficient if not enough dust is found. 

Moisture meter testing

What levels of moisture are safe?

Moisture meters will cost in the range of $1200 to $1500.  In the detail for your question you mentioned a $25 dollar moisture meter. I am unfamiliar with the accuracy of this device. Understanding that what we are looking for is a difference in moisture readings between one section of a wall cavity, either top or bottom or side to side looking for increased moisture and a separate issue is not the actually reading that the device may give but it is the difference itself.  If the device is accurate we would like to see moisture levels no more than 14%.

 

Smell as evidence of water-damaged buildings

Can a house be contaminated with mold or bacteria without smelling musty?

Typically, the musty smell associated with water-damaged buildings (WDB) is most often due to presence of a compound called geosmin.  This molecule is a secondary product of metabolism which is made by filamentous bacteria (also called actinomyctes). Actinomycetes are organisms somewhere between mold and bacteria.  Some experts lump actinomyctes with bacteria and others with fungi.  Others think they are unique.  I am with the last group.

Absence of musty smells usually means either absence of geosmin or an inability to smell it.

Another possibility has to do with the ecology of the WDB. Secondary metabolites are made when the organism has lots of energy available to it, a condition rarely found in the outdoors environment. If actinomycetes aren’t flourishing, geosmin won’t be made.

The question of smells as an indicator of a water-damaged buildings is one that creates credibility issues for some skeptics.  Curiously, those patients with evidence of water intrusion only being musty smells are actually some of the worst-affected patients as presented in the peer-reviewed papers published. Instead of relying on smell, as there is a great variability in olfactory acuity between people, I would suggest doing ERMI/HERTSMI-2 testing. 

Pregnancy and CIRS

I am ill from my home and I am also pregnant. What impact will pregnancy have on my illness and what impact will my illness have on my pregnancy?

The medications we use to treat biotoxin illness and CIRS are listed as Category C (what that means is that the attending physician must decide if the risk to maternal and/or fetal health of no treatment is greater than the risk of treatment). I am aware of patients who have used cholestyramine and Welchol during pregnancy with consent of the attending obstetrician. This is a personal decision for you. Simply being pregnant doesn’t bring relief from CIRS.

We do not have adequate data on the impact of inflammatory response syndromes on fetal health but there is clear evidence that there can be developmental delays and learning disabilities present in children conceived in a moldy environment and carried to delivery in a moldy environment.

There is no list of laboratory values or markers like C4a and TGF beta-1 sorted by fetal age available in any laboratory.  No one has normal values of these compounds in amniotic fluid.

As opposed to rheumatoid arthritis where pregnancy usually brings welcome relief from symptoms, in biotoxin illness with CIRS, pregnancy has no apparent effect one way or another. Interestingly medications such as Procrit (which are worrisome to use without extensive and informed consent) have been used safely in pregnancy for years. 

It is clear that if there is any question about safety of a building that ERMI testing needs to be done promptly and buildings cleaned up during pregnancy.

VCS and Biotoxin Illness

Does passing the VCS mean that I could not have a biotoxin illness?

No. We typically see visual contrast sensitivity defects in affected patients in 92% of all our cases.  That means that 8% of cases do not have a positive VCS. This interesting finding is usually seen in younger patients, especially young woman, as well as people who have an “eye” for a given job.  For example, we often see a normal VCS despite illness in photographers, interior designers, artists as well as some professional athletes like baseball players and tennis players who need to “see” the ball well in their sport. If you are not ill, we expect a normal VCS.  False positives are quite unusual, understanding that the computer test is a screening device.

 

Indoor Mold versus Outdoor Mold

Are there studies that review the difference in illness acquisition from indoor mold and outdoor mold?

Yes, the work done on the SAIIE papers clearly shows that exposure to outdoor mold is not adequate to result in reacquisition of inflammatory response syndrome in people previously sickened by water-damaged buildings.  The prospective study design (called ABB`AB) is one that enables us to assign causation to exposure. To date, no outdoor exposures have shown worsening of inflammatory markers.

