Copyright 2014 by

Ritchie C. Shoemaker, MD

All rights reserved

Permission to reproduce in any form
must be secured from the author.

Please direct all correspondence and orders to

Ritchie C. Shoemaker MD

500 Market St Suite 103
Pocomoke, Md 21851

Printed in the United States of America

ISBN: 9781483533643

PREFACE

Sickened by moldy buildings? Need facts and answers fast? Here is your guide: State of the Art Answers for 500 Mold Questions. Thorough and reliable, “500 Answers” is as current as one can find on a subject where bad information abounds. But, as far as sick people go, what I write here will need to be updated when we finally have genomic information. The world of diagnosis and treatment of chronic inflammatory response syndromes (CIRS) acquired following exposure to the interior environment of water-damaged buildings (WDB) now relies on proteomics and differential diagnosis. Call it “mold illness,” if you will. You need to know the latest and best information about human health effects caused by wet, moldy buildings and the importance of understanding human health effects before remediation begins. The time to share what really is going on in sickened people has been with us for nearly 20 years, yet so much just plain wrong information is out there. Our knowledge has reached new levels as therapies like use of vasoactive intestinal polypeptide (VIP) show us where we need to go to reduce reactivity and stop the systemic inflammation of CIRS-WDB.

But, the final frontier of diagnosis and treatment comes from differential gene activation caused by the many entities found in the indoor air of WDB. We know that genomics is such a big deal; how long do we have to wait to add the vitally important gene information? We think the coming scientific revolution will likely happen before Thanksgiving, 2014. We won't just be talking about genetic susceptibility then, but also gene activation and gene suppression. We won’t be focusing just on commensal coag neg staphs but we will be discussing reversal of the known genomic effects these supposedly benign organisms have. We won’t be talking about using pro-biotics as “just a good idea” any more; we could be discussing the differential anti-inflammatory effects of such use of bacterial supplements to correct abnormal metabolomics from the gut. Thanksgiving is just five months away.

So why write this compendium now if use of genomics will lead us to an entire new plane of understanding? This answer is simple: at www.survivingmold.com (SM) we are still getting the same Top Ten questions routinely. The information gap between established readers of SM and new visitors tells me that we still have a lot of information and understanding to share with people interested in this increasingly common, and increasingly complex medical problem.

And when genomics arrives, the information gap could become a chasm overnight.

I read comments from “mold patients” and “mold docs” that tell me that a lot of really bad information about human health effects is still out there. Some ideas are just silly but others are dangerous, as affected patients might actually believe them, spending huge amounts of money and suffering untold medical and social loss as a result. Whether the bad ideas are from the Inspector General of the EPA, the (intentional?) absence of anything useful from the CDC, or from a mold profiteer taking wheelbarrows full of money in exchange for false hope doesn’t matter. False knowledge is dangerous.

Aldous Huxley told us that the key to understanding is casting out false knowledge. We apply his wisdom in this short book of 500 Answers to prepare for the arrival of new knowledge and new understanding from the human genome that is just around the corner.

Based on what we already know about the proteomics of CIRS, the days of ignorance about the pathophysiology of CIRS should be over, but just as we now celebrate useful therapies, we also know that our understanding has been shaped by less than one hundred blood tests. Compare that understanding to what we can mine from data sets of activity of 22,000 genes.

500 Answers includes new discoveries like the information we obtain from NeuroQuant that shows that the inflammation of CIRS causes the development of a distinctive fingerprint of injury to the central nervous system found just in CIRS-WDB patients. Better still, use of NeuroQuant shows us that the ability to correct the inflammatory response will in turn show correction of localized areas of grey matter atrophy in the brain. This result of treatment is unheard of in the world of brain injury. If you want to confirm that your executive cognitive functioning is due to exposure to WDB, do a NeuroQuant as part of the full work up.

If you simply want to know what to do to obtain a diagnosis that is accurate and begin therapies that work, 500 Answers is a must read. If you need solid information on how to go about testing your home, school and workplace to see if those buildings could be making you sick, 500 Answers is for you as well.

If you don’t have any experience with human health effects cause by wet buildings, and you are understandably overwhelmed by the fuzzy “science” on the Internet, 500 Answers is your portal to a sharp vision of what is wrong and what needs to be done.

500 Answers has a complete Table of Contents, a roster of the many acronyms used and an index that will help you find out quickly what you want to know. The information in 500 Answers is correct but when we add genomics, the jargon terms and new information is going to require a steep learning curve. We welcome you to learn what you need to know now. We will help you with the new understanding too when the time comes.

