Looking at the Literature About Mycotoxin Urine Tests



June 1, 2016

By Lisa Petrison, Ph.D.

Recently in the Facebook group that I run, Mold Avoiders, I mentioned that I didn’t think sufficient science exists to justify the RealTime Laboratories mycotoxin urine test being used to evaluate a patient’s health status.

Since that time, one of the most frequent requests that I have gotten in the group and elsewhere is to provide details on my doubts about that test.

This article is designed to respond to those questions.

The science behind the use of the tests has been presented in several journal papers.

In this article, I will summarize the information in each of the papers and then provide some additional comments.


Hooper et al 2009

The first paper was published in 2009. The authors were Dennis G. Hooper and Vincent E. Bolton of RealTime Laboratories; David C. Straus of Texas Tech University; and Frederick T. Guilford (not noted as affiliated with an organization at the time of publication).

Hooper DG, Bolton VE, Guilford FT and Straus DC. Mycotoxin Detection in Human Samples from Patients Exposed to Environmental Molds. International Journal of Molecular Sciences. 2009, 10, 1465-1475. PMID: 19468319


The goal of the paper was to provide evidence for the usage in human subjects of mycotoxin testing (including urine testing) developed by RealTime Laboratories.

The paper cites just two previous papers looking at mycotoxins in urine (as well as a variety of other references). The first compared levels of ochratoxin A in morning and afternoon urine samples from populations in Spain and Portugal, without attempting to determine the source.

Manique, R.; Pena, A.; Lino, C.M.; Molto, J.C.; Manes, J. Ochratoxin A in the morning and afternoon potions of urine from Coimbra and Valencian populations. Toxicon 2008, 51, 1281-1287. PMID: 18420246


The second looked at a population in the United Kingdom and found that levels of deoxynivalenol (a trichothecene made by the outdoor mold Fusarium) were correlated with consumption of cereals.

Turner, P.C.; Rothwell, J.C.; White, K.L.M; Gong, Y.Y.; Cade, J.; Wild, C.P. Urinary deoxynivalenol is correlated with cereal intake in individuals from the United Kingdom. Environ.Health Perspect. 2008, 116, 21-25. PMID: 18197294


The authors of the paper then described how they had developed a test for three different categories of mycotoxins – ochratoxin, aflatoxin and macrocyclic trichothecenes.

The test was developed by purposely adding mycotoxins to samples (this is referred to by scientists as “spiking” them) and then determining what the lowest level that could be detected by the test was. This turned out to be 0.2 parts per billion (ppb) for the macrocyclic trichothecenes, 1.0 ppb for the aflatoxin and 2.0 ppb for ochratoxin.

The authors tested three different types of samples (urine, tissue and nasal secretions) to determine the best one with regard to sensitivity and specificity. That was concluded to be urine, which had a sensitivity of 94.5% for trichothecenes, 70.6% for aflatoxin and only 17.4% for ochratoxin. Specificity was reported as 100% for all three mycotoxins.

The authors then compared a group of patients who seemed to them to have mold illness with a control group. The patients were described as follows:

Urine and nasal secretions were obtained from hospital patients or out-patients with a history of exposure to mycotoxins or fungi….[This group] was comprised of samples from individuals with reported exposure to non-identified fungi or chemicals. Common symptoms of patients corresponding to group 2 samples included blurred vision, memory loss, fatigue, headache, nausea, loss of balance, cognitive deficits, rhinitis, sinusitis, rashes, and allergies. A detailed history and symptoms from many of the specimens were provided by many of the treating physicians (data not shown).


The 55 people in the control group were described as follows:

[The control group] was comprised of samples from individuals with no reported symptoms or known fungi or mycotoxin exposure.


Of the 178 patients tested for aflatoxin in the urine, 58 (33%) were deemed to be positive (with levels of 1.0 or more ppb). The rest (n = 120) were negative.

Of the 125 patients tested for ochratoxin in the urine, 29 (23%) were deemed to be positive (with levels of 2.0 or more ppb). The rest (n = 96) were negative.

Of the 660 patients tested for macrocyclic trichothecenes in the urine, 437 (66%) were deemed to be positive (with levels of 0.2 or more ppb). The rest (n = 223) were negative.

(Note that the reference range for trichothecenes in Table 4 appears to be mislabeled. The header on Column 3 states “Positive Specimens >= 2.0 ppb (ug/mL),” but based on the information in the rest of paper, it seems that this actually should be labeled “Positive Specimens >= 0.2 ppb.”)

According to the paper, none of the controls tested positive for having any of the mycotoxins in their urine. All tested under the reference values for aflatoxins (<1.0 ppb), ochratoxin (<2.0 ppb) and trichothecenes (<0.2 ppb).

None of the controls came up positive on the other samples (nasal secretions or tissue) being tested for mycotoxins either.

For patients sampled for nasal secretions, the researchers reported that 6/47 (13%) were positive for aflatoxin, 1/27 (4%) were positive for ochratoxin, and 24/63 (38%) were positive for macrocyclic trichothecene.

For patient giving tissue samples, the researchers reported that 10/28 (36%) were positive for aflatoxin, 1/20 (5%) were positive for ochratoxin, and 14/32 (44%) were positive for macrocyclic trichothecene.


Brewer et al 2013

The second paper was published in 2013. The authors were Joseph H. Brewer (a physician in private practice); Jack D. Thrasher (a toxicologist in private practice); David C. Straus (a professor at Texas Tech University); Roberta A. Madison (a professor at California State University); and Dennis Hooper (director of RealTime Laboratories).

Brewer JH, Thrasher JD, Straus DC, Madison RA, Hooper D. Detection of Mycotoxins in Patients with Chronic Fatigue Syndrome. Toxins, 2013, 5, 605-617. PMID: 23580077


The study looked at a sample of 112 patients from Dr. Brewer’s practice in Kansas City, MO. The paper described the patients as follows:

The study was conducted for 6 months from 1 February 2012 to 31 July 2012. Patients with chronic illnesses, many of whom were previously diagnosed with CFS, were seen in a private practice (JHB) which is a consultative outpatient infectious disease clinic in Kansas City, Missouri. Out of approximately 300 patients with chronic illness that were seen for routine follow up clinic visit, 112 met the criteria for a diagnosis of CFS as outlined by Fikuda [sic], et al. in 1994 [4].

These patients were from diverse geographic areas in the United States however, the majority resided in Midwestern states. The patient ages ranged from 15 to 72 years with 84 (75%) females and 38 (25%) males. The duration of symptoms ranged from 2 to 36 years with an average duration of 7.8 years. The illness was so severe that 76 (68%) of the patients were either unable to work, receiving disability or unable to attend school. A past history of mold allergy and/or chronic sinusitis was present in 50 (48%) of the patients. These patients failed to respond to treatments and their CFS symptoms lingered. 


Rather than running a new control group, the authors used the 55-person control group from the previous paper. The paper states:

Healthy control patients with no known toxic mold exposures in water-damaged buildings were previously reported. These controls (n = 55) consisted of 28 males and 27 females, ages 18 to 72 years. These patients were also from diverse geographic areas and resided in various areas of the United States. Urine specimens from these individuals were used to develop reference data for the control group used in this study. Furthermore, the same control subjects were also asked about complaints and/or symptoms related to mold exposure as documented in the peer reviewed literature at the time of this study [30]. Symptoms that were screened included rhinitis, cough, headache, respiratory symptoms, central nervous system symptoms, and fatigue. They did not give a history of water-intrusion or mold growth in the workplace or at home. It was assumed that the controls had exposure to foods and airborne mold spores that occur in their daily activity.


Of the 112 “CFS” patients in the study, 104 (93%) were reported by the researchers as having at least one mycotoxin in their urine. Many of the subjects had more than one mycotoxin. Here are the breakdowns. (Note: AT = Aflatoxin, OTA = Ochratoxin, MT = Macrocyclic Trichothecenes)


Mycotoxin           Positive (N, %)           Range (ppb)               Average (ppb)

AT                               13, 12%                       1.1–9.4                                    4.67

OTA                            87, 83%                       2–14.6                                     6.2

MT                              46, 44%                       0.21–5.72                                0.85

OTA + MT                  24, 23%

AT + MT                     4, 4%

AT, OTA, MT             8, 8%

None                           8, 7%


The results for the patients were compared to the results of the control group used in the previous study (none of which were found to have any detectable levels of mycotoxins in their urine) and statistically significant differences were found.

The concentration of mycotoxins in the urine of patients and controls were statistically analyzed to determine if a difference existed between the two groups. These data are summarized in Table 3. The concentrations were significantly elevated in the patients compared to controls as follows: AT (0.43 ± 1.36 vs. 0 ± 0 ppb, p = 0.0007), OTA (5.26 ± 3.65 vs. 0.355 ± 0.457 ppb, p < 0.0001), and MT (0.422 ± 0.714 vs. 0.0169 ± 0.0265 ppb, p < 0.001).


The paper states that when queried, 90% of the patients reported case histories that suggested exposures to water-damaged buildings:

Environmental histories of these patients were positive for exposure to WDB (many with visible mold) in over 90% of the cases tested, including residential and/or workplace. In the residential group, water damage to the basement was a common finding. However, other sources of water intrusion were noted during history taking, which included water pipe leaks, roof leaks, window leaks and plugged drains. In 24 patients, symptoms, which eventually became chronic, started within one year of the exposure in the WDB.


The paper also reported a few cases in which environmental testing (either for mycotoxins or spores) revealed suggestions of a toxic mold problem in the home. Detailed case studies for two of the patients were included.

Environmental tests (air spore counts, tape lifts and the examination of dust for mycotoxins) were performed in 10 of the situations of the 104 patients (data not shown). In addition, two families discussed below also conducted environmental testing. In the 10 cases mold genera associated with the potential for mycotoxin production were found. In 8 of the situations, Stachybotrys was identified in the WDB. In each of these 8 patients, MT was detected in the urine assay. In addition, Aspergillus/Penicillium-like spores were detected in 8 buildings to which these patients were exposed.

The urine mycotoxin assays identified OTA in 5 patients and AT was present in 2 subjects.

Additionally, dust specimens collected from 5 homes and one office building were sent to RealTime Laboratories for mycotoxin testing on environmental dust. MT was found in the dust samples from all 6 of these buildings. Small amounts of OTA were detected in 4 of the dust samples. There were 7 patients that had been exposed to mold in these buildings. Of these 7 patients, 6 had tested positive for MT in the urine assay, with the levels ranging from 0.21 ppb to 5.72 ppb. Additionally, 4 of the 7 patients had tested positive for OTA with values ranging from 3.7 ppb to 10.2 ppb.


Although Dr. Hooper listed his affiliation with RealTime Labs in the paper, he did not explicitly acknowledge his conflict of interest in terms of his profiting from the sale of mycotoxin urine tests. The Conflict of Interest section states only the following:

Dr. Brewer and Madison declare no conflict of interest. Drs. Straus, Hooper and Thrasher have served as expert witnesses in mold and mycotoxin exposure litigation.


Health Rising Blog

Shortly after the release of the 2013 study, ME/CFS blogger Cort Johnson published a Health Rising article discussing it. Although he seemed to find the study intriguing, he had several criticisms of it:

* He suggested that Brewer was an “infectious disease specialist apparently with a focus in  mold issues” and therefore expressed concern that the study might have had a selection bias.

* He pointed out that the authors’ definition of “water-damaged building” was very broad and wondered if a high percentage of the general population also might qualify as having lived in one.

* He wondered if mold issues might be higher in the Midwest (the home of many subjects in the study) than in other parts of the country.

* He concluded that it was impossible to tell from the study how frequently patients with “CFS” actually have mold as a factor in their illness but stated that the study did suggest that mold might be playing a role in at least some cases of the illness.

Science journalist Jill Neimark made some additional criticisms of the Hooper 2009 and Brewer 2013 studies in the comments section of the Health Rising blog. She expressed concerns with regard to: 1) credibility issues with the journal for the second study (including the fact that authors are charged $1000 to publish articles in it); 2) the low sensitivity reported with regard to some of the testing; 3) the lack of information provided about participants in the 2009 study (including the possibility that they might have been exposed to mold without knowing it); 4) the re-use of the 2009 control group in the 2013 study (rather than the researchers running their own controls); and 5) the possibility that the study might be interpreted to suggest that previous mold exposures were the original cause of the “CFS” patients’ illnesses (when instead they might have just been an exacerbation factor).