Particularly sensitive individuals, namely Erik Johnson and Jonathan Wright, have noticed abrupt deterioration of symptoms with certain outdoor exposures. Erik is well known for his discussion of “plumes” of air containing bioaerosols that have sickened him while he was hang gliding. I suggest that you review the chapters from Erik Johnson both in Surviving Mold as well as Mold Warriors. For others without the sensitivity of Erik and Jonathan to date outdoor exposures are not confirmed to sicken people.

Weight Loss

If a patient with CIRS is losing weight, is that due to enhanced release of toxins from fat cells?

For people with inflammatory illnesses resulting from exposure to water-damaged buildings, the underlying problem of their physiology is capillary hypoperfusion. Innate immune responses to toxins and inflammagens will become the inflammatory responses of CIRS but it is the capillary hypoperfusion that must be understood. What this means is reduced delivery of oxygen into capillary beds.  This reduced oxygen delivery can be measured directly using the Heidelberg Retinal Flowmeter or by measuring lactate using MR Spectroscopy.  In the presence of capillary hypoperfusion there is a problem with efficient use of glucose to generate energy for the cell.  This problem derives from the need for mitochondria, the powerhouse of the cell, to have oxygen available to create 36 molecules of the energy molecule ATP out of the 38 possible ATP that metabolism of each glucose can produce.  Without adequate oxygen, functionally glucose becomes nearly wasted with its reduction of ATP limited to a 5% (2/38) capability. 

In these patients with inefficient burning of glucose, stores of glucose in the complex carbohydrate called glycogen are quickly exhausted.  If a person is continuing to try to do something, like walk up a flight of stairs, in the absence of glycogen, the cell will reach for alternative energy sources, either fatty acids or amino acids derived from breaking down protein. Direct fatty acid burn is accomplished in the presence of high levels of adiponectin, primarily in muscle beds, or release (by low leptin) of fatty acids to be burned directly (this is called beta-oxidation) for fuel.  Unfortunately, (1) low adiponectin is often seen in biotoxin patients and (2) many people will develop leptin resistance as their MSH falls.  What this set of problems means is that functionally fat storage becomes protected. What that leaves as a fuel source then is lean body mass or protein.  This lean body mass is controlled genetically and if amino acids, especially alanine and glutamine, are quickly converted to glucose, the body does so at a loss of the basic building blocks of lean body mass.

Patients then with capillary hypoperfusion can maintain fat stores, just as they are losing protein and not look like they are losing weight, but they are.  Similarly, some patients with reduced fat stores before illness onset will look protein- and calorie-malnourished.

The problem of weight loss here is not due to release of additional toxins from fat cells, it is the ongoing inflammatory response.

Lyme disease, active

Will a low Lyme load result in increased symptoms? 

I am uncertain what you mean when you say “low Lyme load.” The vast majority of patients I see who have a history of Lyme disease do not have active replication of Lyme bacteria in their bloodstream as shown by normal levels of C3a.  This split product of complement activation rises with presence of a bacterial membrane in the blood.  In acute Lyme disease, C3a is invariably elevated; with chronic Lyme disease the presence of high C3a is more complicated.  Please review the discussion of management of Lyme disease in prior questions.  I know of no mechanism to determine number of Lyme organisms living in the body.  Indeed, there is an ongoing problem even considering presence of a culture that purports to show presence of any Lyme organisms. A fundamental flaw with any new culture is presence of false positives. Caution is advised in interpretation of culture results that are not replicated in triplicate.

If you are worried about chronic Lyme disease be sure to verify that you are not also exposed to water-damaged buildings and be sure to rule out asymptomatic carriage of a commensal organism in your nose, the notorious biofilm-forming, coagulase negative staph.

Vitamins, binding by CSM

What vitamins do CSM and welchol bind to?

CSM will bind fat soluble vitamins but Welchol does not have the same concern.

Duration of therapy

How long can patients stay on CSM?