Ritchie C. Shoemaker, MD

Pocomoke, Maryland

TABLE OF CONTENTS

23andme

Absence of HLA susceptibility and illness

Absence of HLA susceptibility and illness due to MARCoNs

Access to care

ACTH, suppression by use of oral cortisone

Activated charcoal

Acute exposure

Acute illness after exposure

ADH

Air conditioners, window units

Air sampling

Alcohol use

Alternative therapies

Ammonia

Androgens, aromatase

Androgens, replacement

Anesthesia

Animals with mold illness

Anti-inflammatory pathways in workplace disputes

Anti-inflammatory pathways, muscles

Aromatase (see androgens)

Aspergillus in sinuses

Autism

Autoimmune response (see T regs)

Avoidance of re-exposure

Bartonella

BEG spray, gentamicin resistant

BEG spray, whole body effects

BEG spray, die-off

Beta glucans

Bibliographies

Bile/gallbladder problems

Bile problems (enterohepatic recirculation)

Biological supplements

Biowarfare

Black tongue

Borax as a cleaning solution

Building testing

C3a

C4a rise from chlorophyll

Candida

Cardiomyopathy

Case definition for mold illness

CD4 and CD25

CD57

CD57 natural killer cells

Celiac disease and HLA

Chiari

Chlorella and mercury

Chlorella, Dr. Klinghardt

Cholestyramine, with liquids

Cholestyramine, re-exposure

Cholestyramine, binding other compounds

Cholestyramine and antibiotics, simultaneous use

Cholestyramine and doxycycline, simultaneous use

Cholestyramine and food

Cholestyramine and mag citrate

Cholestyramine, cessation

Cholestyramine, costs

Cholestyramine dosing

Cholestyramine dosing in children

Cholestyramine intolerance; gastroparesis

Cholestyramine, light

Cholestyramine, long term

Cholestyramine, mixing

Cholestyramine, short duration of Rx not helpful

Cholestyramine, side effects

Cholestyramine treatment before data base

Cholestyramine treatment without a data base

Cholestyramine, use in re-exposure

Cholestyramine, use in (brown) recluse spider bites

Cholestyramine simultaneously with bio-identical hormones

Cholestyramine, used with fatty meals

Cholestyramine, used with non-sweetened almond milk

Chronic inflammatory response syndrome

Cleaning

Climate and CIRS

Coag neg. staph (see MARCoNS section)

Coagulation disorders in CIRS

Cold weather

Colestipol

Colonic irrigation

Communication with other physicians

Consensus statement

Corticosteroids

Crawl space and illness

Crawl space and flooding

Cross contamination

Daughter with 4-3-53 going to college

DDAVP

Demyelination

Denial

Depression

Diagnosis

Diagnosis Lyme, coinfections

Diagnosis, minimum number of laboratory studies

Diagnosis, mycotoxins

Diagnosis, prolonged symptoms after exposure

Diet

Dietary restrictions, carrots

Differential diagnosis

Dishidrosis

Degenerative joint disease

Duration of therapy (See cholestyramine section

Education, patient

ERMI

ERMI/ HERTSMI-2

Erythropoietin

Essential oils

Evaluation of buildings before rental or purchase

Exercise

Exposure, living on a boat

Extreme avoidance

FACT

Flu shots

Food intolerance

Foreign bodies, medical hardware and possible illness

Fungal lung infection

Fungal sinusitis

Gallbladder

Genomics, cure

Genomics, PAXgene tube

Hair loss, catagen versus telogen

Heavy metals #1 (see metals)

HEPA air filtration

HLA#1

HRV/ERV

Hydrocortisone replacement, ACTH suppression

Hypothalamic injury

Hypothyroidism

IgA Nephropathy

Illness, long term

Indoor house plants

Indoor mold versus outdoor mold

Infection from mold

Insurance issues

Intensification

Interstitial cystitis (IC)

IV phosphatidylcholine and IV glutathione

Joint pain

Kidney failure

Labs

Legal

Litigation costs

Lyme, C4a

Lyme disease

MARCoNS

Medication, antidepressants

Melanocyte stimulating hormone (alpha MSH)

Melanotan

Membership

Methylation

Migraines after rifampin and BEG spray combination

Mitochondrial disease

Moisture meter testing

Mold and cancer

Mold and VIP; duration of Rx

Mold in the attic

Mold in cars

Mold growth, winter

Mold illness, concerns

Mold illness, pediatric

Mold in automobiles

Mold in cars

Mold smell on skin

Mold symptoms by mold type

Mold, systemic

Mold testing

Mold versus Lyme

MSH, lab testing

MSH, hypo-pigmentation

MSH, for sale

MTHFR

Multiple chemical sensitivity (MCS)

