Article Summary: I decided to look into the controversy around the use of antifungal nasal sprays in this article. If you read MARCoNS – Fungal Colonization, you know that Dr. Brewer and Dr. Nathan are suggesting that using an antifungal nasal spray is a way to treat mold toxins (mycotoxins). More specifically, they suggest that some fungi in the nose produce mycotoxins and that treatment with an antifungal nasal spray lowers mold toxin levels in the urine – as measured by RealTime labs.
As I’ll show, the significance of of Dr. Brewer’s work and the urine mycotoxin test from RealTime labs is limited. Neither come close to showing nasal fungi create toxins that impair health. Don’t get me wrong. I do believe a trial of a nasal antifungal makes sense for some chronically ill individuals. However, when you look at the data, there is no connection between antifungal nasal spray and treating nose mold, RealTime lab mycotoxin levels, and Chronic Inflammatory Response Syndrome (CIRS).
Hopefully this article will put to rest the suggestion by some that RealTime testing can be used to determine if a person suffers from mold toxicity and indicates the presence of nasal fungi. It does not. Reading your daily horoscope is about as accurate as RealTime testing for these purposes. In this article, I’m going to cover the different sides on the topic of nasal antifungals, discuss how biotoxins enter the brain, and describe how to make your own high-quality antifungal nasal spray. March 31, 2016
- Dr. Brewer and Dr. Nathan on Anti-Fungal Sinus Therapy
- How Accurate Is RealTime Testing?
- RealTime Testing Accuracy Chart
- What Does Dr. Brewer’s Nasal Research Tell Us?
- Who’s Right – Dr. Shoemaker or Dr. Nathan?
- Why Using Nasal Antifungals May Help
- Derealization Caused by Inhaled Biotoxins
- My Experience with Pharmaceutical and Do-It-Yourself Nasal Antifungals
Dr. Brewer and Dr. Nathan on Anti-Fungal Sinus Therapy
Below are my notes from the June 5, 2015 interview of Dr. Joseph Brewer on The Cutting Edge of Health and Wellness Today by Dr. Neil Nathan. In this interview, Dr. Brewer discusses findings from his latest paper regarding treating patients with nasal sprays that consist of an anti-fungal and an EDTA biofilm buster. Of note in this interview are the facts that in this latest study of 151 patients with chronic illness, 94% had at least a 25% reduction in symptoms. Furthermore, over 25% completely recovered! These were folks that just weren’t getting better with other therapies. In addition, both Dr. Brewer and Dr. Nathan mention that treatment may take a year or longer and needs to be ramped up very slowly for those that are particularly sensitive due to impaired detoxification. Many other interesting points are made as outlined below.
- Dr. Joseph Brewer is an Infectious Disease Specialist in Kansas City, a Clinical Professor of Medicine at the University of Missouri in Kansas City, and has special interest in Chronic Fatigue Syndrome, Lyme disease, HIV and AIDS. He has published three papers:
- Detection of Mycotoxins in Patients with Chronic Fatigue Syndrome 2013
- Chronic Illness Associated with Mold and Mycotoxins: Is Naso-Sinus Fungal Biofilm the Culprit? 2014
- Intranasal Antifungal Therapy in Patients with Chronic Illness Associated with Mold and Mycotoxins: An Observational Analysis 2015
How Accurate Is RealTime Testing?
In the 2009 paper Mycotoxin Detection in Human Samples from Patients Exposed to Environmental Molds, the president and medical director of RealTime Labs, Dr. Dennis Hooper, along with others performed testing to determine the effectiveness of urine mycotoxin testing. I was interested in seeing this study because I remember Dr. Shoemaker commenting that RealTime used polyclonal antibodies to detect mycotoxins instead of monoclonal antibodies. Polyclonal antibodies are supposedly susceptible to false positives. A false positive result means the test shows you have mycotoxins when you really don’t. I was interested in seeing for myself how accurate the testing really was.
I found part of the answer to my question regarding accuracy in Table 2, “Sensitivity and Specificity of Mycotoxin Tests”. In this table, the authors list the “sensitivity” and “specificity” for urine mycotosin testing. In terms of sensitivity, they found that urine testing was 94.5% for Trichothecenes, 70.6% for Aflatoxins, and 17.4% for Ochratoxins. In terms of “specificity” the testing was 100% accurate for all three mold toxins. By the way and in case you didn’t know, Trichothecenes mycotoxins come from wet loving Fusarium and Stachybotrys mold. Aflatoxins mycotoxins come from Aspergillus mold and Ochratoxins mold toxins come mainly from Aspergillus and Penicillium molds. Both Aspergillus and Penicillium molds like damp conditions.