Immediately subsequent to the publication of the Health Rising blog article, I wrote to Dr. Brewer and asked him about his subject population. Following is his response, which he agreed at the time to make public:

Although I am an infectious disease specialist, I had no focus whatsoever on “mold issues.” Prior to February 2012 (when I first heard about the urine mycotoxin assay at RealTime Laboratories) I didn’t even have an interest in mycotoxins or environmental illness. These findings surprised me as much as anyone as the results began to unfold last year.

These patients were all randomly tested. These are long standing patients of mine that were previously diagnosed with CFS / ME (basically “average CFS patients”). We simply discussed the test and offered it to them at routine follow-up clinic visits. Very few suspected mold illness until I brought it up at their routine visits.

We only found that they “lived/worked in buildings with visible mold” after we asked. Some patients didn’t even remember the exposure until we prodded a bit (mainly because the exposure had been so far in the past – such as an apartment they lived in college).

I now see patients every week that are shocked when I bring up mold. They have very impressive exposure histories but no one asked.

If these CFS patients who are on the blogs get tested, I suspect ~ 90% will be positive. A doctor from the East coast has found almost identical results to mine in their cases (90% positive). Same for a physician on the West coast.

Anyone that sends a specimen to RealTime Lab must pay for the test “up front” but many of the patients ended up getting reimbursed (at least for most of the testing cost) from the insurance. They were not biased since most were hoping to get reimbursed.

I think is hard for people to get their “arms around this” and want to implicate selection bias but that simply was not the case.

I hope that helps.

Joe Brewer, MD


Dr. Brewer’s contention in this note is consistent with my previous knowledge about him: that he was an infectious disease doctor who had focused on treating Lyme and ME/CFS patients (in many cases seriously ill ones) with prescription drugs. In particular, he was known as being one of the few such doctors using Valcyte, a potent antiviral.

I had never heard that he had any interest in mold at all before his work on this study. So the idea that his subject population consisted of general “CFS” patients (Fukuda criteria) rather than a subset of individuals with a particular connection to mold seems accurate to me.

In addition, I have yet to see any evidence that homes in the Midwest are more likely to have mold problems than homes in other parts of the U.S. Remediators even do a brisk business in the Southwest, which (due to its dryness) logically seems that it would be the least problematic region of the country. Thus, while Cort Johnson’s hypothesis about this is interesting, I tend to doubt that the geographic location of the study participants was a major driver in the reported results.

I also feel that looking at how an academic journal covers its expenses (e.g. from subscriber fees vs. author fees) is no longer a very relevant attribute with regard to judging its quality. Authors generally have their academic institutions pay for their journal publications fees, and many authors prefer to be in open-access journals for articles that they believe will have a widespread public impact so that more people can read them. Therefore, the fact that this article was published in a journal that charges authors does not in itself make me doubt the quality of the article.

The rest of Cort Johnson’s and Jill Neimark’s criticisms of the study all seem valid to me.


Brewer et al 2014

The third paper was written by three of the authors from the previous paper: Joseph H. Brewer, Jack D. Thrasher and Dennis Hooper.

Brewer JH, Thrasher JD, Hooper D. Chronic Illness Associated with Mold and Mycotoxins: Is Naso-Sinus Fungal Biofilm the Culprit? Toxins, 2014, 6, 66-80. PMID: 24368325


In the paper, the authors reiterated the findings of the previous paper and then postulated that a fungal infection may have been responsible for at least part of the results.

The introduction to the paper stated:

Exposure histories often indicated the WDB/mold exposure occurred many years prior to the mycotoxin testing. Many of these patients have not had recent or current exposure to a WDB or moldy environment. Despite the remote history of exposure, these patients had chronic symptoms and the presence of significantly elevated concentrations of AT, OTA and MT in their urine specimens. The persistence of mycotoxins suggests that there may be an internal source of mold that represents a reservoir for ongoing mold toxins that are excreted in the urine. Otherwise, one would anticipate that the toxins would have cleared over time. Herein, we discuss the concept that the nose and sinuses may be major internal reservoirs where the mold is harbored in biofilm communities and generates “internal” mycotoxins.


The paper discussed the previous literature and reported hints that fungi living in the system may be able to produce mycotoxins. The authors suggested that while this seems unlikely to be happening with the macrocyclic trichothecenes (because Stachybotrys is thought to not have the potential of colonizing humans), it is possible that internal fungi in the sinuses or elsewhere in the system are creating mycotoxins and that these are responsible for the urine findings with regard to aflatoxin and ochratoxin.

As with the previous paper, although Dr. Hooper mentioned his affiliation with RealTime Laboratories, he did not explicitly disclose that he was benefiting financially from the sales of mycotoxin urine tests. The Conflict of Interest section stated only:

Joseph Brewer declares no conflict of interest. Dennis Hooper and Jack Thrasher have served as expert witnesses in mold and mycotoxin exposure litigation.


Brewer et al 2015

In 2015, Dr. Brewer and Dr. Hooper published a fourth paper looking at the use of urine tests and sinus antifungals in a population of “CFS” patients. A third co-author on the paper was Shalini Muralidhar, Ph.D., listed as the associate medical director at RealTime Labs.

Brewer JH, Hooper D, Muralidhar S. Intranasal Antifungal Therapy in Patients with Chronic Illness Associated with Mold and Mycotoxins: An  Observational Analysis. Global Journal of Medical Research, 2015, 15:2. 


Although this is stated as being a peer-reviewed journal article, it does not seem to be listed in the Pub Med database.

The study involved 165 patients in Dr. Brewer’s practice, all of whom had been diagnosed with “CFS” and who had came up positive on at least one of the three mycotoxins tested on the RealTime Labs urine test.

Of these patients, 151 were treated with a sinus spray consisting of the antifungal drug amphotericin B plus a chelator. The rest (14 patients) were treated with a sinus spray containing the antifungal drug itraconazole plus a chelator.

Of these patients, 20 chose to have the mycotoxin urine test repeated after several months on the therapy.

Of those who started out as being positive on the aflatoxin test, 5/5 had the levels decrease (100%).

Of those who started out as being positive on the ochratoxin test, 17/18 had the levels decrease (94%).

Of those who started out as being positive on the macrocyclic trichothecene test, 14/19 had the levels decrease (74%).

In addition, patients were asked to make a subjective estimation of whether they improved subsequent to using the therapy. Of patients who had remained on the drug after the initial trial period, 96 out of 104 (92%) stated that they had improved at least “moderately” (defined as a 25% reduction in symptoms).

Further, 26 of the 88 patients (30%) who remained on Amphotericin B rather than discontinuing it due to adverse events rated their improvement as “marked” (improvement of 75% or more from baseline).

Note that these results were only for patients who were able to tolerate the drug for 12 months and that dropout rates in the study were high.

A total of 69 patients (37%) dropped out of the study due to adverse events. If we look at those who reported improvements (96 people) compared to the 165 people who started the study, the success rate for the treatment in terms of producing at least moderate improvements is only 58%.

The paper also describes the outcomes of seven patients who used the therapy for six months or more and then discontinued it (in most cases because they didn’t feel they needed it any more). Of these individuals, six out of seven (86%) relapsed in terms of their symptoms.

In terms of mycotoxin levels, 4/5 (80%) who initially had high ochratoxin levels reported levels of this mycotoxin go up after discontinuation compared to what was reported when they were in treatment.

Of those who initially had high trichothecene levels, 5/5 (100%) had reported levels of this mycotoxin go up after discontinuation compared to what they were when in treatment.

Although Drs. Hooper and Muralidhar listed their affiliation with RealTime Laboratories in the article, there was no conflict of interest section and the fact that they are benefiting from sales of the test was not explicitly disclosed.

Following are some comments about this study.

First, it is important to remember that the RealTime Labs ochratoxin test is reported to have a sensitivity of only 17.4%.  That means that more than 80% of the time when the mycotoxin is present, the test does not pick it up.

That being the case, it is no surprise that the majority of people who tested positive for ochratoxin on one occasion would not test positive for it on a subsequent occasion. Considering how infrequently the test is acknowledged to identify this mycotoxin when it is actually present, it would have been much more of a surprise if the levels had not gone down regardless of treatment.

Second is a standard statistical phenomenon known as regression toward the mean. That means that if a subset of a group that is extreme on a variable is selected out, their scores on that variable on a subsequent test should be expected to be lower than they were on the first test, even if nothing whatsoever has changed.

That being the case, it is no surprise that the majority of those testing as having elevated trichothecene levels on the first test would come up as having lower levels on the subsequent test. That may have had nothing to do with actual improvements as a result of the treatment, and instead merely have been a statistical artifact.

The way to avoid this problem would have been to look at the trichothecene levels for all the patients both before and after the treatment and then to compare them. This data is not reported in the paper, however.

Both the ochratoxin and the aflatoxin measurements also are subject to this regression toward the mean phenomenon. In addition, the aflatoxin sample is so small (only 5 cases) that it is hard to make any judgments at all about it since results may be due purely to statistical error.

Thus, this paper does not do very much to make me more confident about the usefulness of mycotoxin urine tests.

Unlike some researchers, I believe that patients’ reports of subjective improvements have a role to play in allowing us to consider whether treatments are working. While it is true that the methodological design of this study does not eliminate placebo effects or the possibility that patients might have reported more improvements than they actually experienced in order to please the physician, I still find the results to be interesting.

What is of more concern to me is the large number of patients who were unable to tolerate the treatment, as well as the fact that most of those patients who were able to tolerate it (which I would guess were in large part patients who were not all that sick to begin with) experienced fairly modest improvements from it. These results seem to be comparable to those typically reported for a very wide variety of treatments for “CFS,” which of course is an extremely difficult disease to treat effectively (at least, from what I have seen, with anything other than scrupulous mold avoidance).

In addition, the relapse rate of those patients who discontinued the treatment after feeling well from it is a concern. While it may be that taking antifungals indefinitely is preferable to being really sick, the accepted tendency for fungal resistance to occur makes this a less-than-ideal treatment strategy.

One thing that I would like to point out here is that based on my conversations with his patients, I do not feel that Dr. Brewer has been focused very much on avoidance of environmental mold. His assumption (stated in all of his papers) seems to be that in many cases patients were made sick by long-ago exposures rather than current ones. In some cases, his patients have embarked on antifungals without doing an ERMI test, even though it is impossible to know whether an environment has a major toxic mold problem just through appearance or smell.

In addition, although Dr. Brewer has acknowledged that contaminated belongings may be a concern for people moving from a bad building, he has not to my knowledge encouraged patients who may have previously lived in problematic buildings to focus any of their attention on determining whether cross-contamination of their possessions as a result of previous exposures may be having an inordinate effect on them.

I thus wonder if focusing more attention on the issue of avoidance of mold toxins (for instance, as outlined in the book A Beginner’s Guide to Mold Avoidancemight be helpful in allowing a higher percentage of patients to tolerate the protocol as well as to be less likely to relapse when tapering off of it.


MMWR Article

Prior to the publication of the 2013 article, RealTime Laboratories had performed the urine mycotoxin tests for relatively few ordering physicians.

After the article was published, the use of the urine test for patients wanting to know if they had an issue with toxic mold became much more common. The cost of the test panel is about $700.

In February 2015, two MD’s serving as field workers for the Center for Disease Control (CDC) published an article focusing on mycotoxin urine tests  in the agency’s high-profile publication Morbidity & Mortality Weekly Report, read by large numbers of doctors and other healthcare professionals.

Melody Kawamoto and Elena Page. Notes from the Field: Use of Unvalidated Urine Mycotoxin Tests for the Clinical Diagnosis of Illness – United States, 2014. MMWR. February 20, 2015. 64(06): 157-58.


The article describes a situation in which a woman submitted urine tests to the laboratory based on “symptoms involving multiple organ systems” and was informed that she had tested positive for two mycotoxins (trichothecene and ochratoxin).

