Dr. Joseph Brewer: Nasal Fungi, Anti-Fungals and Junk Science

 Dr. Joseph Brewer: Nasal Fungi, Anti-Fungals and Junk Science

Application of the Principles of Integrity in Science and Medicine


1.      Science question: Does colonization of the nose with benign fungi result in production of mycotoxins in mucus that create chronic illness?

Answer: No.

2.      Science question:  Does consumption of food and beverages (all seen in daily fare in the US and in non-third world countries around the world) result in presence of mycotoxins in significant amounts in urine?

Answer: Yes

3.      What scientific studies done on consumption of foods/drink in #2 above show objective injury that casts doubt on inhalation as causative of CIRS-WDB?

Answer: None.

4.      Given the enormity of the scope of the problem of CIRS-WDB, can we allow guesses, assumptions and uncontrolled junk science to substitute for careful science?

Answer.  No.


In 2005, at the height of viciousness of mold litigation, defense interests loved using a California idea (“Geffcken”) that held that if a plaintiff couldn’t show the presence of the same mycotoxins in his body that were found in a wet building, then causation couldn’t be proven. The idea was unfounded for countless reasons, especially absence of logic and real hard evidence but insurance companies didn’t care, because they were winning court cases after an initial onslaught of big verdicts against them in the early 2000s. Fortunately, the mycotoxin mono-causation argument died out quickly but not before many worthy plaintiffs were denied compensation.


Earlier, defense interests tried to convince jurors that ingestion of moldy food was causative of the illness seen in patients with a chronic inflammatory response syndrome caused by exposure to the interior environment of water-damaged buildings (CIRS-WDB). That feeble attempt failed because of the ubiquitous literature showing presence of mycotoxins in countless foodstuffs that were consumed daily never made anyone ill. Moreover, properly controlled clinical trials never showed development of inflammatory effects following ingestion of so-called “fungal foods.” I will talk about aflatoxins in under-developed countries in a later essay.


A third attempt of defense consultants trying to deflect the truth of the issue rapidly followed publication of two studies from the Mayo Clinic, each published in 2005 (seereferences 6, 7 in CRS_ampho B_ not substantiated_01_13_2015). Mayo said fungi were causing rhinosinusitis and an anti-fungal, Amphotericin B, a drug with significant toxicity, could be used safely in a nasal rinse to help chronically ill patients. Here was new fodder for a group of defense-hired docs who were basically paid to say anything they could get away with to defeat plaintiffs. This work followed two poorly received studies from the same group of ENT docs from Mayo published in 1999 and 2002. For reasons unclear to me, the response of the ENT academic community was rapid and unified in one voice in 2005: NO WAY, Mayo (references 11-23 in same bibliography as above). Suddenly, anyone assuming use of Amphotericin B for treatment of fungi in sinuses made sense was ignoring clinical trials, double blinded studies, Cochrane reviews and basically were dangerously close to committing malpractice.  When Amphotericin caused toxic reactions, as it did in 33% of patients that toxicity was solely a failure of the duty of the physician to protect the patient (there was a duty; the duty was breached; the breach caused the injury; the injury caused damages). Thankfully, as we soon saw a remarkable rise in newly found antifungal resistance in benign, nasal-visiting fungi (seemechanisms of resistance to fungicides_1_9_2010), such unsupported use of Amphotericin B never came close to becoming the standard of care.


But in 2015, use of anti-fungals are back, being pushed by small groups of docs, with no data that withstands criticism to support their dangerous and unfounded use of drugs that make no difference in health. Dangerous! Unfounded!


But the defense plowed on, now saying that a little bit of mold in a living room was no big deal, but in the nose, yes the nose, egad, Disaster (some defense guys talk that way)! It didn’t take too long for plaintiff docs to destroy that next bogus defense idea, as essentially 100% of people had fungi traveling through their noses every day. Cases were shown to have 87% incidence of positive nasal cultures but controls had 91%. What does a positive nasal culture mean? Nothing. Nothing at all.


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)) [seebiblio_nasal sinus_epithelium_cell type_12_19_2014, references 1-21]. 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). The paper by Samuel Lai and his colleagues from Johns Hopkins published in Adv Drug Deliv Rev 2009; 61: 86-100 on the micro- and macro-rheology of mucus is a must read.