Cholestyramine has been FDA-approved for approximately 50 years.  Patients have been on the drug for many years without additional complications stemming from use of the drug. People who are on the drug for more than 6 months, I do advise supplementing with a one a day vitamin. 

Outdoor exposure causing illness

As an observing patient, I have seen individuals sickened by outdoor exposures in multiple cities in the U.S. I recognize the difficulty in doing air sampling outdoors to confirm exposure. Have you seen people having a more difficult time recovering in one location compared to another?

This question arises multiple times, particularly in those who are extremely sensitive including Eric Johnson and Jonathan Wright.  These two have given me more information than anyone else about the importance of outdoor avoidance. They have clearly discussed their worsening with outdoor exposures with me multiple times in the past.  I have no reason to doubt their observations but in the absence of seeing inflammatory parameters in blood tests, the data-driven model that I insist on using can not be employed.

I do not disagree that anecdotal evidence is relevant but as such cannot be used to add into a protocol. Having said that, the illness is no different in labs in patients from Phoenix compared to Daytona Beach. As I have said to both Eric and Jonathan, let’s prove your observations with a prospective re-exposure trial. The next step is one of ethics though, if these are such sensitive people, why would anyone suggest re-exposure? I can remember deliberately exposing myself to blooms of blue green algae just to see what the exposure would do to my labs. Looking back on that choice, it was pretty stupid.

The difficulty is some patients are more affected by exposures to others.  Pertinent factors include, but are not, limited to HLA haplotype, history of re-exposures, presence of low VEGF, presence of markedly elevated C4a and TGF beta-1.  Our genomics data holds the key to sorting out additional changes seen metabolically with indoor and outdoor exposures both that would reflect abnormalities not presented in commercially available laboratory testing.

Lyme, toxin, inflammation

Is the inflammatory response typically seen in post-Lyme patients due to a toxin or might there be compounds that are antigens that set off innate immune responses?

The presence of a toxin, called Bb, was patented in 1999 by Sam Donta MD and Dr. James Kilpatrick (I may have this researcher’s name wrong, sorry).  I am not aware of any additional research has been published on this toxin including its size or exact structure.

There is a steady increase in research looking to find the factors that are involved with ongoing inflammatory responses in particular patients sickened with Lyme disease. 

More than the disease types for Lyme (neuro, joint, systemic), the crucial role of HLA DR molecules has been better studied in antibiotic-refractory Lyme then essentially in all other illness that I see represented on PubMed.  Specifically peptides presented by HLA DR molecules in linings of joints of patient with refractory Lyme have been shown to have a sequence of amino acids, 7 in number, that will not permit recognition of particular antigens (called epitopes).  Of these group of non-recognized antigens, endothelial growth cell factor (not VEGF) has been identified as driving T and B cell responses in patients with Lyme disease.  There is an association with increased amount of ECGF in joint fluid and ECGF activity with refractory illness.

It is my opinion that we have not identified reliably the suite of compounds that are associated with the defective antigen presentation of Post Lyme Syndrome.  Toxin production is not ruled out and the patent says we can’t ignore that possibility. I am not sure where the money for this kind of research would come from. Having said that, the consistent observation of elevated levels of C4a and TGF beta-1 in Post Lyme Syndrome after antibiotics but not elevated C3a stands in stark contrast to the elevated C3a seen in antibiotic untreated patients.

VCS Category

Can VCS abnormalities be induce by the antigen/inflammation without evoking neurotoxins?

This is an excellent question. We see inflammatory responses creating capillary hypoperfusion as a basic mechanism of VCS deficits.  We don’t see VCS deficits in patients with non-neurotoxin illness with any significant frequency.  Indeed a false positive VCS, not due to a biotoxin exposure, is extremely rare.

The problem with this analysis is that inside a building that has water damage will be a variety of toxins, including endotoxins, not to mention inflammagens.  How can we assess specific causation when there is no single causative agent in a mixture of what is inside a building in Nature.