Multisystem, multisymptom illness

Musical instruments as a source of CIRS

Muscle twitching

Mycology labs

Mycotoxins

Mycotoxins and food

N95 mask

Neuropsychiatric symptoms

NeuroQuant, reading the test results

New home construction

No-amylose diet

Non-porous possessions

Nose bleeds

Obtaining medical advice

Omega 3

Ongoing therapy with ongoing symptoms

Outdoor environmental exposures

Outdoor exposure causing illness

Outdoor illness

OWCP

Ozone

Panchakarma

PANS/PANDAS

Paralysis

Pediatrics

Personal air ionizers and diffusing thieves' oil

Pets and CIRS

Phase I detox compounds

Physician certification

Physician question, cholestyramine endpoint

Physician referral information

Physician request, case management. Case #002

Physician training

Porous materials

Post exertional malaise

Post-remediation testing

Pregnancy and CIRS

Purifier, air

Rashes

Re-exposure comments

Regaining health

Relapse after re-exposure

Remediation, fogging

Rheumatoid arthritis

Scorpion envenomation

Serotonin, melatonin, dopamine

Sicker-quicker

Silicone implants

Skin changes

Smell and evidence of mold

Smell as evidence of water-damaged buildings

Spore trap versus ERMI

Steroids (see corticosteroids also)

Sudden onset of severe symptoms

Supplements

Success rate of remediation

Swiffer testing

Swimming, indoors

Symptoms

Thyroid cancer

Thyroid therapy

Tick bite

Tinnitus

Toll receptors

Tongue, nodules

Toxic black mold

Toxins, storage in fat

Treatment approach

T regulatory cells

Unknown mold

Unusual lab abnormalities

Urinary testing for mycotoxins

Vasculitis

VCS, non-neurotoxins

VEGF, high

VIP, baseline labs

Viruses

Vitamins, binding by CSM

VOC

Weight loss

Welchol

Worms and mold

Zeolite

FOR THE FUTURE

APPENDIX 1 Glossary of acronyms

APPENDIX 2 HERTSMI-2 scoring sheet

Index

STATE OF THE ART ANSWERS TO 500 MOLD QUESTIONS

1. 23andme

I have 23andme genetic testing but can’t find a way to understand HLA SNPs vs. the specific tests recommended. Also, I have been told I have protomyxzoa rheumatica infection. Please help.

The future of medicine will include accurate genomic testing. I have little knowledge of the basis for the use of 23andme testing in clinical medicine. I am happy to review any data that you have that supports specificity and sensitivity of these tests underlying clinical illness.

It is my opinion that use of SNP testing is fraught with a significant possibility of error as mere presence of an SNP has nothing to do with gene activation/suppression. Presence of a SNP tells us nothing about regulation of the entire gene by microRNA.

I have never been able to confirm a diagnosis of protomyxzoa infection though I have seen a number of patients who have had testing done by Dr. Fry's lab in Arizona.

I am happy to review any data that you have to confirm this diagnosis with a particular eye to objective proteomic findings separate from findings on peripheral smear.

Please forward these findings to the website so that I may be of assistance to you.

2. 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.

3. 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.

4. Access to care

Is it possible to self-treat using your protocol?

The protocols that I use employ lab tests and diagnostic procedures that must be ordered by a licensed health care professional. I do not agree that it is safe for individual to take on this task without the ability to share what they want to do and what they should be doing with a trained expert. There are multiple physicians who have certified in this protocol listed on this website.

5. ACTH, suppression by use of oral cortisone

I know cortisone can suppress immune system as well as suppress the adrenal output but generally those rebound after cortisone is stopped. How does CIRS change this?

I am uncertain what you mean when you say cortisone can “suppress the immune system,” but please recall that both ACTH and MSH are members of a hormone system called melanocortins. There is interaction between ACTH and MSH in the production pathway involving proopiomelanocortin in the hypothalamus.

For those with MSH deficiency, persistent suppression of ACTH following exogenously administered cortisol (or any of the related adrenal steroid compounds) is common and can be an ominous finding. Steroids have an important role in medicine; if the use will bring about needed changes in physiologic parameters, then the risk of suppressed ACTH is not too great. But optional use of prednisone for dermatitis, a mild flare of lung disease or sinus problems, for example, is best avoided.

6. Activated charcoal

My doctor thinks I am too ill to take cholestyramine and wants me to use activated charcoal in the middle of the night instead. Will that be as effective as cholestyramine?

There are a number of questions that we have answered on this website regarding alternatives to cholestyramine. We have abundant objective data showing that Welchol performs the same duties as cholestyramine but to date no other nostrum has been shown to be effective by publication of objective parameters before and after individual use. I am aware that a number of people value use of activated charcoal, particularly since it is not a prescription item. If you are going to use activated charcoal, please be sure to collect a database on inflammatory mediators before you start the medication and after one month to see where you are. Also, please don’t use multiple simultaneous interventions if you are collecting data.