The laboratory referred the woman to a clinic specializing in mold illness, which diagnosed her with mold toxicity and prescribed a variety of “non-standard” treatments. She then went to her workplace and asserted that it had a toxic mold problem. The employer spent $25,000 on destructive testing but no evidence of water damage or significant fungal growth was found. The employee remained convinced that she had had an damaging mold exposure in the workplace, and some of her co-workers also became concerned about their own health.

Neither the mold testing laboratory nor the mold illness treatment center was mentioned by name in the article.

The authors of the article criticized the urine tests primarily for the fact that they had not been validated, suggesting that this made it difficult to know whether they were measuring a legitimate health effect:

The laboratory mentioned its Clinical Laboratory Improvement Amendments (CLIA) certification on its reports and noted that the urine mycotoxin testing was not approved by the Food and Drug Administration (FDA). CLIA regulations require any laboratory that performs testing on patient specimens to have an appropriate CLIA certificate and to meet applicable quality and analytic standards to ensure accurate and reliable test results.* CLIA regulations, however, do not address the clinical validity of testing (i.e., the accuracy with which the test identifies, measures, or predicts a patient’s clinical status). FDA clearance or approval of a test provides assurance that the test has adequate analytical and clinical validation and that it is safe and effective.§ There is no FDA-approved test for mycotoxins in human urine.

During the past 10 years, CDC’s National Institute for Occupational Safety and Health has received many requests for workplace evaluations based on the results of unvalidated laboratory tests purported to diagnose occupational and environmental illnesses caused by exposure to fungi (including molds). Using unvalidated laboratory tests to diagnose work-related illness can lead to misinformation and fear in the workplace; incorrect diagnoses; unnecessary, inappropriate, and potentially harmful medical interventions; and unnecessary or inappropriate environmental and occupational evaluations.

Mycotoxins are metabolites of some fungi that can cause illness in humans and animals, primarily after ingestion of contaminated foods. Low levels of mycotoxins are found in many foods; therefore, mycotoxins are found in the urine of healthy persons. Mycotoxin levels that predict disease have not been established. Urine mycotoxin tests are not approved by FDA for accuracy or for clinical use.


The MMWR article concludes by referring the reader to the CDC’s own information about mold, which suggests all mold in buildings should be treated the same and that no testing of the building and no biological testing is recommended.

Although I originally believed that the laboratory in question in this case was RealTime Labs, upon further examination it seems that it was more likely a laboratory called Biotrek, which offers a panel of tests for the same mycotoxins that RealTime Labs tests for.

Biotrek appears to be owned by the same company as the National Treatment Centers for Environmental Disease, which is based in Atlanta (near the CDC headquarters). Based on reports that I have gotten from members of the Mold Avoiders group, that organization appears to be extremely controversial in the online mold illness community.

This organization recently was the subject of an investigative report by the local Fox TV station in Atlanta.

I have been told by patients of the National Treatment Centers that a protocol mentioned in the MMWR paper – eating only canned chicken and white rice for a period of time – is a standard recommendation there. That being the case, it seems reasonable to think that this lab is recommending that patients who get the test from them then seek out treatment from the center also owned by their company.

In addition, in their comments below, RealTime Laboratories strongly denies that this CDC report is focused on them.

However, most of the CDC’s criticisms are about the concept of mycotoxin urine testing in general, rather than about the practices of this particular organization. Thus, their criticisms would seem to apply to mycotoxin urine testing done by other organizations, such as RealTime Labs.


Unvalidated Tests

Generally speaking, I am no fan of the CDC. It is my belief that the organization has done everything that it possibly could for the past thirty years to cover up both the phenomenon of toxic mold illness as well as the illness that it named and still dismissively refers to  as “chronic fatigue syndrome.”

The information on the CDC’s website about dealing with mold is particularly inappropriate and has the potential of causing severe injury or death to individuals due to the fact that it does not encourage enough caution when remediating mold, I believe.

The idea that the CDC wrote the MMWR article with the express goal of continuing to suppress the phenomenon of toxic mold illness and its connection to “CFS” is not lacking in plausibility, in my opinion. It certainly would be consistent with the agency’s history.

On the other hand, as someone who has spent the past decade immersed in the “CFS” community, it has become abundantly clear to me that insofar as people are selling tests (especially very expensive tests) without providing any verification that the tests are doing what they say they are doing, skepticism is wholly appropriate.

For instance, several years ago, “CFS” was reported in a study published in a highly respected journal, Science, to be associated with the retrovirus XMRV.

Immediately after the paper was published, the individuals heading the organization sponsoring the study (the Whittemore Peterson Institute) started offering to the public testing for the virus, at costs of up to $650. These were sold for almost two years.

Eventually the researchers agreed to participate in a study designed to protect the blood supply, in which they were given blinded sample to analyze. It turned out that not only was there no association between “CFS” and the virus, but that the laboratory’s assays were not even able to consistently identify the virus when it was actually there (in purposely spiked “positive control” samples).

It also was later revealed that some of the samples in the original paper had been treated with a “demethylating” substance, generating the suspicion that this was responsible for the results posted in the original paper.

The important scientific events with regard to the remarkable story of XMRV and “CFS” are summarized on a page of the Paradigm Change website.

A number of years before XMRV became a topic of discussion in the “CFS” community, many patients sent off samples to be tested for an “antigenic epitope resembling ciguatoxin” developed by Professor Yoshitsugi Hokama of the University of Hawaii. Virtually all “CFS” patients were reported by the researcher to be positive for this substance.

Recently I was told that this test – like the XMRV test – had been persuasively demonstrated not to be reliable. (Unfortunately I have been unable to find any details online, but it does seem that the test is no longer available.)

Especially in light of the incidents with the XMRV and ciguatoxin tests, I am extremely hesitant to believe that any proprietary test is actually doing what it is supposed to be doing, even if the laboratory has published its data in a peer-reviewed journal, unless it’s been validated in a blinded case/control test by a researcher not associated with the laboratory.

There’s too much financial upside in selling a test to the public and (at present) too little downside with regard to selling a bad test for any laboratory to be trusted not to be careless or fraudulent in order to justify the use of a test.

Even when people have solid backgrounds and seem wholly honest, it is impossible to know that those who stand to profit from laboratory test sales have not cut corners or shaded the truth or even blatantly made up data submitted to journals if tests have never been validated in any way.

In the case of the urine mycotoxin tests, there never has been any kind of public blinded experiment where control samples and patient samples were sent to the laboratory for analysis. Thus, the only way that we can assume that the test is doing anything at all is to put our faith in Dr. Hooper, who is the laboratory director and who is presumably profiting financially from sales of the test.

As a general principle, that concerns me.


Author Backgrounds

When evaluating the validity of scientific research and laboratory methods, I personally look almost exclusively to the literature.

That seems to me a much more direct and useful method than trying to guess whether the individuals associated with the project likely are competent and honest enough to be doing things right.

However, since some people do consider scientists’ backgrounds as an important method of estimating their credibility and trustworthiness, I will briefly discuss the backgrounds of the authors of the three relevant papers here.

David Straus is a professor of immunology and molecular microbiology at Texas Tech University Health Sciences Center (retired in 2013). He has been on the faculty there since 1981 and has written many papers on the effects of Stachybotrys and other toxic molds. He also was the dissertation adviser for the author of one of my favorite papers on mold toxins, Enusha Karunasena. I have a good deal of respect for his work.

Jack Thrasher is an immunotoxicologist (now semi-retired) with a Ph.D. from UCLA. He has written many papers on the effects of both toxic mold and chemicals on humans in water-damaged buildings and has served as a consultant and expert witness on the topic. He is on the board of directors for the Global Indoor Health Network (GIHN). He states that he did some consulting work for RealTime Laboratories in 2005/2006 but has not been financially associated with them since then.

Joseph Brewer is an infectious disease doctor in private practice in Kansas City, MO. He sees many patients with Lyme and ME/CFS, and I have received generally favorable reports about him from his patients. He is on the clinical advisory board of the Whittemore Peterson Institute. He also is on the Infectious Disease/Scientific Committee of RealTime Laboratories.

Roberta Madison (now deceased) held a doctorate of public health and was a professor of statistics and epidemiology at California State University of Northridge.

Frederick Guilford is an otolaryngologist working for Your Energy System (manufacturer of the glutathione product ReadiSorb and other nutritional supplements) in Palo Alto, CA.

Vincent Bolton previously was listed as employed by RealTime Laboratories and has co-written several journal articles. He appears to be currently practicing medicine as an anesthesiologist in Maine.

Shalini Muralidhar earned a Ph.D. in molecular and cell biology from the University of Texas at Dallas. She has been the associate medical director at RealTime Laboratories since January 2015.

By far the most controversial is Dennis Hooper, who is the director of RealTime Laboratories and listed as a co-author on all four papers.

Dr. Hooper earned an MD from the University of Nevada at Reno and later worked as a pathologist for the US Naval Hospital in San Diego. He left that position in 2001; worked for a time as a pathologist for a Texas hospital; and then started RealTime Laboratories in 2004.

In 2004-2005, the Los Angeles Times wrote a series of articles about Hooper’s previous work as a pathologist, suggesting that errors he had made were responsible for a number of patient deaths. The article also stated that Hooper had filed bankruptcy and been sued by investors in connection with previous private laboratory ventures that he owned.

The newspaper reported that immediately after the publication of the initial article in the series in 2004, Hooper resigned from his job at a San Antonio, TX, hospital. He then admitted to some errors during an administrative hearing before the Medical Board of California and eventually was placed on five years’ probation in that state, the paper reported.

Please note that I do not have the knowledge to make any judgment at all on the extent to which the information in these articles is accurate and unbiased. Here are the links.

One Doctor’s Long Trail of Dangerous Mistakes – December 7, 2004

Hospital Places Former King/Drew on Leave – December 8, 2004

Ex-King/Drew Doctor Resigns Post in Texas – December 15, 2004

Ex-King/Drew Doctor Admits Diagnoses – August 26, 2005

Ex-King/Drew Doctor Gets Probation – December 20, 2005


Control Group

My own main concern about the RealTime Laboratories mycotoxin urine test (other than the unvalidated nature of the tests and the conflict of interest) is with the control group that was used in the research studies.

My first concern is related to the fact that a number of articles in the literature have suggested that mycotoxins consumed in food are related to the amount of mycotoxins that are excreted in the urine.

As stated earlier, the original paper (Hooper et al 2009) referred to one such paper in its own references.

Urine mycotoxin tests also have been used in a widely cited series of papers looking at the connection between aflatoxin exposures in foods and the development of AIDS in patients in Africa. The research is headed by Professor Pauline Jolly of the University of Alabama at Birmingham and demonstrated that individuals eating a larger amount of foods known to be contaminated with mycotoxins (such as corn) had higher levels of aflatoxin in their urine than individuals whose diets consisted primarily of foods lower in aflatoxin.

In addition, the CDC’s Kawamoto and Page noted in the MMWR paper that previous research has found that random samples of individuals may have mycotoxins in their urine.

Ahn J, Kim D, Kim H, Jahng KY. Quantitative determination of mycotoxins in urine by LC-MS/MS. Food Addit Contam Part A Chem Anal Control Expo Risk Assess 2010;27:1674–82.

Duarte SC, Pena A, Lino CM. Human ochratoxin a biomarkers—from exposure to effect. Crit Rev Toxicol 2011;41:187–212 PMID: 21401326


A first question therefore is why none of the control subjects in the original study were found to have any mycotoxins at all in their urine (as well as none in their tissue or nasal secretion samples) in the light of other findings.

The U.S. food supply is highly contaminated with mycotoxins. Aflatoxin is regulated (meaning that food is not as contaminated as it can be in Africa), but the allowable levels are much higher than they are in Europe.

Ochratoxin also is heavily present in the U.S. food supply and is not regulated at all in the U.S. (Dave Asprey’s business selling low-mycotoxin coffee and cocoa is largely based on providing an alternative to ochratoxin-contaminated products, for instance.)

The U.S. food supply also is contaminated with large amounts of trichothecenes, but to my understanding most of these are non-macrocyclic trichothecenes made by Fusarium mold and so in theory should not be coming up on the RealTime Laboratories urine tests. (Although macrocyclic trichothecenes made by Stachybotrys can be present in hay, and although these toxins may be passed on to humans through the consumption of meat or dairy products, I tend to agree that that this particular exposure route is likely comparatively minor.)