Getting back to Table 2, by definition, “sensitivity” is defined as the percent of people that actually have mycotoxins that will test positive for mycotoxins. Conversely, “specificity” is defined as the percent of people that do not have mycotoxins that will test negative for mycotoxins. Looking over Table 2, you see that according to the RealTime study, if you do not have mycotoxins in your urine, then there is a 100% chance they are correct. In particular, the “specificity” was 100% for all three types of mycotoxins. However, if RealTime testing shows you do have mycotoxins in your urine, the tests will come back positive showing mycotoxin levels 94.5% for Trichothecenes, 70.6% for Aflatoxins, and only 17.4% for Ochratoxins. So according to this paper, RealTime testing does not produce any false positives but may very well show false negatives.
So this is what RealTime is purporting. Now let’s look at why some of these percentages can’t always be trusted. Unfortunately, RealTime uses “polyclonal” antibodies to determine the presence of Aflatoxins. In Round Table: How do I know a scientific paper isn’t junk?, microbiologist Francis W. Ruscetti and molecular biologist Judy Mikovits state that “polyclonal antibodies by definition recognize more than one antigen”. In this case, the antigens are mycotoxins. In other words, for the 70.6% of the time that RealTime says a person has Aflatoxins in their urine, many of these may be false positives; they may have much lower or no levels of Aflatoxin.
Continuing on with the discussion about the accuracy of RealTime testing, at 2:25:00 in the 2015 presentation, When Inflammation Becomes Chronic, Dr. Shoemaker says that in order for urine mycotoxins testing to at least have a chance of being accurate, it’s important to go on a mycotoxins free diet for at least one month prior to testing. Dr. Shoemaker mentions that the mycotoxin called Ochratoxin that is made by Aspergillus and Penicillium molds is commonly found in foods such as cereals, coffee, dried fruits, wine, beer, cocoa, nuts, beans, peas, bread and rice. There are plenty of studies supporting this claim.
He also points out that Deoxynivalenol (DON), also known as Vomitoxin, is prevalent in grains and is a type of Trichothecenes that will influence urine levels. As a consequence of these mycotoxins being in grains, they are also found in meat, especially pork and poultry. So do these statements by Dr. Shoemaker matter when it comes to the accuracy of RealTime testing?
In the case of Aflatoxin and Ochratoxin, it quite likely does matter. Is RealTime using tests that can discriminate between Aflatoxin and Ochratoxin found in moldy buildings versus Aflatoxin and Ochratoxin found on food? Not that I’m aware of. If they aren’t, then when a test comes back positive for these two mycotoxins, how do you tell if they’re from nasal fungi, a moldy building, or moldy food? You can’t.
On the other hand, when it comes to Trichothecene, RealTime uses a test antibody for macrocyclic Trichothecene. Given that Vomitoxin common found in food is non-macrocyclic and the Trichothecenes found in moldy buildings are typically macrocyclic, Dr. Shoemaker’s point is moot when it comes Trichothecene – the mycotoxin from Stachybotrys. RealTime testing results for Trichothecenes should be solid.
Dr. Shoemaker finishes his comments about RealTime by pointing out that the 2009 paper by Dr. Hooper does not use a good control group – people that have good ERMI scores and have been on a mycotoxin free diet. In the RealTime study, the authors write, “Specimens from patients with no known toxic mold exposures were tested…” In other words, it may be entirely possible that many of those in the control group actually had measurable levels of mycotoxins in their urine even though RealTime testing showed negligible levels 100% of the time for this group. Said another way, if your RealTime test comes back negative, it’s unclear if your urine really is free of mycotoxins. Not to mention the fact that having mycotoxins in your urine is not proof of a fungal infection in your nasal cavity.
The bottom line is that if RealTime says you have mycotoxins in your urine, then it appears they are likely right for Trichothecenes and Ochratoxins. Although when it comes to Ochratoxin, you won’t know if you have high levels are from moldy food or being in a moldy building. The statistics say they will miss 5.5% of people that actually have Trichothecenes and will say there are no Ochratoxins when there really is in 82.6% of people. When it comes to a positive result indicating the presence of Aflatoxins, the result simply can not be trusted. Furthermore, for people with testing that comes back negative for any of the three mycotoxins, they may actually have levels of mycotoxins in their urine when the testing says they don’t.
For us moldy folks that tend to lean toward the more paranoid, it’s unfortunate the testing isn’t good at finding Aflatoxin and Ochratoxin. In addition, when testing comes back positive for Aflatoxins, positive for Ochratoxin, or negative for all three mycotoxins, it can’t be trusted. A person really has to know the ins-and-outs of this test to glean useful data. Oh well, it’s always good to know the facts about testing accuracy.