I am uncertain as to why you would take activated charcoal in the middle of the night if you have a chronic fatiguing illness where restorative restless sleep is compromised. As always, of course, your physician has a duty to answer your questions and if your physician feels that taking charcoal in the middle of the night is the right way to go, then by all means you should listen to your doctor.

7. Acute exposure

I went camping this past weekend at Camp Woodlands in Annapolis. Shortly after we turned in for the night, one of my friends developed a significant cough, headache and congestion. Another friend had a flare of her pre-existing asthma. We left after one hour. Should we seek medical care?

Exposure to any number of environments can cause the acute onset of respiratory symptoms without necessarily being an inflammatory response syndrome caused by exposure to the interior environment of a water-damaged building. Classic chronic inflammatory response syndrome is symptomatic for over a month; we cannot say that applies to an exposure of less than 3 hours associated with an illness of less than 3 days.

You mentioned that you are beginning to feel better now several days after your exposure. If you do not have a multisystem, multisymptom illness it would make sense to observe and not initiate treatment. Having said that, if the visual contrast sensitivity (VCS) test is positive at this date, the likelihood that this finding will resolve without treatment is quite low. Having a VCS test done now provides a reasonable basis to look back 2 weeks from now to see whether this is developing into an ongoing syndrome.

I do not object to you having baseline labs done, including C4a and TGF beta- 1, together with MMP-9, as the acute exposure is not likely to have enough time to lower MSH and VIP but did have enough time to drive up inflammatory responses.

8. Acute illness after exposure.

My Mom's house flooded when she was away and it sat soaking for weeks. I went in for six hours scrubbing mold from walls in the home. I now am ill with sinus problems, sore throat and lung congestion. I now am irritable and moody with red eyes and temperature intolerance. Is this serious?

Certainly you have met the requirement for the potential for exposure and you have multiple health systems represented with multiple health symptoms. I would suggest that you take a look at the visual contrast sensitivity (VCS) test to gain a better idea of what all symptoms you might actually have and then to correlate those symptoms with an objective screening test. At some time it would make sense for your physician to evaluate you with the labs that we look at routinely as represented on the physician order sheet in the diagnosis section of this website. You need to have the labs present to secure the diagnosis and initiate treatment. Do not ignore your illness. I think that you have made a good start by contacting us. I hope you will follow through.

9. ADH

After a dose of cholestyramine I find my urinary frequency doubles to approximately 10-12 times per day. What is happening to me?

We would need to look at your level of anti-diuretic hormone (ADH) and simultaneously measured osmolality to get an idea of what is happening to you. Cholestyramine is not absorbed and can not be doing anything directly to ADH; the link to frequent urination is usually inflammatory in origin. Unfortunately, there is no way to answer your question without looking at simultaneously measured laboratory studies before and after your cholestyramine dose. I would look at TGF beta-1, C4a, VEGF, ADH and osmolality before the dose and after the dose over a course of every two hours for a total of three more blood draws.

This is a cumbersome approach in trying to answer a simple question but it's the only way I know to have any data to rely on.

10. Air conditioners, window units

I found mold on the outside window sill and cover of my window air conditioner. Are window air conditioners safe for those with biotoxin illness?

Any air conditioning unit can create problems with condensation and possible microbial growth. Window air conditioners are designed to deliver condensation to the outside world with such delivery enhanced by having a slight angle of the air conditioner with a down hill side directed to the outside. If there is evidence of microbial growth on the inside of your home related to the extra moisture created by the dehumidifier effect of the air conditioner, I would suggest that you have that looked at with a tape lift sample. This procedure costs approximately $35 in a mycology lab. In my experience, the normal organisms found around condensation areas from air conditioners are Cladosporium and Alternaria. These organisms can create some problems with allergy but are not toxin formers.

11. Air sampling

Can you please discuss the spore trap method in detecting mold in a building? Is it reliable and how does it compare to ERMI?

Air sampling for spores was the industry standard for years. Attempts to determine if a building was moldy or not using air sampling, however, is so fundamentally illogical I cannot understand why people still consider these tests to be reliable. They are not.

In this approach to sampling a vacuum device is attached to a filter and then turned on for either five or ten minutes such that air above the sampling device (usually placed in the middle of the room) would be pulled through the filter. Particles smaller then the pore size of the filter would go right through but particles bigger then the pore size would be retained. The pore size was established at 3 microns which made it an effective device to measure large, intact spores. The problem is that for every intact spore, ranging in size from 3 to 8 microns, there will be 99 fragments of spores that sail right through the device, right back into the room to continue to make people sick by inhalation.