Dr. Straus argues in his response to this article (below) that people can breathe in large amounts of mycotoxins from living on a long-term basis in a moldy buildings, and likely he is right about that. Still, the amount of mycotoxins consumed from food sources by most people is substantial enough that it seems expected that it should be coming up in the tests of random control subjects, as it has in previous published papers.

In addition, as Jill Neimark pointed out, a high percentage of U.S. buildings have toxic mold problems and a high percentage of people living or working in those buildings have no idea that they are being exposed. Thus, even if the control subjects denied having had exposure to any water-damaged buildings, it seems likely that at least some of those individuals were unknowingly getting substantial environmental mold exposure.

Mycotoxins in the urine demonstrate the successful removal of the toxins from the body. Therefore, even if individuals are not susceptible to being made sick by these toxins, it nonetheless seems that if they are taking the mycotoxins into their systems via exposures (either by ingestion or inhalation), then they should be leaving the body through the urine.

In a response to a question by physician Jacob Teitelbaum, Joseph Brewer stated that to his understanding, the control patients had not been heavily screened to eliminate all possible mold exposures and were more like a random sample of the population.


When you talk about having had some mold exposure, almost everybody has had some if you ask them. ‘Oh, yes, I lived in this mildewed place in college.’ So I’m wondering if the lab – how many people did they have to screen to get those 55 pure, no-mold-exposure people? I’m wondering if that was a pretty representative sample.


Dr. Hooper could answer that best. Dr. Hooper at RealTime Laboratories could answer that better than I. But in talking with him about that group, and I’ve talked to him in some detail about that group, and they have shared the actual raw data with me since we put it in our paper. And he was an author on that paper.

I don’t think they had to cherry pick. In other words, I think that they would accept someone who said, well, you know, it might have been a little musty in my basement in the past. I don’t think that would have been excluded. This wasn’t, you couldn’t have had any exposure whatsoever. It was just, you know, a screening history of mold exposure.


It therefore seems very peculiar to me that 0% of subjects in the control group would have had any mycotoxins in their urine.

Considering how prevalent both food mycotoxins and moldy buildings are in the U.S., it is hard to believe that none of the 55 control subjects would have had a significant enough exposure for the toxins to be positive on the test. It seems more likely to me that there was some kind of problem that occurred when the control subjects were being tested and that the results reported were inaccurate.

Since it is difficult for even expert reviewers to detect flaws in a technical study such as this one, and since almost no details are given about how the controls were selected or queried, it is hard for an outsider to know exactly what might have gone wrong with the control group. But in general, all things considered, the idea that 0% of these control subjects would have come up as positive does not seem plausible as an accurate outcome.

It therefore is unfortunate that the authors of the second study (Brewer 2013) did not run their own control group and instead just used the same one that was used in the original study.

If the authors not working for RealTime Laboratories had submitted a mix of patient and control samples, blinded so that the laboratory did not know which was which, and if even a reasonably large difference between the two  groups had been found, then I would be much more convinced that the effect being asserted was real.

Another problem with the control group that was used was that the individuals reported “no known toxic mold exposures in water-damaged buildings.”

If the goal was to determine whether “CFS” patients are more likely to have mycotoxins in their urine than the average person, then the control group should have been a group of random healthy people, not people that had been selected for lack of exposure to mold.


Clinical Use

Another factor that has concerned me about these tests is that the results that patients have reported to me do not seem to be consistent with what one would expect if the test were measuring an actual effect.

In particular, frequently patients have reported currently or previously living in an environment where (based on the species of mold present and on symptoms) particular mycotoxins would be expected to be present, but not having those mycotoxins come up on the test.

For ochratoxin, this is not a surprise. With the test having a sensitivity of only 17%, that would mean that the test identifies this toxin when it is actually present less than 1/5 of the time.

It is my own personal feeling that this introduces such a large element of randomness to the test that even if the test is working precisely as the authors of the studies suggest, it is pointless to get the ochratoxin test done at all.

With that low of a level of sensitivity, if that mycotoxin does not come up, it is impossible to even make a reasonable guess whether the reason is because it is not present in the system or because the test is simply not registering it.

And if it does come up on one occasion, it seems particularly pointless to repeat the test since even if it is still present, there is a greater than 80% chance that it will not come up the next time.

The reported sensitivity for the aflatoxin test is 70.6%. Although this is high enough that the results are not being totally driven by randomness, it would explain some of the inconsistencies that I have seen in the testing results.

The macrocyclic trichothecenes test is reported to have a sensitivity of 94.5%, which is quite high. It thus was surprising to me that many people with exposures to documented major Stachybotrys problems did not come up as positive for this toxin on the test, either while in the home or after they moved out.

My first hypothesis about this was that perhaps some people were storing the toxins in their systems rather than excreting them, due to detoxification impairments. I have since been told that this is the explanation that RealTime Laboratories gives to people who inquire about this phenomenon as well.

However, after being given details about their case histories by a great many patients, I am less convinced that this is the right explanation.

For instance, in a number of situations with Stachybotrys-contaminated buildings, family members who were experiencing only mild symptoms (and thus would be expected to be excreting the mycotoxins) have been tested and have come up negative for macrocyclic trichothecenes.

In addition, many individuals who have moved out of a Stachybotrys-contaminated building said that they were doing much better and believed that they were detoxifying heavily but also came up negative for macrocyclic trichothecenes.

Of course, there also are reports of individuals with exposures to Stachy-contaminated buildings who have been found to be positive on the test, either while they were living in the building or after they started to recover.

Nonetheless, it seems to me that the results of the testing are inconsistent enough with people’s actual experiences for both the macrocyclic trichothecenes and the aflatoxin that it raises concerns that the test is not actually measuring what the laboratory says it is measuring.

And again, for ochratoxin, the sensitivity level for the test is acknowledged to be so low that the usefulness of running the test at all seems questionable to me.



Dr. Joseph Brewer and host Dr. Neil Nathan (another “CFS” physician) discussed their clinical use of the RealTime Laboratories test and their treatment protocols with regard to mold and mycotoxins in an Internet radio interview on the program “The Cutting Edge of Health and Wellness Today” in December 2014.

RealTime Laboratories was listed as a sponsor of the show.

Dr. Brewer and Dr. Nathan suggested that it was their belief that treating the patients with glutathione or sauna prior to getting the RealTime Labs urine test done resulted in more mycotoxins being excreted. They referred to this as a “challenge” test:


We have indeed picked up more than a dozen patients who were negative with an ordinary test and then tested very positive once they had glutathione improving their ability to detoxify. 


I probably most often do the test without a challenge. But I do think that one would pick up more, as you have found, and as I and others have found, there would be even higher test results with doing a challenge.


With regard to binders, Dr. Brewer stated:

There appears to be some difference in which binders work the best. Charcoal seems to be pretty broad spectrum. Cholestyramine is pretty broad spectrum. Bentonite clay seems to be best for the aflatoxins. So sometimes we will design a binder program based a bit on the toxins they have.


Both Dr. Nathan and Dr. Brewer stated in the interviews that they had experiences observing patients on their treatments having the amount of mycotoxins in the urine decrease over time and said that this often correlated with those patients improving.


The thing that we look for is patients improving, that’s what we want most of all, to have patients improve and have a dramatic reduction of their symptoms and return to good health. And we do see that. The other thing that we’ve seen is that if we repeat the urine assay – so we treat somebody to break up the biofilm and to try to get rid of the mold, particularly out of the sinuses, and we repeat the urine assay, we see dramatic drops in the mycotoxin levels. And we have a few now that are getting very close to zero.


I don’t see patients feeling better until they get those mycotoxin levels back in the normal range.


But Dr. Brewer also said that in some cases, patients’ levels increased over time:

Unfortunately I’ve had some patients that if I test them a second time sometime down the line, they’ll show up with a second toxin that maybe was not there the first time. Or that was there maybe in a smaller amount the first time and that is there in a larger amount the second time. And of course, this will be without treatment or if you did some kind of a sauna provocation. So for the worst of these patients, I assume that they may have these three toxins plus possibly some others that we can’t test for.


Dr. Brewer and Dr. Nathan both suggested that they had had success in treating their patients with nasal sprays to address sinus fungi. The sprays that they used contain an antifungal (such as amphotericin B or nystatin) along with a biofilm “buster” (such as colloidal silver or bismuth). Dr. Brewer said that the best results were obtained when patients used the sprays consistently for six months or more.

In general, the treatments suggested by Dr. Brewer and Dr. Nathan seem to have some merit for the treatment of patients with toxic mold illness.

Binders are certainly popular treatments and many of the participants in the Mold Avoidance Survey have stated that cholestyramine or other binders have been helpful to them.

Treatment of fungal sinus infections also have been highly rated in the Mold Avoidance Survey.

I myself used an anti-fungal sinus treatment of the exact type that Brewer and Nathan discuss here almost a decade ago, while living unknowingly in a very moldy house and then after moving out. Although my health continued to decline until I moved out of the house, I found the treatment to be helpful enough to continue using it for a few years. Eventually I concluded I did not need it any more and stopped that treatment.

Whether the mycotoxin urine tests are providing any helpful information with regard to allowing doctors to appropriately prescribe and monitor the success of those treatments seems much less clear to me, however.

Even if the RealTime Laboratories test is measuring the excretion of mycotoxins as accurately as the paper claims, the mycotoxins could be originating from a number of different sources:  food mold, environmental mold or internal mold. In addition, what is being measured could be the result of a current exposure or could have been stored in the body from previous exposures and released at the time of the testing.

Dr. Ritchie Shoemaker posits that pathogenic mold growing in the sinuses would not get enough activity of water to make toxins. Whether that is true, I don’t know.

However, insofar as molds are capable of making toxins in the body, it seems to me that they would be more likely to be ones like Wallemia that thrive on low-moisture conditions in the external environment than ones requiring a larger amount of water (such as those known to make ochratoxin and aflatoxin).

Although Dr. Brewer and Dr. Nathan appear to believe that the urine tests often reflect patients’ clinical status, they also acknowledge that they have encountered some inconsistencies in testing that sound similar to the ones that I have heard about from patients.

In addition, the argument that mycotoxin testing is needed in order to determine what binder to use seems to me a stretch in terms of what the literature will support.

I personally have spent a very considerable amount of time reviewing the abstracts of all of the thousands of papers in the Pub Med database on aflatoxin, ochratoxin and trichothecenes (including satratoxin) and organizing them for a review article and have found little evidence for this idea.

Almost all of the literature about binders comes from the agricultural field. And although there is more literature about the efficacy of binders with regard to some toxins (such as aflatoxin) than others, I have not seen any evidence that suggests that binders that work for some mycotoxins are ineffective for others.

For instance, here is an article that suggests that bentonite indeed can be helpful for binding mycotoxins other than aflatoxin (in this case T-2, a trichothecene toxin).

In general, then, while it seems to me that the treatments discussed by Brewer and Nathan may be very appropriate for people with mold-related illness, the idea that the RealTime Laboratories test is going to be helpful (much less necessary) as a gauge to determine the likely usefulness or actual efficacy of these treatments seems much less clear.


Dr. Ritchie Shoemaker Blog

In mid-October of 2015, I sent a preliminary version of the material above to a number of people to get their comments prior to releasing the blog to the public. Included were the individuals mentioned in the article as well as mold physician and researcher Dr. Ritchie Shoemaker, who had expressed misgivings to me about mycotoxin urine tests in the past.

Dr. Shoemaker immediately responded to me with a few comments. Then, on November 10, he published a blog of his own related to the topic of mycotoxin urine tests, called “Dr. Joseph Brewer: Nasal Fungi, Anti-Fungals and Junk Science.”

In the blog, Dr. Shoemaker reiterated his position that the activity of water in the sinuses would be insufficient to allow the growth of fungi producing mycotoxins. He wrote:

Thankfully, nasal mucus, a viscoelastic fluid, is such an inhospitable environment for fungi.  They rarely even grow in mucus and don’t make mycotoxins even if the fungi can eke out a cell division or two.  Mycotoxins are never made in biological materials with such a low water activity (A(w)). At first, the idea of mucus being too dry might appear odd; we think of a “runny nose” not a sticky nose. But the mucus layers along the respiratory tree are such that while there is water in mucus, it is contained within biological interstices such that the water is unavailable for use by fungi, hence the low A(w).