The defense didn’t argue much more about Mayo’s fantasyland ideas.


In 2006, at a conference arranged by Sharon Kramer for Senator Kennedy’s Senate Health, Education and Labor committee, one of the Mayo authors, David Sherris, by then having moved to SUNY-Buffalo with his Mayo colleagues, presented an elegant talk about fungi in sinuses with illness not due to production of toxins but due to production of an inflammatory compound, IL-13.  Dr. Sherris taught us that the source of the rhinosinusitis was eosinophilic major basic protein (MBP), stimulated to be released by eotaxin. At the 2011 International Fungal Conference, sponsored by Dr. Eckhart Johanning, in Albany, NY, Dr. Eugene Kern, now also at SUNY-Albany and having also been a Mayo author, was discussing the mysterious role of MBP and eotaxin. He was unaware that eotaxin is regulated by genes controlled by TGF beta-1, a major player in CIRS-WDB. Fungi in the nose had nothing to do with the illness at all! Indeed, the link from TGF beta-1 to eotaxin was a primary mover in inflammatory diseases characterized by eosinophilic infiltration in lungs, esophagus and possibly liver as well.


Actually, presence of fungi in sinuses (never the nose) stimulated migration of eosinophils to the inside surface of sinuses (see Eosinophils_MBP_EMT_TGF beta-1_01_14_2015), where they released packets of MBP which killed Alternaria fungi, the genus most commonly found there, (with Cladosporium next in the list of common colonizers).  Note:  neither genera of these fungi contains species proven to be to date as being toxigenic in WDB. As our work on TGF beta-1 suggested, and literature has confirmed, the release of eotaxin was the result of effects of TGF beta-1 on transcription factors changing cell types (epithelial to mesenchymal transformation; EMT). Dr. Kern showed interest as his group had already abandoned the idea of fungal infection and use of anti-fungals.


The reader might find of possible interest an essay published on www.survivingmold.com, “Owls Under a Beaver Moon” for additional information on A(w) and fungal growth (or lack of same in lower A(w)). And the Beaver Moon of October remains of interest this time of year.


By 2011, no one was talking about fungi making mycotoxins in noses but the immune literature showed cell-type transformation caused by TGF beta-1 was hugely important in the role of MBP in lungs, esophagus and sinuses. NOT NOSES.


Bizarrely, in 2013, we started seeing reports that a CFS-treating physician, Joseph Brewer, now ordering ELISA urinary mycotoxin studies, was finding problems and claiming that over 90% of people with CFS had urine full of mycotoxins. Therefore, the urine meant something was causing them to be ill from mycotoxins. His paper on mycotoxins and CFS was shredded by Gary Rosen as junk science earlier this year (Urine Testing for Mycotoxins, Junk Science or Not? www.Mold-Toxins.com). Please also see the Round Table on www.survivingmold.com for a frank discussion of ELISA testing, especially in urine. ELISAs are never specific without showing validation of the antibody used (not done) and absence of activation of the antibody by epitopes of the putative antigen (not done); nor reliable without stringent controls.  His reports on the methods used to collect urine did not show use of such stringent controls.


Moreover, in his report, he tried to tell us that while he had no controls, he would use controls from a prior study that never showed presence of urinary mycotoxins.  No comment about dietary restriction was made. Dr. Rosen goes into additional detail unveiling this paper as scientific junk. I will return to the idea of no controls showing mycotoxins when I discuss dietary effects of foodstuffs. See also the Centers for Disease Control and Prevention (CDC) publication, Morbidity and Mortality Weekly Report (MMWR) of 2/15. I have not read any authoritative reference in this field ever suggest that large groups of people who eat real food and drink real beverages won’t show some mycotoxins in urine.


But Dr. Brewer did not express concerns about reliability of ELISA assays in 2013 just as he also had not objected a few years before to use of an ELISA purporting to show presence of a retrovirus called XMRV.  We all heard of Dr. Brewer’s use of anti-retrovirals, including some compounds used in treatment of HIV. I had personal contact with one patient who told me of benefit from this viral killing concoction. We then witnessed the scientific community rising against the developer of the XMRV research, Dr. Judy Mikovits. I suggest reading her book, Plague, published in 2014, for another perspective on the XMRV debacle. The XMRV ELISA was pulled from the market.