An additional problem with spore trapping is that the spores are identified by using light microscopy, often at a mere 200 power. Such microscope work will not distinguish any of the species of the Aspergillus genus; similarly the Penicillium species could not be sorted out. Even worse all Aspergillus itself could not be separated from all Penicillium. What we see in spore trap reports with be 'Asp/Pen,' a classification that wholly ignores the vastly more important role for A. versicolor and A. penicilloides, for example. If particular spores were particularly sticky, as those of Stachybotrys are supposed to be, air samples would often not show any spores of this important mold as spores would not be released from their “stuck on” habitat easily. Further, Wallemia has never been reported in any spore trap I have seen.

Using ERMI, a DNA analysis of dust collected not from the air but from areas where dust is settled in a given room, has the opportunity to identify up to 136 species with remarkable accuracy using QPCR. As opposed to guessing about Aspergillus and Penicillium and never even knowing about Wallemia, the QPCR tells us about these very important organisms specifically, inexpensively and rapidly.

Spore trapping has been exposed as inadequate in countless discussions including the World Health Organization report of 2009. WHO suggested that if spore trapping is to be used then multiple samples should be taken from multiple locations in each given room throughout a given day with multiple days per week and multiple weeks per month. The cost of such sampling is prohibitive.

Let's not forget that by using ERMI or HERTSMI-2 you can obtain health information from building information. Such correlation has never been done from air sampling and frankly never can be done reliably given the limitations discussed briefly above. If you are a landlord and want to hide evidence of a moldy building, use a single 5-minute spore trap taken from the middle of a room with the windows open. If you are concerned about health effects of WDB, use ERMI or even better, use HERTSMI-2.

12. Alcohol use

I think I become less tolerant of alcohol when I developed CIRS. Does this happen to other people to?

Changes in alcohol sensitivity is quite variable with the most intolerant being people with ciguatera. As a general rule, use of alcohol does not create an additional burden for affected patients understanding that excessive use of a known chemical toxin is not a great idea.

13. Alternative therapies

I am recently concerned about the possibility that my complex illness is related to mold exposure. We have air samples showing Penicillium and Aspergillus. We have problems with duct work and vents containing excessive moisture.

I have been recommended to use low dose antigens for treatment of mold illness. I am also taking reverse T3 for diagnosis of Wilson Syndrome. My son has an unusual depression and anxiety as well that is ruining his life. I have been told to obtain a SPECT scan. He has had a neurotransmitter test and is being treated with serotonin and norepinephrine.

Over the years I have had a chance to see multiple different approaches to treatment of complex illnesses such as yours and that of your family. I am uncertain as to what antigens are being suggested for you but if you have HLA-based susceptibility, the problem of defective antigen presentation will be a factor that you will need to take into account. We saw a variation of this somewhat ominous idea for treatment stemming from the Lyme vaccine given years ago in the thought that it would help prevent Lyme disease. In the Lyme case, an antigen, OspA, was given intramuscularly on three separate occasions purporting to force the body make antibodies to OspA which would protect against the invading Lyme bacteria. Unfortunately, those with HLA DRB1- 4 (and there were multiple haplotypes that included HLA DRB 1-4, see below) had difficulty processing this antigen. In essence, the Lyme vaccine became an exercise in asking the question, “If I give antigen to those who can’t process it, will I create a chronic inflammatory response syndrome in those with given HLA susceptibility?” The answer to this question, of course, was absolutely yes. Needless to say, the Lyme vaccine was a disaster, for those with HLA DR 4-3-53, 4-4-53, 4-7-53 and 4-8-53.

Therefore, please identify which antigens you are going to be given.

I am uncertain as the diagnosis of your thyroid dysfunction. Given that inflammatory responses will down regulate the intracellular enzyme 5'-deiodoinase that converts T4 to T3, I am reluctant to blame unusual thyroid problems on any syndrome in the absence of correction of inflammation. In my experience such correction of inflammation often heals the putative source of the thyroid disorder.

Instead of a SPECT scan, one that shows abnormalities in arteriolar function, and these abnormalities have no bearing on capillary hypoperfusion, I would suggest performance of a NeuroQuant which will give volumetric data in an FDA-cleared program.

Finally, I have not seen any data showing benefit from treatment with norepinephrine and serotonin for alleged neurotransmitter abnormalities. There are uses of norepinephrine in particular illnesses but I am concerned that here there may be anecdotal use of medications without clinical basis. I would be happy to review the literature that your physician can supply to support such treatment.

14. Ammonia

I have been told that ammonia denatures mycotoxins. Is this correct?