Note: For another excellent review on the work of Dr. Brewer and RealTime labs, see Lisa Petrison, Ph.D. article:
Looking at the Literature About Mycotoxin Urine Tests
|RealTime Testing Accuracy|
|Aflatoxin||unknown (1)||unknown (3)|
|Ochratoxin||unknown (2)||unknown (3)|
- unknown (1): RealTime says it’s 70.6% but there can be false positives so your levels may be much lower.
- unknown (2): RealTime says it’s 17.4% but some of those tested lived in moldy homes and ate moldy food. As such, if your test comes back positive, you may actually have much lower levels.
- unknown (3): RealTime says it’s 100% but some in the control group lived in moldy homes and ate moldy food. As such, if your test comes back negative, you may actually have much higher levels.
What Does Dr. Brewer’s Nasal Research Tell Us?
In a September 2015 article written by Dr. Shoemaker titled “Dr. Joseph Brewer: Nasal Fungi, Anti-Fungals and Junk Science“, Dr. Shoemaker lays out his arguments as to why nasal antifungals should not be used except in those cases where CAT scans or some other proven diagnostic method (like a nasal swab from MicrobiologyDX) is used to confirm the presences of mold colonization. Here are some of the points he makes and my comments.
- Roughly 90% of people with and without health issues have some level of mold in their noses. In addition, the mold in people’s nasal cavity and sinuses simply does not have enough water to make mycotoxins. The water activity (Aw) needs to be around 80% for mold to make mycotoxins. It’s about 20% in nasal and sinus mucus. That’s not nearly enough of freely available water. My comment – Dr. Shoemaker does a good job showing why there simply isn’t enough water for fungi to make the energy intensive chemicals called mycotoxins. Still, maybe fungus in one person’s nose isn’t a problem but it is in another? Isn’t it possible that the fungi could be making some other unknown inflammagens?
- The study, Mayo Clinic Study Implicates Fungus as Cause of Chronic Sinusitis has been discredited with follow up clinical trials, double blinded studies, and Cochrane reviews (systematic review of the available research). My comment – Follow up work to the Mayo study is showing that mold in the nose is not the real issue. This does not negate the fact that ENT doctors in the Mayo study, Dr. Sherris and Dr. Ponikau, found that repeated Functional Endoscopic Sinus Surgeries (FESS) were no longer needed when folks with chronic sinusitis used nasal anti-fungals as explained by CIRS advocate Sharon Karmer in the comment section of Looking at the Literature About Mycotoxin Urine Tests. So using anti-fungal nasal sprays can be helpful but it’s unclear why. Dr. Shoemaker purports its all about how high TGF-beta1 causes an inflammatory response in the sinuses. You can see why Dr. Shoemaker is upset about Dr. Brewer and Dr. Nathan making claims that mold in people’s noses is a problem. There just isn’t any data to support this claim.
- The antifungal, Amphotericin B used in the Mayo study and by Dr. Brewer on nasal fungi causes toxic reactions 33% of the time. The overuse of antifungals causes mutant and resistant strains of fungi to develop. My comment – this is one more good reason not to use Amphotericin B and to limit azole antifungals. However, for people that have diligently been trying to get better for a long time, I think its OK to use a tame antifungal like Nystatin and even an azole like Itraconazole especially when there are gut issues. When it comes down to it, if a person is really concerned about the development of mutant fungi in response to the overuse of antifungals, they should really focus their attention on the chemical industry and conventional agricultural. There is a whole lot of blame that needs to be laid on leaders in this industry that have turned a “blind eye” to the known implications of using too may antifungals. Leave the poor soul that has suffered for year after year and is trying to carefully evaluate treatment options out of the equation.
- A lot of food has a degree of mycotoxin contamination. These mycotoxins show up in the urine. My comment – along with the human studies Dr. Shoemaker sites, there are plenty of animal studies that correlate ingestion of mycotoxins and elevated levels in the urine.
- Eating mycotoxin laden foods does not cause CIRS. My comment – Although human studies may not be present showing a correlation between eating moldy food and the specific adverse health effects in CIRS, there is loads of data from the agricultural industry showing that when animals eat moldy feed, they get all sorts of illnesses including reduced productivity, increased disease incidence, chronic damage of vital organs and decreased reproductive performance.