I actually have no idea what Dr. Brewer was treating with potentially toxic HIV drugs and I had no idea what his “CFS” patients actually had. But he wasn’t the only prominent CFS researcher taken in by the XMRV idea. What an embarrassment to those docs! Sadly, we are seeing more than a few now becoming self-appointed experts in human health effects caused by exposure to moldy buildings!


Dr. Brewer then wrote another paper, the subject of this junk science investigation, trying to convince us that fungi found in noses were making mycotoxins, in turn then showing up in urine. Further, he claimed that in three patients (including an 8-year old!) he could correct their chronic health problems by using anti-fungals as part of a protocol that employed no proteomic or genomic factors.  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. The cases themselves are not persuasive. There are no controls.


Meanwhile, the same results of dietary sources of urine mycotoxins appeared in countless studies were found year after year in peer reviewed documents (seemycotoxins_dietary measurements_6/25/2015; mycotoxins in food_2/27/2014; ochratoxin A_12_17_2014; deoxynivalenol_trichothecene_DON_12_04-2014). The papers I cite are largely written before Dr. Brewer’s two publications. As an aside, I note Dr. Brewer claims to be reviewing literature carefully yet omits hundreds of long-published studies that would impeach his ideas.


The CDC remained silent on this topic until February 20, 2015.  In a weekly publication, the MMWR, the CDC commented on “Use of unvalidated urine mycotoxin tests for the clinical diagnosis of illness-United States 2014. In just over two pages, this missive (64(06); 157-8) rips apart all aspects of the urine testing cited by Dr. Brewer.  Who are we to believe?


We will return to this topic to discuss the absence of academic support for health consequences caused by inflammatory illness (CIRS-WDB) after ingestion of mycotoxin-containing foods despite the irrefutable data showing sometime massive levels of urinary mycotoxins after eating particular foods.


So what have we found as I write this in October of 2015? First, the research principles that all members of the Professionals Panel of Surviving Mold have agreed to are relevant for us.  Second, sloppy ideas, sloppy science, sloppy medical practice and downright money-grabbing are rampant in the “mold” field. All deception and flawed science must stop. Patients need to become better-educated consumers.


Back in the day when there were just a few of us testifying for plaintiffs and treating mold patients, we had enough to worry about with defense fabrications.  Now that peer reviewed literature has shown that we are in the Golden Age of therapy, with a major paper on genomics of treatment of CIRS to appear next month, a major concern is the rising incidence of unscrupulous profiting on human suffering caused by moldy buildings.  I hear it every day. When someone says they are a mold doctor, demand to see their credentials, publications, protocols and annotated use of peer reviewed literature. When you see they have nothing, or are using someone else’s published work as their own, without accreditation, send us a copy. We will publish their names and their attempt(s) at misrepresentation.


I submit to you that integrity in medicine in CIRS-WDB begins with published peer reviewed studies that hold up to scrutiny.  Real Mold Docs must be able to pass a rigorous test (provided through www.survivingmold.com) and must be able to recognize dubious practices. Use of anecdotal data (“well, it worked for me”) is not science. And use of worthless nostrums provided by the handful with promise and hope that simply are designed to make money must be condemned. 


Our first step in finding understanding is to cast out our false knowledge (with thanks to Aldous Huxley). We looked at Dr. Brewer’s publications hoping to find understanding but we did not. All we found was JUNK science!


Stop the fungal nasal cultures; stop the anti-fungals. Go back to rigorous science. Our patients are relying on us to tell them the truth. When the urinary mycotoxin testing can satisfy the demands of science, let us give its proponents a blinded trial to assess validity.





The paper we read that proposes the nasal fungal/mycotoxin hypothesis, written by Joseph Brewer MD and colleagues, “Chronic Illness Associated with Mold and Mycotoxins: Is Naso-Sinus Fungal Biofilm the Culprit?” It is published in Toxins in 2014, Volume 6, pages 66-80.


We refer you to the Research Criteria of CRBAI and the Professionals Panel of Surviving Mold.  Please also review the criteria for Junk Science published by the Professionals Panel of Surviving Mold.