I know of no published data showing that ammonia (NH3) is effective to remove health risk from exposure to mycotoxins. I routinely recommend people use quaternary ammonium compounds (NH4+) to help with cleaning and removal of dust and particulates that have been in bioaerosols. The key here is not attempting to denature just any part of the mycotoxin molecule. As long as the exposed acetyl groups of mycotoxins are detectable by ficolins, part of the MASP-2 signaling system, the mycotoxins will continue to set off inflammatory responses.

15. Androgens, aromatase

I have been in a water-damaged basement for five years. Over the last year I have had multiple health symptoms appear without explanation including cognitive problems, vertigo, headaches and erectile dysfunction. Is erectile dysfunction a common symptom from exposure to a water-damaged building?

There are several elements in your question that I think need to be addressed. First is that if you still have exposure to the interior environment of a water-damaged building you are not going to have the same response to treatment as those who have accomplished the first goal which is removal from exposure. I strongly suggest that you obtain ERMI or HERTSMI-2 (please use Mycometrics understanding that I have no conflict of interest to report with that entity) to adequately define what organisms you are exposed to and just how bad your basement continues to be.

In the inflammatory response to antigens found in the chemical mixture existing inside water-damaged buildings there is direct adverse impact on levels of MSH. As MSH falls, as it does in over 95% of affected patients, there will be development of abnormalities in androgens in over 40% of patients. We look at levels of total testosterone (don’t spend the money for free testosterone), DHEA-S and androstenedione. We also measure levels of estradiol at the same time. The problem with erectile function in patients with low MSH stems from up-regulation of the enzyme called aromatase. Aromatase will convert testosterone into an estrogen, estrone, which in turn is converted to estradiol. The more active the aromatase is the worse the androgen problem is for males.

Should you seek medical attention for your erectile dysfunction and simply use testosterone replacement without affecting aromatase, you are doomed to failure. On the other hand if you correct the inflammatory process and normalize aromatase it is likely that your testosterone levels with stabilize.

A word of caution regarding aromatase inhibitors: These drugs, used in post-chemotherapy regimens in breast cancer, will cause a typical CIRS syndrome in people with low MSH.

16. Androgens, replacement

I read that it is not a good idea to replace testosterone, can you elaborate on that?

To assess correction of deficiency of androgens, we must look at MSH-deficient compared to MSH-normal patients. If MSH is deficient, very often there will be disruption of normal pituitary release of hormones called gonadotrophins (LH and FSH). For many people, low testosterone is recognized as an illness for which treatment is indicated. Simply using androgen creams or testosterone supplements delivered in a variety of ways can paradoxically make the deficiency of testosterone worse.

Why? The rebound suppression of gonadotrophin release happens in a manner similar to use of birth control pills. By giving the end organ hormone (testosterone) we actually suppress gonadotrophin release, as the pituitary “thinks” that there is enough androgen present and therefore reduces the release of the pituitary hormones that stimulate peripheral production.

An additional concern with low testosterone has to do with the function of the enzyme called aromatase. Aromatase will convert testosterone to estrone which in turn is converted into estradiol. Aromatase activity is often increased in inflammatory illnesses independent of MSH levels. If one has enhanced aromatase activity and takes testosterone, the testosterone is converted even more rapidly to estrone. What this means is that the patient may initially feel better with increasing testosterone levels only to find levels crashing shortly thereafter. In fact, increasing aromatase activity creates an additional burden of additional feminizing hormones being produced. What does a person do? “The testosterone helped at first but now it isn’t working, so I need to take more.” Aromatase really gets cranked up now! The vicious cycle continues.

It is important to understand that androgen deficiency is best treated by reducing inflammatory burdens first and then using upstream precursors of androgens that eventually will be funneled into testosterone production.

17. Anesthesia

Is it ok to get minor surgery with diprivin anesthesia while taking cholestyramine?

Cholestyramine is not absorbed and will not bind to anesthetic agents.

18. Animals with mold illness

Do dogs or other animals have mold illness?

There is no question that humans are not the only animals with inflammatory response syndromes. I have collaborated with veterinarians in the past looking at creatures as diverse as hawksbill and green turtles; race horses and riding mares; horses with Sarcocystis and Lyme; dogs, cats, pelicans; and many more. The difficulty a veterinarian faces is how to access the laboratory studies needed to confirm the diagnosis.

19. Anti-inflammatory pathways in workplace disputes

Asking my local doctor to run the blood tests.

I have been working in a trailer with leaky roof and visible mold for the past seven months. An outside agency has suggested the building be vacated but yet my employer continues to require me to attend work in this building. I have multiple health symptoms. What should I do?