The contention by Dr. Brewer and Dr. Nathan that mold in the nasal cavity and sinuses is producing mycotoxins has been shown in many ways to be highly questionable. There are serious issues with Dr. Brewers study methodology along with lots of unaccounted for confounding factors – moldy food, moldy homes, lack of controls, lack of specificity, conflicts of interest, and so on. My comment – skimming over this article and Urine Testing For Mycotoxins Junk Science or Not? shows in many ways that Dr. Brewer and Dr. Nathan do not have sufficient evidence to make the claim the nasal fungi produce mycotoxins and that these mycotoxins are showing up in urine. Dr. Brewer’s papers fall way short of supporting this position.
Not making it very clear to the general population that very little can be concluded from Dr. Brewer’s work and RealTime urine testing results in a lot of confusion. For example, I often hear doctors and individuals suggest that the way to test for mold induced illness is with urine testing. This is just wrong and my concern is that a lot of people won’t get the treatment they need because of it. All we really know from Dr. Brewer’s work is that when nasal antifungals were applied over a period of time, some chronically ill folks felt better
There needs to be a whole lot more emphasis put on the fact that positive RealTime urine test results do not mean a person has nasal fungi producing mycotoxins. That claim is about as substantial as my suggestion that nasal antifungals may provide some protection against toxins entering the brain via the olfactory system. At this point, it’s just a lot of guessing! This type of unqualified conjecture regarding mold and its adverse health effects hurts the mold community. This doesn’t mean Dr. Brewer’s work doesn’t have value. It’s just that he and Dr. Nathan need to be a lot more clear that they’re just guessing about nasal fungi.
Who’s Right – Dr. Shoemaker or Dr. Nathan?
In November 2015, Dr. Nathan responded to Dr. Shoemaker’s article in Junk Science or Junk Blog. One of the main points that Dr. Nathan makes is that there is a lot more to learn about treating health issues from mold. In regard to Dr. Shoemaker’s claim that Dr. Brewers study is not “scientific”, Dr. Nathan counters by saying that imaging that the work of Dr. Shoemaker “has achieved the status of a science is a considerable overstatement”.
I’m not going to get wrapped up in the nuances related to what Dr. Nathan wrote too much here. There are well established criteria that researchers use to ensure their study results are meaningful. It’s important for all CIRS people that research on mold health effects is well done. Otherwise, poorly done studies will invariably be used against our community. In my interpretation, I don’t think Dr. Shoemaker is saying his work on CIRS constitutes a science. Instead, he’s making the point that Dr. Brewer and Dr. Nathan need to be a lot more careful about the conclusions they’re drawing based upon fairly dubious RealTime testing and sketchy methodology.
Dr. Nathan goes on to make the point that many of his patients have more than just CIRS and that treatment with antifungals has been helpful. This is an important point. Even in spite of the fact that RealTime testing is mostly inaccurate and there isn’t any evidence that nasal fungi are an issue, nonetheless, 94% of the 151 patients Dr. Brewer treated with nasal antifungals got at least 25% better. Granted the measurement for getting better wasn’t based upon lab work, but clearly a good percentage of chronically ill people felt better. Given that it’s very unlikely that nasal fungi were the culprit, the question is why.
At this point, no one knows. In fact, this is similar to the situation when it comes to understanding what part of the body’s defense mechanism stops working with CIRS. No one knows why people’s immune systems go haywire with CIRS. In fact, there is very little data to support Dr. Shoemaker’s claim that the body loses the ability to make antibodies. It’s just conjecture at this point. Now, that doesn’t mean his protocol isn’t scientific. It is. Unlike Dr. Brewer’s work, what Dr. Shoemaker has shown is that when CIRS folks get exposed to mold, specific inflammatory blood markers shoot out of range. Furthermore, when his protocol is followed, these markers generally correct and people get their life back.
As such, Dr. Shoemaker’s work is defined whereas Dr. Brewer’s work is not. In Dr. Brewer’s case, we don’t really know how to tell who should take antifungals. We also don’t know how to tell when the antifungals have done their job – other than the subjective opinion of the patient. All we really know is that when you take a population of chronically sick folks and give them nasal antifungals for an extended period of time, many of them will feel better. That’s all. Note: Instead of looking at urine mycotoxin levels and trying to deduce the presence of nasal fungi, why not test for them directly with a nasal swab from MicrobiologyDX in Bedford Massachusetts at 781-276-4956.
When it comes down to it, I’m guessing that Dr. Nathan’s main objection to Dr. Shoemaker’s paper is to be found in his closing remark. Dr. Shoemaker writes in bold-face letters, “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.”