As references, Dr. Shoemaker lists numbers 1-21 in this PDF document.  He cites a technical paper on micro and macro rheology of of mucous that does not include any mention of mold or fungi – Lai et al, 2009 – as a “must read.”

Dr. Shoemaker points out that mycotoxins in foods have been shown to show up in urine tests and speculates that insofar as mycotoxins in urine samples are found, it seems likely that they would be coming from ingested exposures from foods.

Dr. Shoemaker also spent a significant amount of time referring to the Mayo Clinic studies on fungal sinus infections that took place in the late 1990’s and early 2000’s.

The Mayo Clinic first made news by publishing findings that most sinus infections were caused by fungi rather than bacteria, suggesting that treatment using antifungals might be appropriate. Later, Mayo Clinic researchers published a few studies suggesting that the use of antifungals is not appropriate for this after all.

Dr. Shoemaker refers to the Mayo Clinic work in suggesting that the use of antifungals by Dr. Brewer and colleagues is “dangerous,” “unfounded,” “unscientific” and “inappropriate.”

Dr. Shoemaker’s particular concern about antifungals seems to stem from his belief that the use of these drugs eventually will result in fungi that are not only resistant to everything that we can throw at them but also more capable of making worse toxins. He already has posited (in the book Surviving Mold) that the antifungal crop chemical Benomyl has resulted in more toxic strains of mold, and he seems to fear that the use of medical antifungals will do the same thing.

I had a compounding pharmacy tell me that they were making a knock-off BEG spray that contained either one of the anti-fungals itraconazole or Amphotericin.  I got worried. It is one thing to make up the idea that fungi in low A(w) conditions did anything really bad (they don’t), but to now say, “Oh my, we must kill this placid little contaminant” using drugs that are not benign and are ones for which resistance would create a major public health issue.

The docs who are demanding itraconazole and Amphotericin B possibly have no knowledge of ketoconazole, secoconazole and other azole resistances that rapidly followed their use.  Sad. If we want a resistant organism, let’s use itraconazole for 12-months to see how fast we can make the fungi laugh at what desperate patients put up their noses.


Most of the rest of the long blog consists of criticisms of methodological issues in the Brewer et al body of work.

Dr. Shoemaker also makes two more comments of note.  First, with regard to physicians treating mold illness patients, he writes:

Real Mold Docs must be able to pass a rigorous test (provided through www.survivingmold.com) and must be able to recognize dubious practices. 


Second, Dr. Shoemaker brings up a Surviving Mold virtual roundtable discussion on the topic of “How Do I Know That a Scientific Paper Isn’t Junk?,” in which I participated in early 2015. With regard to that discussion, he wrote:

Aside from the ELISA, a test noted to have significant problems by Dr. Rosen and then Dr. Petrison in the Round Table, Dr. Brewer presented no evidence to support his contentions. 


Dr. Neil Nathan Blog

On November 8, 2015, Dr. Neil Nathan published his own blog as a response to Dr. Shoemaker’s blog. The title was, “Junk Science or Junk Blog?”

Dr. Nathan spent much of the article detailing his own historical friendship with Dr. Shoemaker and then rebuking Dr. Shoemaker for what he called the “unprofessional” tone of his blog. However, he also made some substantive comments.

One of his comments was to suggest that despite the efforts of Dr. Shoemaker and other caring physicians, the field of mold illness was not yet a science. He suggested that we were still in the early stages of figuring out what was going on and therefore that experimenting with different treatment methods was appropriate.

In addition, he suggested that different types of practices attract different types of patients, and that this can and should influence the specific treatments that are used.

I know that Dr. Shoemaker has confined and focused his work on patients who have, exclusively, mold exposure. On the other hand, I know that Dr. Brewer and I, and many others, have practices filled with patients who have mold toxicity AND exposure to other environmental toxins, including heavy metals, Lyme disease with its attendant coinfections, chronic viral infections, multiple chemical sensitivities and many other factors, making comparisons between our patient populations, observations and results, difficult. 


Finally, he asserted that the binder and antifungal protocols that he and Dr. Brewer had been using had been helpful to their patients:

Patients who were treading water under my care are now improving or well. Patient after patient relate to me their improvements on the expanded use of biotoxin “binders” and to their use of antifungal medication taken as nasal sprays and orally. For most of my patients, it simply works.


Dr. Gary Rosen’s Article

In his blog, Dr. Shoemaker referred to an article on the mycotoxin urine tests published by Gary Rosen, PhD. The title of the article is “Urine Testing for Mycotoxins: Junk Science or Not?”

Dr. Rosen is a mold remediator and building contractor located in Florida. He has a doctorate in biochemistry and molecular biology from UCLA and has written several books on the topic of mold remediation and mold toxicity.

One of the assertions that Dr. Rosen makes in his article is that mycotoxin urine testing is fraught with inaccuracies even with the best of equipment. He thus says that he does not believe that the RealTime Labs tests are very reliable:

When Real Time Labs (RTL) is testing for Ochratoxin, Aflatoxin or Trichothecene in urine they cannot actually test for these toxins because these toxins never exist in urine. Only the detoxified (biotransformed) derivatives (also called metabolites) of these mycotoxins are present in urine. The detoxified derivatives of Ochratoxin, Aflatoxin or Macrocyclic have different chemical properties and molecular weights from the original mycotoxins and as such do not consistently cross react with immunoassays developed to detect the actual (nondetoxified) mycotoxins one is exposed to from either foods or moldy indoor environments.

So when you read in an article that tests for mycotoxins in urine by RTL where they claim that they purchased pure mycotoxins from such and such a source to calibrate their equipment … there’s a problem. They are using a completely different chemical to calibrate their systems than what they are attempting to measure in urine which is the biotransformed derivative of the toxin and not the original toxin ingested or breathed.

Furthermore, in the papers published by Brewer, Real Time Labs uses (as explained in their papers) a different toxin — roridin and not satratoxin — to develop and calibrate their equipment for analysis of Satratoxin (which RTL calls Macrocyclic Trichothecene.)

Studies by leading researchers find that detection of mycotoxins in urine even with much higher end equipment than used by labs doing commercial urine testing are fraught with problems including false positives.


Dr. Rosen also brings up the Mayo Clinic studies, suggesting that the species that Mayo had found to colonize the sinuses would be unlikely to be making mycotoxins that would show up on the urine tests in question.

Without citing a reference, he suggests that trichothecenes made by Fusarium (a food contaminant) may be mistaken for macrocyclic trichothecenes in lab tests:

It is widely known that the methods used by Real Time Labs to test for Satratoxin (which is a type of trichothecene) cross reacts with other Trichothecenes that are very often found in food.


In addition, Dr. Rosen cites a 2010 study in which mice that are exposed to satratoxin begin to excrete it immediately. He uses this as the basis for the following argument:

Furthermore, Stachybotrys toxins are not present in commercial foods. Therefore, if  1) Not from food & not from growing in the body for example not growing in sinuses;  2) Not stored in body fluids as the body starts to detox Satratoxin in minutes; and  3) Not from the environment as patients are no longer in the water damaged home, then

The only possible conclusion for finding Stachybotrys toxin in patient urine is that what is being measured is a false positive and that there is a major problem with the RTL measurements of toxins in urine.


Dr. Rosen also expressed some concern that certain RTL tests had been labeled as “Trichothecene Group” and wondered if Fusarium toxins might be included in that. In more recent RTL test reports, “Trichothecene Group” was specified as “Macrocyclic,” however.


Some Comments

First, I would like to state my appreciation for the enormous contributions that Dr. Shoemaker has made to the study of mold-related illness and for the help that his protocols have provided to very large numbers of patients. I myself decided to pursue mold avoidance only after reading his book Mold Warriors, and so I am personally grateful to him as well.

I am in agreement with many of Dr. Shoemaker’s comments on the methodological limitations of the papers on  mycotoxin urine testing published by Dr. Brewer and colleagues.

Although I looked through the references that Dr. Shoemaker supplied on the activity of water in the sinuses, I am not sure whether or not I agree with him on this topic.

Certainly, it seems to be the case that activity of water is a limiting factor with regard to Stachybotrys, which requires a great deal of water to grow and which is generally believed not to have the ability to grow in the human body.

It also may be the case that other molds that create aflatoxin and ochratoxin require sufficient amounts of water that they cannot manufacture substantial amounts of toxin in the body. I’m not sure about this, but it is plausible since those molds do generally require a fair amount of water to grow and release toxins.

However, it also is the case that there are some species of toxic mold (like Wallemia) that require less water and that can grow and make toxins just fine even on the condensation in HVAC systems.

Considering how fast mold seems to be mutating into virulent forms, the idea that a strain of mold not requiring much water might adapt itself to be able to colonize the human sinuses and make toxins there does not seem to be wholly implausible to me.

I bring this up because of the large number of reports that I have gotten over just the past year or so from trusted and successful mold avoiders that a subset of mold sensitized people seem to be colonized with toxin producers, to the point that they have become far more toxic to other sensitized people than even the worst bad buildings.

At first I doubted the veracity of these reports, believing that these individuals instead were carrying around large amounts of cross-contamination from particularly bad residences or excreting toxin through sweat or breath.  But after doing a lot of probing interviews, I have become fairly convinced that this is an actual phenomenon and that a particularly problematic microorganism – referred to as Hell Toxin in a previous blog – does appear to have the potential of colonizing mold victims and producing unusually bad toxins in their bodies.

If this indeed is an emerging phenomenon, then it might have the potential of explaining why the research from Mayo Clinic from 15 years ago would have shown no evidence of fungi with the ability to make particularly bad mycotoxins being present in sinuses, and also why some patients with mold illness appear to be benefiting to a significant extent from sinus antifungals and/or systemic antifungals.

If this phenomenon is a legitimate one, I feel reasonably confident that it is not being caused by fungi manufacturing aflatoxin, ochratoxin or macrocyclic trichothecenes.  The symptoms do not match the ones those toxins are known to cause, and the molds that make those toxins do require a fair amount of water.

Rather, my guess would be that it is a mutated form of another mold that does not require much water.

Ideally, of course, a sophisticated researcher would look into this and find out, but such a researcher has yet to present himself or herself. Hopefully that will occur in the near future.

In terms of Dr. Shoemaker’s other points:

I am in strong agreement with Dr. Shoemaker that the threat of antifungals causing mold to mutate into more problematic forms is of significant concern with regard to the future fate of the world.

Erik Johnson (who has been studying the phenomenon of toxic mold since the mid-1970’s and whose opinions I trust far more than I do anyone else’s) has said many times that he does not believe that we are going to be able to chemical-ize our way out of this situation – and that he believes that instead, the more that we try to kill off the mold with chemicals, the worse it’s going to get.

I agree that that is likely true. Therefore, the idea of using antifungals to kill mold in patients’ bodies makes me worried.

On the other hand, people who appear to be colonized with this emerging pathogenic fungus seem to be having an inordinately hard time even when engaging in really scrupulous mold avoidance and pursuing a variety of other treatments to the best of their abilities.

It is really heartbreaking for any caring person to see these individuals suffer when it is possible that there is a treatment that may help them, even if it also seems that the overuse of that treatment may have negative consequences for the world at large.

I thus see this as a social dilemma – one that practitioners treating this illness eventually may need to resolve both in their own minds and as a community.

On another topic, I am not of the belief that passing the test to become a Shoemaker certified practitioner or practicing according to the Shoemaker protocols should be considered a requirement for an individual to be considered a “real mold doctor.”

Rather, I am in agreement with Dr. Nathan that it is too early in the scientific process for anyone to come to the conclusion that certain treatment protocols are mandatory for treating mold-related illness or that other protocols do not have the potential of being very helpful for this. Much, much more research will be needed before we can reach such conclusions.

I also am in agreement with Dr. Nathan that study of the Shoemaker Protocol has been focused on a subset of patients with mold-related illness and these experiences cannot and should not be generalized to all patients who are inordinately affected by mold toxins.