NB: This paper breaks a record.  It has ALL ten (of ten) criteria that each taken singly can define Junk Science


At least ten times in the past few months www.survivingmold.com has received an inquiry regarding practitioners who advise (1) use of nasal rinses to identify fungi that (2) then are reputed to cause illnesses from fungal manufacture of mycotoxins.  Therefore, the nasal fungal practitioners believe (3) that treatment with anti-fungals for months on end without any defining parameters will result in abatement of the undefined illness. There is no published data on a series of cases and controls regarding this idea.


Sounds like this idea would be easy to confirm or refute.   What we look for are reliable methods and credible data presented according to standard scientific principles. We found nothing.


OPINION: Dr. Brewer’s paper needs to be retracted as unsuspecting but desperately ill patients are at risk if they, or their treating physician, actually believe that this paper presents an acceptable method to correct chronic illness.


Fact check: A whole series of excellent studies (NB: remember these studies exist when we talk about specific Junk Science Criteria) have shown repeatedly that not only are fungi ALWAYS found in everyone’s nasal rinses but the environmental conditions (“A(w)” or water activity) make it impossible for such fungi, benign as they are known to be, to serve as the source of any reservoir of mycotoxins that could theoretically (but not actually) make people chronically ill.  Further, the idea that fungal colonization of the nose bears any resemblance to what is actually going on in the special environments of actual sinus cavities is not confirmed.


How could anyone take the nasal/mycotoxin idea to the next step, that of treating patients for months with unproven (and potentially dangerous) therapies?  Anti-fungal use is not benign (and not new): Amphotericin B is poorly tolerated and caused all sorts of problems for at least one third of people that use it. And taking itraconazole for months on end is just plain dangerous.  All of the azole drugs can rapidly create fungal resistance.  Frivolous use of anti-fungals should be rapidly condemned by all academics and individuals concerned with safe-guarding patient care as they were the last time this bogus approach to fungi in noses was espoused in 2005. Please read the chapter on benomyl in Surviving Mold to review what happened with benzimidazole. Within a few years of introduction of this fabulous fungal killer across the globe, we saw emergence not only of resistant strains of fungi, but the genes for resistance made them potentially aggressive threats to human health. DuPont was forced to pay out over $1.5 billion in damages for crop injury but never paid a nickel for human health effects from the mutated fungi.


The argument against the role of fungi in nasal rinses goes on and on: (1) nasal mucosa is not the sinus; (2) trapping fungi in mucus in nose is a defense mechanism to eliminate inhaled fungi; (3) the organisms aren’t growing and therefore aren’t making metabolically “expensive” compounds of secondary metabolism like mycotoxins; (4) the organisms aren’t making new fungi; (5) there is no such thing as fungal sinusitis that is identified by nasal rinses that is silent clinically, i.e. sinus infections do exist but aren’t illnesses that don’t cause local symptoms; (6) this issue has been extensively reported in many clinical studies with one and only one conclusion: there is no role in any acceptable science to treat benign nasal fungi with long and expensive courses of anti-fungals without any objective evidence that such therapy has ever shown consistent benefit. And  (7) no one, as we are asked to believe in the Brewer paper, can suggest that “CFS” of 35 years duration is due to presence to a benign fungus vacationing in someone’s nose now.


Imagine the discussion in a Daubert hearing in a court case about causation of illness from a specious N=1 study about longstanding illness from fungi growing in the sinus when they never have been shown to grow in the sinus and make toxins at the same time.


Q  “Tell me, doctor, you have testified that fungi found in sinuses can make toxins that create CFS and that in your opinion this factor caused the disability of Mrs. Conidia. 

A:  Correct.

Q:  What was the organism found in the patient’s maxillary sinus 35 years ago?”

A.  “There was no culture.”

Q.  “Can you present any evidence that will prove to us as we sit here today that the patient had fungi making mycotoxins to cause CFS back then.”

A. “There is no proof. All I can say it might have been true.”

Q.  “What makes you think it might have been? Isn’t it possible the patient could have one of ten thousand events happening back then-actually you don’t know when.”`        

A.  “Well, you can’t say it wasn’t, now can you?”

Q. “Doctor, this is a court of law.  We are talking about science and truth here, not some pie-in-the sky speculation. You have testified that Mrs. Conidia is sick now because my client had a moldy outhouse that was used by Mrs. Conidia when Mrs. Conidia was a child.  Did you see her then? Did anyone who saw her then make a comments such as yours? Did anyone who has seen her since makes such a comment? What basis do you have to convince this judge that you should be allowed to testify in this case?”