At one time the National Toxicology Program proposed to do isolated studies in animals looking at the effect of a unique presence in an environment and not a mixture in an effort to short cut which member of the mixture did what.  This research went no where as NTP focused on looking at allergy and IgE and not inflammatory markers as a source of analysis.

Mold symptoms by mold type

If I am exposed to Stachybotrys will I be sicker than if I were exposed to Aspergillus?

There is no difference in any data ever presented looking at mixtures of water-damaged buildings that would separate symptoms from one particular kind of organism versus another. This idea, called specific causation, was used effectively for years by defense lawyers to defeat allegations of mold illness filed in court.  The particular legal opinion, called Geffcken, published in 2003, was effectively destroyed by the U.S. GAO report of 2008 and the World Health Organization of 2009, both of which said symptoms can not be ascribed to specific causation.

Heavy metals

Does CSM or Welchol bind to heavy metals?

No.

Mycotoxins and food

Are mycotoxins in food a concern?

There is a significant world literature looking at aflatoxins found in food creating illness in animals.  There are exposure limits set by the FDA (which are quite high) for presence of aflatoxins in food stuffs.  Animal feeds are routinely protected from fungal growth to prevent toxin contamination.

I have not yet seen a patient with a persistent illness due to consumption of food. In one remarkable small study I found non-allergic volunteers willing to eat 4 giant jars of Skippy crunchy peanut butter in a two hour period (during this time they watched Young Frankenstein and danced to Putting on the Ritz). There was no change in inflammatory parameters before and after said consumption and no changes in blood results in the next two days.  Fortunately, the patients did not suffer bowel perforation from this gross consumption of peanut butter. 

Absence of HLA susceptibility and illness

Is it possible to become ill and stay ill without one of the HLA haplotypes associated with susceptibility?

Yes, we see approximately 95% of cases having one of the six HLA haplotypes that in turn comprise 24% of the normal population.  That means 5% of ill people (cases) do not have HLA-driven susceptibility. The good statistical news is that for those 5% their prognosis is much better than those of the other 95% of cases.  Treatment is still necessary for the non-HLA susceptible individuals.  Even though they don’t have the HLA we are accustomed in seeing in cases, they will not self-heal. The standard response to the predictable response of “how does HLA alone determine susceptibility that I have used in the past is that biology is never 100% and HLA research is in its infancy.”  That statement is still correct.  In order to perform the research needed to show how defective antigen presentation is occurring, we would need a very large prospective study to be done on a multi-site basis.

Don’t forget, once MSH falls to below 35, additional susceptibilities to inflammatory illness develop.

Absence of HLA susceptibility and illness due to MARCoNs.

If a non-susceptible individual acquires an CIRS illness could that condition solely be due to colonization for MARCoNs with its own genomic affects.

This is an interesting question from a reader from Australia. Specifically we are still counting on fingers on one deformed hand the number of people with true MARCoNs without MSH deficiency. If MSH deficiency is the mechanism for MARCoNs colonization (please don’t say infection; it is not an infection) then we can restate your question. Is there a mechanism to get sick solely due to MSH deficiency? That answer is yes. What we don’t see are people ill just from MARCoNs and without low MSH.  What this means is that treatment with BEG spray alone will not take care of an inflammatory illness acquired following exposure to an interior environment of water-damaged buildings. Similarly, use of cholestyramine and subsequent protocols will not eradicate the MARCoNs. That treatment is specific for this biofilm-forming commensal.

Please note that researchers from Newcastle University in Australia were among the first to note the importance of MARCoNS first in facial pain first and then in Chronic Fatigue Syndrome. As I recall Dr. Timothy Roberts and Dr. Butts were early and prolific researchers in this field.  It has been nearly 10 years since I have spoken with that group and hope that they have adopted use of MSH profiling as part of their susceptibility rosters for acquisition of MARCoNS.  We hope to be publishing soon the genomic results of the MARCoNS biofilms study we completed not long ago.