In the book Mold Warriors, Dr. Shoemaker acknowledged that he did not have much ability to help “CFS” patients. Although he has added a few treatments to his protocol since then, reports made to me have not suggested that these additions have made a major difference in terms of the ability of that protocol on its own to bring these unfortunate individuals to an acceptable level of wellness.

I have a particular interest in this topic, since these very ill individuals tend to gravitate to my Mold Avoiders Facebook group (as well as, apparently, to the practices of Dr. Nathan and Dr. Brewer).

In a high percentage of cases, these individuals cannot tolerate cholestyramine or Welchol at all (or can only tolerate those drugs after they have achieved a much higher level of mold avoidance than Dr. Shoemaker suggests). A high percentage cannot tolerate the other Shoemaker drugs either.

On the other hand, most of these patients report benefiting from treatments that the Shoemaker protocol does not recommend – generally very specific mixes of therapies tailored with great care to their own particular situations.

That being the case, I have a substantial problem with the idea that Dr. Shoemaker’s approach is the only way to treat mold-related illness and that any physician who does not follow that approach is doing something wrong.

Certainly, it is a legitimate decision to have the Shoemaker protocol focus on moderately ill patients who are relatively easy to help, rather than on more severely ill patients who are much more difficult to help.

But it is quite another thing for anyone to suggest that the only appropriate treatment strategy for mold-related illness is one that very frequently is not successful in helping the most severe patients, since that would leave those patients who are most in need out in the cold.

Moving on with one more small point: although I was quite critical in the “Science and Integrity Roundtable” of the RealTime Labs urine tests as well as of proprietary testing in general, I never made any comments with regard to ELISA testing.  I am by training a social scientist, not a medical scientist, and thus have no specialized knowledge about ELISA testing. I would not venture a comment as if I were an expert on something that I do not know much about.

With regard to Dr. Rosen’s article, I found the idea that mycotoxin urine testing often has a lot of false positives to be interesting.

The possibility that derivatives of trichothecenes made by Fusarium mold could be mistaken for derivatives of trichothecenes made by Stachybotrys is even more interesting. I wish that Dr. Rosen had provided some support for that notion.

The idea that just because mice start excreting satratoxin right after exposure to it means that people cannot be excreting satratoxin from long-previous exposures does not make sense to me though.

For one thing, various mammals are not all equally good at excreting all mycotoxins. That being the case, maybe mice are a lot better able to handle this particular toxin than humans are (or than humans with certain genetics are).

Another possibility is that some humans have their detoxification abilities impaired due to factors that the mice were not experiencing, such as burdens of heavy metals or particular parasites or methylation problems or nutritional deficiencies or ongoing exposures. If that is the case, then detoxification of previous exposures may be noted in some individuals long after those exposures occurred, subsequent to these problems being remedied.

I thus do not believe that it is appropriate to use this one mouse study to suggest that there must be a laboratory error present if trichothecenes are identified through the test. That is too big of a leap.

Finally, I am almost as suspicious of the Mayo Clinic as I am of the CDC with regard to their positions on “CFS” and mold illness. I have heard stories from many patients with this kind of illness who have sought treatment from Mayo, and even in recent years, these individuals always have emerged with referrals to psychiatrists and no useful treatments of any sort. This makes me question whether the Mayo Clinic really has the best interests of individuals with mold-related illness in mind and thus whether their recommendations that no one use antifungals for sinus issues may have been motivated by something other than pure science.

Thus, I feel less inclined than Dr. Shoemaker or Dr. Rosen seem to be to take the Mayo Clinic’s conclusions on any of these matters to be definitive.


Gliotoxin Testing

On January 8, 2016, Dr. Brewer again was a guest on Dr. Nathan’s radio program, “The Cutting Edge of Health and Wellness.”

The two physicians reiterated many of the same discussion points as in their previous radio broadcast. They also expressed considerable concern about patients with mold-related illness being misdiagnosed as having purely psychiatric illness and about the well-being of their particularly severe patients.

In addition, they brought up a new component of the mycotoxin urine test offered by RealTime Laboratories. This is for a mycotoxin called gliotoxin, which is made by certain strains of Aspergillus mold (and possibly also by Candida) and which has been implicated in a few papers as being associated with multiple sclerosis (MS).

Dr. Nathan commented:

The gliotoxin is made by Aspergillus, which is one of the common toxins that people get exposed to that make them sick. But in addition to that, many people believe that gliotoxin is also made by Candida. This may be a more specific way for us to know which of our Candida patients really are being affected by it and then give us a more specific way of monitoring how we work with them.

Having said that, we just got yesterday our first few gliotoxin assays back. I specifically was looking at some of my patients that I was certain had mold toxicity but could not get a positive test from them. I had a particular woman who had been sick for many years, and we have tested her over and over for Lyme disease and mold toxicity and anything I could think of. She has the full constellation of symptoms. But we haven’t had any positive testing. She’s one of those folks who really needs to know that she has this before she’s willing to embark on a complicated treatment program. Her gliotoxin test was 3.54, with the upper level of normal at .3. Meaning she had 10x above the limit of the test. So I think I can take the information back to her now and say, “Okay, we can really confirm your diagnosis and start treating.”

I think in patients like this, that this test will be especially helpful.

Clinically we do see that we have quite a few patients that we’re treating for mold that we have had more success when we have added a treatment more specific for Candida….What we suspect, just because our patients have done well clinically, that the treatments that we are using include treatment for the species that make gliotoxin. If we can get a series of these assays on patients that we’ve already treated, then we can really define that and help the whole medical world to know what we’re doing here.


Dr. Brewer added:

We’re excited because we have a new toxin that we think is important. Probably a very toxic toxin that impacts the immune system in a number of deleterious ways and has mitochondrial toxicity, etc. Now that we can test for it, it may guide us in some different directions on treatment.

We don’t know which binders may work best for gliotoxin. We do think that the antifungals that we use, nasally and so forth, do have a pretty broad activity for gliotoxin.  But in some patients it may raise the question of whether Candida may be an issue along with the molds.


The idea of gliotoxin gaining more attention is of considerable interest to me, because I feel that it has not received nearly a much attention as it likely deserves with regard to mold illness patients up to this point.

In addition to the MS connection, I became intrigued when the autism researcher Kerry Scott Lane, M.D., made to me in 2010 an offhand comment that “Gliotoxin from Candida and Aspergillus can bind to disulfide linkages similar to glutathione.”

I brought this comment up to Dr. Rich van Konynenburg (“Rich van K”), a career physicist who spent his retirement years prior to his death looking at the role of glutathione and methylation in ME/CFS.

He wrote to me the following in response:

In response to your request, I looked into gliotoxin a little.  That is really diabolical stuff!  But then, I’ve never met a toxin I really liked.

O.K., here’s the story.

First, some background about glutathione and how great it is:

As I think you know, glutathione is very important to our cells, and does many wonderful things for us.  One of its main roles is to control the redox potential inside the cells.  The redox potential is basically sort of like the market value of electrons in terms of energy.  The more “reducing” the redox condition, the more available electrons are, and the more “oxidizing” the condition, the less available they are.  

Normally the inside of cells runs at a more reducing condition than exists outside the cells.  This relatively reducing condition is maintained by glutathione.  Glutathione does this by being able to exist in two states: the sulfhydryl or thiol state (called GSH), and the disulfide state (called GSSG).  The thiol state is more reducing, while the disulfide state is oxidized.  A balance is struck between these two in the cells, where the GSH form is normally much more abundant, so the cell is more reduced, chemically.  It’s the ratio between these two states that determines the redox potential.  This redox potential has a big effect on biochemical reactions, especially the so-called redox reactions that are very important in the mitochondria as well as in other parts of the cells. Chemistry, after all, is all about electrons, how they are exchanged between molecules, and how they bind molecules together.

O.K., so much for background.  Now, what about gliotoxin?  The important thing about this toxin is that it contains a disulfide bridge in its molecule.  This bridge can exist either in its oxidized state, in which the two sulfur atoms are bound together in a disulfide bond, or in its reduced state, in which there are two thiols, i.e., each sulfur is bound to a hydrogen atom.  This is called the dithiol state.  So it’s sort of like glutathione in this respect, except it’s all within one toxin molecule, instead of two separate glutathione molecules.

Now, it so happens that the natural state of gliotoxin is the oxidized or disulfide state.  In this state, it is able to enter cells. However once it gets inside a cell, it starts reacting with glutathione and also with some of the proteins in the cell that have thiol groups in them.  When it reacts with them, the gliotoxin converts to its reduced state, and it oxidizes the glutathione or protein thiol groups.   The reduced state of gliotoxin cannot leave the cell, because it will not pass through the cell membrane.  So it builds up in the cell.  As more glutathione becomes oxidized, the cell, in desperation, exports the oxidized glutathione (GSSG) in an effort to maintain a high ratio of GSH to GSSG, in order to hold the redox potential in a reducing condition.  If there is enough of the toxin, it can overwhelm the capacity of the glutathione to control the redox state.  Sadly, the cell then has to commit suicide by apoptosis.  In the process the gliotoxin reverts back to its natural, oxidized state, and escapes from the dying cell.

Now here’s the really devilish part:  the gliotoxin can now invade another cell and do the same thing over again!  So this makes it a very efficient killer.

Now, you asked about the context of the topic under discussion here. Well, I can only speculate, but I suppose that if a cell that has a provirus in its DNA is attacked by gliotoxin, it will have its glutathione depleted, which in turn will diminish its ability to keep its methylation potential up.

This could cause the provirus genes to become unmethylated and therefore unsilenced, and could thus allow the propagation of the retrovirus.  I guess it would depend on how much toxin there was in the cell, and thus whether it causes apoptosis before the provirus can produce its progeny.  It would seem likely that there would be cells that receive some gliotoxin, but not enough to kill them, and these might serve as breeding grounds for the retrovirus.  I’m projecting a bit here from what I think I know, but it would seem reasonable to me to suspect that this could happen.  So this makes the gliotoxin a trigger for propagation of the retrovirus.

Doesn’t this sound mean to you?  But then, we scientists are cold and unemotional!  I have to confess to you that when I first learned that the cavalry in the form of the cell-mediated immune response does not arrive in ME/CFS, so that the cells are abandoned to the attack of viruses, I actually cried!

Just a small nit pick:  the disulfide bridges are formed under oxidizing conditions and are broken under reducing conditions.  They involve the linking of two cysteine residues together in a disulfide bond, to effectively form cystine, which is the oxidized form of cysteine.  One thing Dr. Cheney did not mention is that glutathione depletion is what leads to the oxidizing conditions that allow these disulfide bonds to form.  Many pathogens require the formation of these bonds, for example the whole herpes family of viruses as well as Chlamydia intracellular bacteria.  If glutathione levels can be normalized in the cells where these pathogens reside, they will go into latency.


Considering the apparent importance of glutathione with regard to ME/CFS patients, and also considering the frequency of Candida overgrowth in these patients, I have been very interested in the potential role of gliotoxin in this illness ever since having this conversation. And there is at least a small amount of evidence in the literature suggesting that Candida and Aspergillus in the body have the potential of making gliotoxin.

So I am pretty interested in this new gliotoxin test from RealTime Labs.

The problem is that there is even less publicly shared evidence that this is a legitimate test than there is about the other three mycotoxin tests being offered by the company (i.e. at least thus far, no evidence whatsoever, as well as no information on sensitivity or specificity of the test). That makes it hard for me to take the test results seriously.

As a side note: I am really grateful to Dr. Brewer and Dr. Nathan for bringing up the issues of the suffering of severe patients and of the psych misdiagnoses. I have no doubt that regardless of whether these individuals are right in terms of the mycotoxin urine tests having any validity, they are both very caring physicians who have their patients’ best interests at heart.


Better Health Guy

Scott Forsgren is a mostly recovered chronic illness patient who runs a website and Facebook page called Better Health Guy. In addition, he wrote (along with Dr. Nathan and Dr. Wayne Anderson) an article for the July 2014 edition of Townsend Letter, called “Mold and Mycotoxins: Often Overlooked Factors in Chronic Lyme Disease,” and he frequently has spoken about mold-related issues in high-profile presentations and on his blog. I am very grateful to him for his efforts in bringing mold toxicity to the attention of the Lyme community.