Judge: “Doctor, can you support your opinion with any published literature from informed professionals that supports your contention to a reasonable degree of medical certainty?”

A.  “No.”

Judge: “The witness may step down.  Motion to exclude is affirmed.”

* * *


But the truth be known, I have become accustomed to hearing all sorts of other unsupported ideas in this field brought forth from the “fringe.”  Perhaps we need to know when an idea on causation of illness supported is.  Start with an idea that is based on logic, physiology and science; and tested with proper informed consent using a reasonable study design. New ideas become paradigms of new science when the “anomalies” identified are observed by others and expanded. Thomas Kuhn, in his classic book, The Structure of Scientific Revolutions, taught us these principles and more back in 1965. For those who want nasal rinses to become a new paradigm of science, has any one used “Dr. Kuhn terms” about a revolution in thought about illness acquired following exposure to the interior environment of water-damaged buildings? No; since we have seen no science from the fringe groups, would we expect a positive answer to the anomaly question?


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. 


Given that President Obama is mounting a $1.3 billion program (3/28/2015; President’s Council of Advisers on Science and Technology; USA Today, page 3B) to stop inappropriate use and over-usage of antibiotics, one that is broad but non-specific in scope, let me volunteer to take such unscientific and inappropriate use of anti-fungals to the national chopping block. Cut it out!


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. Please cease and desist!


I am wondering what is driving the misguided idea that fungi magically can become toxigenic inside the nose. Sure some docs have claimed that anti-fungals help but have never presented any data (NB: odd, isn’t it? If a therapy works, aren’t there measures to confirm the subjective change?). I read Dr. Brewer’s paper looking for the elements of good research. I found none. I looked for elements of Junk Science; I found the Comstock Lode of Junk.


Understanding that the underlying peer review process provides a basis to screen out aberrant papers so that they won’t be published, I have to wonder (1) what were the possible reasons for submitting this manuscript in its existing form? And (2) what peer reviewer agreed that publication was merited? We don’t know.


I remember the wonderful evenings of speculation about testing and treatment for CIRS in the early years. We wondered if there were an endogenously produced neurotoxin. There is some evidence that suggest that Charcot Marie Tooth disease (both Types A and B) might do so and maybe toxin production has accompanied one or two people’s illness from fungal infection but no none has ever shown that nasal colonization actually creates a CFS-like clinical picture.  Note I don’t say that “some think that is the case;” no proof has ever been shown.


What we needed then and will always need is sound science based on integrity of the highest order. Let’s go back to some basics. Take a look at the Round Table in the www.survivingmold.com section called Integrity on Medicine and Science. Let us see how the Brewer paper fares under established criteria for junk science.


Please note the parallel references from 1) Gary Rosen 2) Elena Page of NIOSH/CDC writing in MMWR; 3) papers reviewing the absence of illness related to aflatoxin exposure in the U.S. and 4) a litany of papers showing that dietary contributions to finding mycotoxins in urine are nearly 100%.




1.      The first junk of ten Junk Criteria focuses on methods. Unfortunately, in the Brewer paper there are none. This study is not prospective! Causation cannot be concluded. This study is not even a case/control study either. We can’t compare the three trivial cases included to anything as no actual biochemical or environmental data is presented. The paper claims it contains a review of the literature but this claim is unsupported. I presented seven bibliographies of papers that would be reasonable to see referenced in any “complete review.” None are. Where are the references from past and current literature that show an even-handed and thorough review? Just look at the short list of academic papers included above that by themselves destroy any credibility of the ideas of the authors regarding use of anti-fungals and nasal cultures.


What we see are a seemingly interminable series of speculations and open ended attempts to link unrelated issues presented as an argument purported to withstand criticism. That attempt fails.  We don’t even see logical concatenation of the far-ranging leaps of thought in this paper. Frankly, with no methods, there is no paper. JUNK IT.