I think the first order of business is to have you collect a sample of dust from your trailer to run an ERMI on it to confirm that this is a water-damaged building. Please note that the EPA and CDC would say mere presence of a leak or visible mold was enough and you didn’t need to have environmental sampling done. In contrast to that opinion, one that always loses in court, is the reality that if your employer has ignored reasonable informed opinion to vacate the building, you are going to need additional evidence to vacate on your own. All employers have a clear duty to provide a safe workplace.

I think it reasonable to sit down with your employer once you have unmistakable evidence of contamination and inform the employer of your adverse health effects. If your employer is unwilling to assist you, you have the option of taking the physician order sheet to your doctor together with the 2010 Expert Treating Physicians Consensus Report (available as a free download on this site) together with the paper from Health (also a free download) published March 2013 to a local doctor with your request that labs be done. If the physician refuses, then you should have as a fall back option to contact one of the physicians who have certified in my protocols. Their contact information is on the website.

20. Anti-inflammatory pathways, muscles

Do muscles act as an endocrine gland to decrease inflammation?

The important regulators of inflammation remain the neuropeptides, MSH and VIP. These hormones will have a variety of effects on metabolic pathways and muscle; but muscle itself is not an endocrine gland. ACTH and cortisol are important mediators of inflammation as well, though under regulation of MSH and VIP, among others, but muscle effects are due to other hormones, including ACTH and cortisol.

21. Aromatase (see androgens)

How do aromatase and low MSH fit into fertility issues?

If we have up regulated aromatase due to inflammatory responses in CIRS, and this is incredibly common, we will see enhanced conversion of testosterone to estrone and then to estradiol. Such disruption of normal androgens can have fertility effects both on men and women.

MSH has a significant role in regulation of LH and FSH, the gonadotrophins that regulate production of sex steroids. If there is evidence of abnormalities of FSH or LH, correction of MSH is a desired part of treatment.

22. Aspergillus in sinuses

I am diagnosed with having Aspergillus and Pseudomonas in my sinuses that are reportedly the triggers for my chronic bronchitis. I have read that UV light will be of benefit in eradicating these organisms. Do you know of a mechanism to deliver UV light to sinus conditions?

First, I hope that your culture was done of material obtained by sinus drainage and not from nasal aspiration. Obtaining material from sinuses is difficult; children often are given the inviting prospect of having sinus puncture done at the bed side. I cringe even talking about this. Endoscopy in adults can help to obtain pure sinus materials for staining, PCR and culture.

There are a variety of fungi found in sinuses that can create a chronic rhinosinusitis (CRS) as work from David Sherris and his colleagues (who were at Mayo but now are at the State University of New York at Buffalo) have shown. Unfortunately, control patients in the early Mayo studies also had fungi found in sinuses. They key was to identify interleukin 13 and IL-17 in sinuses related to colonization (not infection) from particular non toxin-forming species. Pseudomonads are gram negative bacteria that can be a very dangerous pathogen if in blood, soft tissue or lung. A study done years ago looking at nurses new to working in the ICU showed that they picked up nasal colonization of gram negative rods, including Pseudomonas, within one month of occupational exposure.

What this means is that you need to be very careful saying that you have sinus infection with Pseudomonas versus simple nasal colonization. Similarly, finding a fungus in a nasal swab does not equate to having a fungal sinusitis. Thirdly, having fungi found inside sinuses does not necessarily convert over to a source of an ongoing fungal infection requiring antibiotics, at least according to the Mayo and SUNY data.

23. Autism

Do I have statistics regarding the prevalence of visual contrast sensitivity deficits in children with attention deficit and autism? I am a developmental optometrist. Also, is there a role to assess visual evoked potentials in these children?

To date, I have only evaluated 12 children with confirmed autism, understanding the case definition of autism is still based in psychiatric terms and not on objective biometric parameters. As far as attention deficit disorder goes, I see many children diagnosed with this condition but when the inflammatory burden placed on the blood brain barrier in the central nervous system by innate immune activation is cleared, the ADD disappears. It is therefore hard for me to answer your question.

Simply stated, if attention deficit disorder is a catch-all diagnosis in which children are placed in part due to lack of consideration in underlying mechanisms, then how can we develop a meaningful pathophysiology? No physiology, no targeted cure. Dr. Norman Swartz sent me PAXgene tubes on two patients with autism. These assays will be run through the genomics program when funding is restored.