On May 10, 2016, he published a blog article entitled, “My Experience: Urinary Mycotoxin Testing.” He explained in the article that when he first got the test done in 2013, he was doing well and that all three mycotoxin tests then available came up negative.

Then, in 2015, when he knew he was being exposed to mold and experiencing some symptoms, the test came up highly elevated for ochratoxin and gliotoxin and close to the positive level for trichothecene and aflatoxin.

Finally, in 2016, after he had moved from the problem environment and was feeling better, all the tests came up as negative.

He described the test as a “huge help” to him, stating:

I don’t think that urine mycotoxin testing is a single test done in isolation. I think it is one of many things that may be helpful when mold is suspected. I absolutely suggest the Mycometrics ERMI as well as all of the standard Shoemaker biotoxin illness markers such as TGFb1, C4a, MMP9, MSH, and others. The urine testing is, in my opinion, one more indicator; one more piece of a complex puzzle.


If all the stories I heard about the mycotoxin urine tests had results similar to this one, I might be inclined to agree that it was potentially useful despite its lack of scientific validation.

Unfortunately, though, these types of commonsense results seem to me to be the exception rather than the norm.

What I hear much more often are results that seem on the surface really counterintuitive.  Such as whole families with known exposures to massive amounts of Stachybotrys who never show any trichothecenes on the test, while in the exposure or at any time after getting out. Or people who are highly positive for one mycotoxin and one point in time and then – without seeming to have done any substantial detoxification at all and without having been in a new problem environment – are negative for that mycotoxin but highly positive for a different mycotoxin at a later time. Or clearly mold-sick people who appear to be in the midst of detoxification who come up negative for all the mycotoxins. Or families where members are positive for totally different toxins from one another.

Of course, if we try hard enough, we can come up with explanations that do not involve the idea that the results are due to food mold or test problems for any of these events. Such as the idea that people had impaired detox capacity. Or that they already had engaged in successful detox. Or that they had gotten a pathogen under control.

But after seeing a large number of these apparently random results, they have begun to seem to me to qualify as “Just-So stories” – meaning, something that has totally left the realm of scientific exploration and moved into the realm of pure conjecture. And that is not something that I feel comfortable endorsing.


Mold Group Poll

Finally, I was interested in finding out whether the results reported in the Brewer et al paper from 2013 were consistent with the results that mold illness patients in online groups who had taken the test had received.

Therefore, I did an informal poll in several mold-oriented groups on Facebook from May 9-11, 2016. Of the 76 respondents, 45 were from my own group, Mold Avoiders. The rest were from Black Mold Symptoms; Toxic Mold – Rediscovering Health and Wellness; Toxic Mold, CIRS and Lyme Support Group; and Toxic Mold for Dummies 101.

Participants were asked to supply their results from the first time they had the mycotoxin urine test done. Only results for the RealTime Labs test were included.

Following are the breakdowns of the numbers reported in Brewer 2013 compared to the poll numbers. AT = Aflatoxin; OTA = Ochratoxin; MT = Macrocyclic Trichothecene.


Mycotoxin           Paper (N, %)           Mold Groups (N,%)               

AT                               13, 12%                       8, 11%

OTA                            87, 83%                       32, 42%

MT                              46, 44%                       48, 63%

OTA + MT                  24, 23%                       20, 26%

AT + MT                     4, 4%                             5, 7%

AT, OTA, MT             8, 8%                             4, 5%

None                           8, 7%                          10, 13%


Overall, the results are quite similar to those reported in the Brewer et al 2013 paper. The main difference is that a higher percentage of the mold group participants reported having been positive for macrocyclic trichothecenes and a lower percentage reported having been positive for ochratoxin.

In addition, a slightly lower percentage of mold group respondents reported being positive for any mycotoxin than were reported in the paper (87% vs. 93% in the paper).

This is reassuring with regard to the patient component of the Brewer study. However, my problem with the research on the RealTime Lab test never was with the patient groups.  Rather, it was with the lack of proper controls against which to compare the patient data.

Therefore, although these results are of some interest, they do not relieve my doubts about the validity of these urine tests.

Perhaps most critically of all, one thing strikes me as odd about these numbers.

In the original paper attempting to prove that the tests were legitimate (Hooper 2009), the sensitivity of the ochratoxin test was stated as 17.4%. This means that even if high levels of ochratoxin were present in the urine of all individuals, we would see it come up on the test as positive only 1/5 of the time.

And indeed, in the patient sample in the Hooper 2009 paper, this is how the results came out, with 23% of the patient population being reported to be positive for ochratoxin.

However, in the patient populations of the Brewer 2013 paper and of my poll, far greater percentages of patients registered as being positive for ochratoxin (83% and 42%, respectively). This makes me suspect that the test that is being used has been changed to make it more sensitive.

Of course, from a general perspective, a more sensitive test is a good thing.

The problem is that the Brewer 2013 test compared the results against the 2009 control sample using the original test.

It is not appropriate scientific practice to use one test on one group of individuals and a different test on another group of individuals, and then to make a conclusion that the two groups are inherently different from one another if the test results come out as disparate. Obviously, in that case, the difference could have been due to the testing being used rather than anything inherent to the groups.

Unless this matter is cleared up, it is my position that the reports about ochratoxin in the Brewer 2013 paper cannot be taken to mean anything at all.

This also makes me question whether the aflatoxin and trichothecene tests used in Brewer 2013 were the same ones that were used in Hooper 2009, or whether they also might have been changed.



Insofar as the RealTime Laboratories test actually does what it is claims to be able to do, it could be a very helpful test.

I actually was interested in doing a study using this test myself, when David Straus first brought the test up to me in 2010. And so I can see why both patients and physicians have been so drawn to the test.

However, after having looked closely at the literature, I am no longer convinced that as the evidence stands now, this test is worth using.

In particular, the many problems with the control group for the studies and the conflicts of interest involved are too great for me to feel comfortable with it.

My concern increased a number of months ago, when an ME/CFS researcher expressed doubts to me about the idea that a very high percentage of patients with that illness actually were affected by mold, citing as evidence the fact that not very many of their own patients had come up as positive on the mycotoxin urine tests.

The idea that an inaccurate test would cause researchers to become less interested in the relationship between mold and ME/CFS is, in my view, an issue of serious concern.

I therefore believe that it is necessary for questions about this test to be resolved prior to its continuing to be used.

A simple way to do this would be to send to the laboratory a group of random control samples and a group of patient samples – blinded so that the laboratory cannot tell which is which. And then to compare the results.

It seems to me that the owners of RealTime Laboratories are likely making enough money selling these expensive tests that if the tests indeed are legitimate, it would be worth it for them to do this experimental testing for free.

I would personally be happy to contribute my own time to a project like this, in conjunction with others who might be interested in participating.

In the meantime, at a minimum, I am going to venture to say that I think it would be inappropriate for any physician to deny treatment for mold-related illness issues to patients due to either their unwillingness to spend the money on the test or their not coming up with specific results on this test.

The questions surrounding the test are too numerous and too substantial for it to be the deciding factor in important treatment decisions, in my opinion.

In addition, I sincerely hope that ME/CFS researchers will not put any weight on these test results when considering the question of whether toxic mold is an issue in that illness.

For them to turn away from the whole topic of toxic mold due to a problematic test would be a tragedy for all concerned.


Addendum 2/28/18: Dr. Ron Davis of Stanford University made a critical comment about mycotoxin testing in a panel discussion.



Individuals mentioned in this article were provided with a preview copy and given a chance to submit comments on it. Here are the submissions that I received back from them.

Please note that I made some changes in the blog in accordance with these comments and thus that all remarks may not pertain to the final version of the blog.


From Joseph Brewer, M.D.:

There has been an explosion of on line journals (which are called Open Access Journals) and as you are probably aware is the growing trend in scientific publication.

When we were looking at potential journals in which to publish our papers, we contacted several Open Access journals, of which all charged a fee for review and publication. We picked Toxins because it was a good match for our type of data and findings, not how much they charged.

These journals are peer-review formats with rules for fairness. They maintain strict “arms’-length”policies. The journal Toxins (which published two of our papers) has a very good reputation and is tightly controlled.

Our paper from 2013 was retrospective observational analysis of what I observed in my practice. A control group was impossible. This was not a prospective case – control study. I did not have access to any other control data.

A large case–control study would be great but who would pay for that? I haven’t seen or heard anyone stepping forward to do that.

RealTime already did the study on the 55 controls at their expense. They are working on another control group study at present.

We have never stated that mold exposure and mycotoxins were the “cause” of CFS. We have published an association.

We do believe that mycotoxins may be an important piece of the puzzle. How readers “interpret” the data is up to the individual reader. Our study is not unique in that regard.


From RealTime Laboratories Management (including Dennis Hooper, M.D., Ph.D.):

We are answering your request for a response to your blog article titled, “Looking at the Literature About Mycotoxin Urine Tests”.   We appreciate your courtesy to ask us to respond.

First,  we commend you for attempting to take a very difficult subject and condense it to a few pages.  Your attempt to give your readers an educated and well thought out explanation of mold and mycotoxins and the science provided by Real Time Labs was valiant.   We do, however,  believe that some deficiencies in your evaluation need to be corrected if your blog is an honest attempt  to improve patient care in the area of molds and mycotoxins.