2. Control groups.  There are none. Table Two is supposed to show controls but no data are presented. This table found in Brewer’s paper is at best deceptive as he states that no controls showed mycotoxins in urine, citing another paper that doesn’t show any controls either.  Fact check: only a few papers he lists actually tested mycotoxins in urine.  The few studies that reported mycotoxins are tainted by the criticism from the CDC in MMWR; mycotoxins are found nearly ubiquitously in people who eat food! Where are the dietary data clearing the putative control group from consumption of the many foods found to contain mycotoxins?  And even if the urine testing were accurate, where is the discussion of polyclonal aspects of ELISA testing? Without such validation, how do we know an assay for one kind of trichothecene won’t light up when other trichothecenes, like vomitoxins (DOC) are ingested? JUNK IT.


3. Unsupported speculation and dubious authorities. These two elements describe this paper. Reference 63 ­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­­ is vital to Brewer’s argument yet it is simply a poster. We cannot find out anything about his study from the reference. What reviewer let that unpublished, uncontrolled small study pass?  JUNK IT.


4.  Variables are non-existent in scope. There is no attempt to present any information to sort out any variables that might apply both to a 71 year old patient with 35 years of illness to an 8 year old girl with enlarged turbinates (major confounder!) who is alleged to be ill for a while. The same criticism regarding rigorous case analysis applies to case 2. No reasonable, informed member of the mold field could possibly agree these three cases aren’t without marked variability. JUNK IT.


5.      Dr. Brewer says he has no conflict of interest yet he joined the clinical staff of the Real Time Lab in 2014. When did that contact arise? Dr. Thrasher does not disclose his role of medical director of RTL, though his CV posted in the GIHN website (accessed 3/12/2014) shows such conflict from at least 2011.Dr. Hooper does identify himself as attached in some way (does not specify: owner) to Real Time Labs. JUNK IT.


6.  Biased populations. Cases 2 and 3 are patients evaluated in a different paper co-authored by Dr. Thrasher. We are given no biochemical data to confirm they are cases as published in the Expert Mold Treating Physicians Consensus Report, co-authored by Dr. Thrasher in 2011. JUNK IT.


7. Absence of methods to confirm specificity of ELISA. The reference to Dr. Hooper’s work shows RTL states his antibody detects roridin. Does it detect other trichothecenes? If so, does it detect DOC and call it the same as all other trichothecenes?


Dr. Brewer says without reference or basis that the urine test is specific. Dr. Hooper fully acknowledges the test is polyclonal (personal communication 10/23/2013). Please see the Round Table on Integrity in Medicine and Science pages. JUNK IT.


8.  Treatment claims. Dr. Brewer makes a progressive series of statements that might lead an unaware reader to believe that intra-nasal therapies are the gold standard for treatment for patients sickened by WDB. But he presents no data. None. He relies on personal communications from Dr. Michal Gray but presents no data. Dr. Brewer’s attempt to use Mayo Clinic, amply refuted by multiple studies, and amply refuted by references provided earlier, to support his hypothesis is disingenuous at best. He discusses use of EDTA to disrupt biofilm but presents no evidence any of his three cases had fungal biofilm. This is a serious error in this paper. To fail to present any data to support the preferred therapy is anathema to any clinician. JUNK IT.


9. IRB approval.  There is nothing here. No clinician can escape the reality of IRB approval in this era of regulation of science writing. To make treatment suggestions without informed consent and clinical data based on informed consent is fatal for publication. JUNK IT.


10. Thorough references. Despite including 86 references, the failure to review and comment on papers not supportive of his hypotheses means failure for this criterion. 


Dr. Brewer has scored 10 out of 10 failures to meet standard elements of good science. Any single failure is usually enough to make a paper junk science.


How does Dr Brewer fail thoroughness? Simple, he ignores the ubiquitous dietary sources of mycotoxins. The literature is full of references to show that dietary mycotoxins give assay positivity for urinary mycotoxins. Anyone who wrote up 86 references could have spent the 17 minutes I did to develop a roster of studies that show both trichothecenes and ochratoxin moieties on urine (there are at least 19 variations of ochratoxin found in urine). Dr. Brewer failed to even cite one study that is diametrically opposed to his ideas and to make it worse, cites 2 papers by Ebbens group as supporting the idea of nasal Rx of anti-fungals. Incredible.  Dr. Ebbens and his colleagues have published extensively showing why anti-fungals make no clinical improvement!  JUNK IT.


Please help your fellow humans. If you see them taking nasal anti-fungals or following what the CDC calls unproven lab testing protocols, make them stop.  Take away their credit cards and make them read the references included herein. And then beg them to stop.

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