Regarding visual evoked potentials I would more interested in pursing use of NeuroQuant in children as this would require 10 minutes of magnetic resonance imaging time and has provided a fingerprint showing physiologic disturbances in adults with mold. Here we will see distinctive fingerprints of microscopic interstitial edema in some areas of the brain and caudate atrophy. Similarly, with Lyme disease we see reduction of forebrain parenchyma size together with reduced putamen. Also, in Lyme we see increased cerebellum and increased thalamus size as well. If these disorders are similar in adults and children then we expect to find central nervous system changes that can be readily treated and documented as the course of treatment proceeds.

24. Autoimmune response (see T regs)

I have autoantibodies to gliadin and cardiolipins. My HLA is 1-5 and 13-6-52C. Are there other foodstuffs to which I may have autoantibodies? I am preparing to test my blood for antibodies to food.

The mechanism for autoimmune illness remains less well defined then what we might like. Specifically, we know that there is a tremendous importance of both high TGF beta-1 and levels of T-regulatory cells that are too low that are important in the pathogenesis of autoimmunity. Normally, rising levels of TGF beta-1 will cause the migration of T-regulatory cells into tissue to suppress inflammation and suppress autoimmunity. In tissue, if the levels of the retinoic acid orphan receptor (ROR) are too low bad things will happen to our friends the T reg cells: they are converted to pathogenic T cells that make more TGF beta-1! The vicious cycle that is then created sets off the syndrome with elevated TGF beta-1 and low T regs. This tissue basis of uncontrolled inflammation is an additional burden for CIRS patients.

There are problems with abnormal control mechanisms in autoimmune illness, particularly in CIRS, where we commonly find autoantibodies. Children, more than adults, will have autoimmune problems. In 2009 our group showed that (i) low dose losartan safely lowered TGF beta-1 and that (ii) lowered TGF beta-1 was accompanied by resolution of autoimmune defects. This study was flawed in that we did not have a good T-regulatory cell assay at that time.

The mechanism of autoantibody production that we see most commonly involves antigliadin antibodies of the IgG class and anticardiolipins of the IgM class. There are other autoantibodies made to gliadin and cardiolipin.

Separate from the issue from autoimmune problems are the concerns regarding antibodies to foods. This is an area of some controversy. I have seen lab results to show terrible food allergies when there is no clinical evidence of food allergy at all. I urge extreme caution in diagnosing food allergy in the absence of a diagnostic re-exposure trial.

A special condition is Food Protein Induced Enterocolitis (FPIEC) which is now recognized as a CIRS. Together with (i) MSH deficiency-associated gliadin autoantibody positivity and (ii) true celiac disease, both of which also are CIRS, these three CIRS illnesses demand immediate attention in treatment as opposed to simple exclusion of foods. There illnesses are not an antibody illness; these are an autoantibody illness.

There are a group of people with food intolerance, for example, most commonly to gluten, in which there is no autoantibody or antibody found. Patients simply can’t eat the given food safely. The reasonable, prudent physician will suggest that such foods not be consumed. Along with that avoidance of consumption, after a period of stability, approximately 3 months, a diagnostic re-challenge can be undertaken to follow inflammatory parameters appearing in blood following a reintroduction of the food stuff (usually gluten, diary, soy, corn) into the diet. If illness symptoms develop and inflammatory markers develop then there is no question that those foods most be avoided.

25. 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 cross-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, 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 stereotypical 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.

26. Bartonella

With 27 different known species of Bartonella and with only the ability to test for 2, how can one be certain whether Bartonella is present or absent?

This is an excellent question. To my knowledge, there are 28 species of Bartonella that Dr. Breischwerdt has identified as causing disease in dogs. It is not clear that these veterinary organisms will also create a zoonosis.

Galaxy Laboratories has been working for at least 4 years to develop sophisticated testing for Bartonella as the available tests for Bartonella are confounded with false positives and false negatives.

Short of a tissue biopsy showing the organism with a methenamine silver stain, this diagnosis is usually made by guess in the US.

27. BEG spray, gentamicin resistant

A physician writes, “A patient with exposure to a water-damaged building and a low MSH has an MRCoNS that is resistant (as shown by the antibiograms) to gentamicin. May I still use BEG spray?

Yes, as the level of resistance (MIC) seen in the antibiogram is usually less than what levels of gentamicin are achieved with topical intranasal use. In cases like this one I will add Rifampin 600mg, taken once a day with food in the morning, to the high dose BEG spray (2 sprays, each side of the nose, 3 times a day). I obtain a culture routinely after one month. Caution is advised with Rifampin as red urine, nausea and possible drug interaction can occur. Moreover, use of oral antibiotics can create an additional resistance, i.e., Rifampin resistance. If this is the case, often a one month use of intranasal EDTA will alter the mucosal habitat adequately to permit removal of the unusual MRCoNS.

28. BEG spray, whole body effects

Does BEG spray eliminate all MARCoNS found in the body?