  1. There were 28 references cited in the paper  listed in the “reference” section. You decided to only mention two (2) of them in an attempt to discredit the validity of the study.  In our opinion, this has not been a sufficient literature rebuttal to this 2009 paper.   The paper cites exquisite work conducted by Groopman, et al,  and Brasel, et al, to only mention a few.
  2. Your statement on the Brewer et al 2013 paper and the Brewer et al paper of 2014 appear to be correct.
  3. You then address issues that are raised in “Health Rising Blog” by Cort Johnson. We have then, and again now, read Johnson’s critique and have comments on your excerpts: a) Dr. Brewer might have had a selection bias. To clarify,  Dr. Brewer selected his patients and was  the treating physician. Patients and Physicians  are “selected” by each other.   When a physician reports the findings in his practice, it is exactly that, a finding in his practice. It should not be misconstrued, to mislead the readers the readers as a “selected bias”. b) The points made on the “water-damaged building” definition were broad and a high percentage of the general population might indeed qualify as having lived in one (ibid….a WDB). Again, Brewer et al reported on a select population in Brewer’s practice.  It was never intended to be an “end all” about mold-mycotoxin exposure and the relationship to Chronic Fatigue Syndrome (CFS). c) Johnson’s supposition that mold issue might be higher in the Midwest.  Brewer et al, does not dispute or support that supposition. Again, the population reported by Brewer et al was small and consistent with Brewer’s practice. d) Brewer et al, as well as RTL staff, take the conclusions of Johnson as helpful and note that Johnson did state “the study did suggest that mold might be playing a role in at least some cases of this illness”. Again, to say anything further would be an injustice to the patients.  Brewer et al, reported their findings as fact, with suggestions listed in the Discussion section. This is not inappropriate to do.
  4. You then cite Jill Neimark (jillneimark.com), “a veteran science journalist and author of adult and children’s fiction, as well as a contributing editor and feature writer at Discover Magazine.” (from Home page of www.jillneimark.com).Although Ms. Neimark  may be an  accomplished and respected author, we strongly disagree with her assessment of credibility in publishing in Open Access publications. We cite the following publication for your review: Van Noorden,  The True Cost of Science Publishing.  Nature 426 (495), 28 Mar 2013.   (Exhibit #1) This excellent article cites Michael Eisen, University of California, Berkeley. A few issues covered: a) Libraries are charged by Publishers an undisclosed amount, covered by a non disclosure agreement. Private communication indicates this, in some cases, can be as high as $30,000 annually per journal per library. b) The cost average for submission to journals not on Open access prior to 2013 was 4000-6000 per journal article from the submitting author. At present, there is a one time fee for Open Access journals averaging $650-$1350.  To date,  RTL has paid on the average $400/journal submission. c) If a scientific investigator desires a copy of a published journal and he/she is not a member of the journal (i.e. Proceeding of XXXXX),  the cost per journal is $39-$50 to the inquiring investigator/scientist. There  is no charge to the inquiring investigator for an open-access journal. d) The data submitted to a publisher becomes the publisher’s data. The data in open-access is solely  owned by the investigators. There is no copyright violation to the investigator.
  5. You then cite quotations from Joseph Brewer, M.D. You further agree with Brewer that his patients were not a “subset” of individuals with a particular connection to mold. We also agree that the contention that Midwest homes have more problems than homes in other US areas,  but this is difficult to evaluate given the present scientific literature. We again disagree with  Ms. Neimark’s statement of Open Access Journals (See RTL response, #6, above).
  6. Your review of and citation of an MMWR Article of February 2015, focusing on mycotoxin urine tests by Kawamoto and Page.   You explain a patient situation and assume that this test and treatment was conducted by RTL. This is not the case.  We would take exception to your conclusions and note that they are considered “hearsay”.  This was not RTL’s test and RTL does not recommend treatment plans. RTL does not promote or suggest any treatment plan especially one of eating canned chicken and rice as a standard protocol. RTL’s testing procedure is validated to identify the analyze (the mycotoxin only).  RTL’s procedure is not meant to be a diagnostic test. This can only be accomplished if the test can be linked to a specific disease process, which, at the present time, it has not. Of note:   RTL prints a disclaimer at the bottom of the result sheet which states “….Ibid…these lab results are intended to help the physician in the diagnosis of the patient’s problems.”
  7. You go on to discuss Unvalidated Tests: The staff and management of RTL, respect the work conducted by the CDC.  It is the authority in health conditions in the US.  RTL  believes that the work that has been done and will continue to be done will benefit patients. RTL  also believes ultimately CDC’s views on toxins from various sources, including molds, could change with enough data.
  8. RTL strongly disavows any knowledge or association with the Whittemore Peterson Institute. We would strongly recommend anything that can even potentially cause the reading public to draw any association between the two institutions be removed.
  9. You further state that Dennis Hooper did not list his interest in RTL. That is not true.  On all papers, Dr. Hooper states his affiliation with RTL. In every presentation at medical meetings, it is a requirement to report to the Continuing Education Committee, that an individual holds financial interest in the company either on the paper or in the presentation.
  10. You further mention the different  author’s background on these papers. If you need further information on any of them, please feel free to contact us. a) David Straus, Ph.D. of which you hold in high esteem. b) Jack Thrasher, Ph.D., a toxicologist. c) Dr. Brewer, M.D., an infectious disease physician, is held in high esteem by RTL. Dr. Brewer is now on the Scientific Advisory Board of RTL to assist RTL in better patient care.  He has divulged that in scientific conferences and elsewhere. d) Roberta Madison, Ph.D., a statistician, is now deceased. e) Frederick Guilford, M.D., an owner of YES, Inc., Palo Alto, CA. and a California licensed otolaryngologist. f) Vincent Bolton, M.D., a licensed anesthesiologist and on the  board of directors of RTL. g) Dennis G. Hooper, M.D., Ph.D., licensed M.D., in Texas and California. Dr. Hooper has asked that he respond personally to this at the end of this evaluation.  (See Exhibit #2)
  11. Your review address the subject of Control Groups: RTL agrees that finding appropriate Control Groups are very important to evaluate the clinical relevance of the analytic test developed by RTL. Of note, aflatoxins are in many foods throughout the US diets, however, RTL finds less than 5% of all urines tested over the last ten years as  having been positive for any detectable amounts of aflatoxins. It is unclear to us what this finding means. RTL  has found that there is no agreement as to where the mycotoxins originate, food , infection, or environment. It is  of interest that through private communications with physicians that they have observed patients testing positive for mycotoxins such as ochratoxin A or trichothecenes, do not change their diet while under physicians’ care, and improve in their symptom presentation with treatment. Also, note, RTL staff and scientific committee members are not aware of major food groups that have macrocyclic trichothecenes present, thus eliminating the argument that the test is detecting  food contamination in positive patients. Scientifically, macrocylcic trichothecene producing organisms are in contaminated buildings. These  trichothecenes are far more toxic than simple trichothecenes. Why patients in the same exposure area are non-susceptible to the same amount of mycotoxins is an area which needs to be further explored. We do believe that there are some genetic components involved in this observation as well as the patient being immunocompromised. Also, for your clarification, no specimens submitted to RTL from ANY physician is identified as to a study, the symptoms, or otherwise. All  specimens are accessioned as they arrive in the laboratory and are tested in the same manner. Study specimens that are identified by a Principal Investigator (PI) and are labeled as such are not processed any differently. None of the Brewer specimens were differentiated as to patients with CFS or otherwise.  Thus, the specimens were blinded to the laboratory as to patient type. Dr. Jacob Teitelbaum asked specific questions of Dr. Brewer which were handled well by Brewer.
  12. Your review reports patient’s statements, to support an argument, yet you do not indicate how  many  patients (1, 100?), what specimens (urine, blood, tissue, nasal secretions). There are no specifics. It does not help the cause of your argument,  if you are not specific. Again these statements become hearsay. We would recommend you review the literature further and take note that mycotoxins act intracellularly (i.e. protein synthesis, DNA synthesis) and thus are not always available for measurement in the extracellular milieu.In your clinical use section you report “after seeing a great many cases, you are less convinced”. We ask, how many cases have you seen? What type of cases are they? In what capacity were you allowed to review the cases without violating HIPAA? Without those clarifications, RTL can not respond.
  13. RTL has no response on treatment. The laboratory is providing a test that is used in assisting the provider in their patient assessment and diagnosis. There is very little published on the actual treatment protocols of mycotoxins.
  14. You state that you have reviewed “abstracts of thousands of papers in Pub Med database”.   It is RTL suggestion, that to review only abstracts is not an adequate method to develop a comprehensive understanding of a topic. You need to review the entire paper and evaluate it for the science it is reporting.


RTL lab finds it difficult to understand  why you are convinced that RTL tests are not useful. However, your arguments are considered and RTL suggests the following:

  1. RTL would agree that a group of random control samples and a group of patient samples (blinded) be sent to RTL. Thus results can be compared. The methods on control group selection should be highly evaluated and agreed to by all reviewers prior to testing.
  2. RTL does not agree to your implications that the money is the only reason the test is performed. We have worked hard to reduce the price of the test in getting Medicare approval, Insurance payments, and reducing the price of follow up tests.

Further, in summary,  we believe that RTL’s test  look for the analytes of mycotoxins. To find these does not lend towards interpretation or diagnosis of any disease entity.   These tests are meant to help the physician make his/her diagnosis of the patient’s presenting symptoms.

Thank you for the opportunity to evaluate your presentation.

(RealTime Laboratories also wrote a response to the 2014 CDC paper.)


From Neil Nathan, M.D.:

While I agree that we need a lot more science to provide clearer answers for our patients, accepting what we now have to work with, I personally find the RealTime mycotoxin test of significant value.

The tests developed by Dr. Shoemaker are useful, but are often too general to help me with diagnosis and treatment. To be more specific, an elevated c4a or TGF beta-1 reflects inflammation, but in my complex patients who have CFS/ME, FM, Lyme with co-infections and mold toxicity, those levels do not help me to tease apart the components of their illness so that I can orchestrate treatment better.

High mycotoxins in the urine are very specific, and although we can question the absolute accuracy of those numbers, from a clinical perspective I can use that information to define what I think the patient needs, and in what order.

This brings up an important point. I do not think that those of us who treat CFS/ME are always looking at the same patient population. I practice on the West Coast, and my patient’s results agree quite closely with what Dr. Brewer is finding in the Midwest. Then again, he sees a patient population with a large infectious disease component, as do I.

I have worked with Dr. Shoemaker for a long time, and his population is much more of a “pure” mold toxicity group with much less infection.

Similarly, I have looked at Dr. Paul Cheney’s patient population, which looks quite a  bit different to me as well.

So I would take with a grain of salt any clinical results referring to mycotoxins from different clinic populations since we need to be sure we are comparing apples to apples ; I am not aware that we can do that very well, but I think it matters.

I would also like to be sure that we don’t miss the very important point, that Dr. Brewer and I have separately noted, (and I personally have no financial ties to any laboratory or supplement company) that the information we have gleaned from the RealTime test has led to significant clinical improvement in many of our patients who were treading water before we pursued this line of treatment.

From my perspective, that is the single most useful comment I can make. Our understanding of mycotoxin illness is in its infancy and we should stay open to all of the information available to us as we move forward.

It seems to me we all want the same thing: a lot more research so that we can make responsible diagnoses and provide the best medical care possible. The public does not realize how prevalent mold toxicity is. We desperately need this information, and we need it now.


From David Straus, Ph.D.:

One of the things I wanted to make sure in the Brewer et.al paper of 2013 was that this paper does not state anywhere in it that mycotoxin exposure is the CAUSE of CFS. The paper simply states an association so any one that states that it does is mistaken. Certainly a further examination of this association is warranted.

Regarding the surprise that people express regarding a lack of mycotoxins found in the control group: I will point out that in a 2004 paper (Brasel et al., “Detection of Trichothecene Mycotoxins in Sera from Individuals Exposed to Stachybotrys chartarum in Indoor Environments,” published in Archives of Environmental Health, June 2004, pp 317-323, vol. 59 (#6)), where we looked at the presence of trichothecene mycotoxins in human serum, we found only one positive in 26 serum samples (Table 4) from people who reported no exposure to Stachybotrys.

In that study, we were able to show that in sera from people who were in documented Stachybotrys infested buildings, there were significantly higher levels of MT than in normal human serum (people not exposed to Stachybotrys).

This test therefore was very good in showing a difference between mycotoxin levels from those with obvious documented Stachybotrys exposure and those who had no obvious Stachybotrys exposure.

In that paper we found 77.7% (Table 2)  of the samples where people with documented Stachybotrys exposure were positive for the mycotoxin examined and 34.6% of the samples (Table 3) with reported Stachybotrys exposure (but not documented) were positive for the examined mycotoxin. These studies were done before I ever met Dr. Hooper.

So this type of analysis is possible. We were the first lab to generate a quantitative test for trichothecene mycotoxins (MT) in human tissue and we did it looking at human serum.

As regards intoxication vs. ingestion and those who say it is impossible to get enough MT into the human body via inhalation, I say this. We actually measured MT levels in the air in Stachybotrys infested houses and although the levels were low (Brasel et al , “Detection of Airborne Stachybotrys chartarum Macrocyclic Trichothecene Mycotoxins in the Indoor Environment,” Applied and Environmental Microbiology, Vol. 71, pp 7376-7388, 2005), each time a person takes a breath in such a building, he or she inhales the MT in the air, and it is therefore only a matter of time before the inhaled levels rise to a potentially toxic dose.

Think how many breaths a person takes in a day. The result of the inhaled MT is additive.


From Jack Dwayne Thrasher, Ph.D.:

You have failed to understand and repeat exactly word for word what Hooper et al stated under section 3.2 Validation Samples. They followed standard protocols and  the tests were validated with and without spiked samples according to standard acceptable methodology in the control subjects as well as those exposed to mold. I trust that you will eventually become educated with respect to standard procedures for validation.

Furthermore, RealTime Laboratories is routinely inspected by CLIA with CLIA validation of the testing.

Finally, all papers that have been published have gone through peer reviews and accepted for publication without revision. The only exception to this is the paper on Sphenoid Aspergilloma. I had to add to the discussion the reasons why the diagnosis of sphenoid cancer was an error.



Everything in this article is based on my current understanding of the tests, gained as a result of reading the medical literature about them. I do not have any special knowledge about this topic beyond what is presented here.

Nothing in this blog or anything else that I might say should be taken as medical advice. Individuals who are sick should collect as much information as possible from various sources and preferably discuss their situations with a licensed healthcare practitioner before making any decisions related to trying to improve their health.


About the Author

Lisa Petrison earned a Ph.D. in marketing and social psychology (with a focus on research methodology) from the Kellogg School of Management at Northwestern University in 1998. She then worked as a tenure-track professor at Loyola University Chicago until becoming disabled with myalgic encephalomyelitis (ME) in 2001.

She now is mostly recovered and is the executive director of Paradigm Change.



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