Well, that’s Dr. Shoemaker for you. If you haven’t figured it out all ready, the guy is a radical. He’s not the warm and fluffy type. And truth be told, we absolutely need a Pit Bull Terrier like him to clear a path for a new mold paradigm. We need someone that tears apart the junk science that has been used against CIRS folks for far too long. It’s actually good he’s willing to take aim at anyone that doesn’t adhere to the currently accepted research standards. When doctors like Brewer enter into the realm of publishing papers, they need to be precise.
Having said this, I return to the point made in Dr. Brewer’s paper that many chronically ill people felt much better using nasal antifungals. Granted it makes sense to avoid systemic antifungals like Amphotericin and Intraconazole. It’s also clear there isn’t anything but guesswork as to why this therapy works. Still, I agree with Dr. Nathan. Let’s not throw out this “baby out with the bathwater”. From where I stand, a trial of antifungals makes sense for folks that just can’t seem to be able to recover their health.
I’ll close with a few quotes from the truly wonderful Sharon Kramer. If you don’t already know about the important fight she’s taking on for the mold community, please watch Sharon Kramer for Lawless America. In a well written accounting of Dr. Brewers, Dr. Shoemaker’s, and Dr. Nathan’s positions on this matter, Sharon wrote, “From the standpoint of advancing public health policies so everyone may receive viable treatment from mainstream physicians, the last thing we need at this point in time is the claim (by Dr. Brewer and Dr. Nathan) that antifungals combat Biotoxin Illnesses with no research studies to back that claim up…Being backed by the government and the insurance industry, the “naysayers” in the mold issue make for formidable foes… I feel quite certain that Dr.
Brewer did not mean to throw a monkey-wrench into the war for proper public health policies…One (Dr. Brewer) works to advance treatment options for those who can afford to go outside of their healthcare provider systems. The other (Dr. Shoemaker) works to advance that physicians who work within healthcare systems are educated to provide proper treatment to the masses.” Thanks for all your hard work Sharon.
Why Using Nasal Antifungals May Help
When it comes to recovering from CIRS, I’m taking the long and winding road. If you’ve been reading some of my writings, I’m sure you know that I’ve been struggling to get our home remediated. Perhaps foolishly, I decided to try to fix the brand new home we built. It had an ERMI over 23 with Aspergillus counts over 24,000! Being the knucklehead that I am, I dug in. It was a brutal learning curve. However, just recently, the latest ERMI came back at 0.09. Yippee! I hope to eventually write down what it means to do remediation right so others don’t have to struggle like my wife and I did.
As a result of deciding to remediate, I’ve been getting hammered with mold toxins for years after my initial CIRS diagnoses. On top of living in a moldy home, our home is surrounded by woods. If I go tromping around in the lower parts of these woods, I’ll pay the price. It’s a lot of mold for someone with a pair of 11-3-52b haplotypes and inflammation from CIRS to work with.
We all know what happens in CIRS. In part, an important hormone called MSH plummets while inflammation goes sky high. When MSH is low, the mucosal linings of the nose and gut are diminished. Partly due to this effect, I’m now treating MARCoNS for the third time! There so much to say on the subject of MARCoNS, that I’ve learned since the first article I wrote on the subject, that I’m saving it for a separate piece. On top of MARCoNS, a recent Small Intestinal Bacterial Overgrowth (SIBO) came back positive indicating that I’ve got some pretty serious gut issues too. Just like all the new MARCoNS information, this is a subject of another article.
Given that I knew I needed to get my house cleaned up before continuing on with Dr. Shoemaker’s protocol, I’ve been in a holding pattern for over 5 years. Yes, that’s right, 5 years. Knowing that I had gut issues and not wanting to sit and wait, I decided to give nasal antifungals a try. To be clear, I did not do this because I believe using antifungal nasal sprays has anything whatsoever to do with treating CIRS. I did it simply based upon the fact that for some unknown reason, a significant number of chronically ill folks that used the spray got better. That’s it.
In fact, my personal belief is that part of the reason using nasal antifungals are effective has to do with fact that a certain amount of what gets sprayed in the nose ends up in the gut from swallowing saliva. I’ve tried oral doses of a systemic antifungal (Sporanox) in the past and got really strong adverse reactions. Over the years, I’ve learned how to discriminate between symptoms from gut dysbiosis and inflammation from CIRS. The nasal spray was definitely addressing gut flora. For myself, using small doses of Nystatin with EDTA nasal spray to bust up the biofilms is a much more gentle, albeit slower, way to work on my gut until I’m finally able to get VIP onboard. I’m hopeful that once I’m taking VIP, much of my gut issues will resolve on their own.
Now you may ask, why would I use Nystatin as a nasal spray when I’m of the belief that part of the reason it was effective on Dr. Brewer’s patients had to do with treating Candida or some other fungal overgrowth in the gut? If that’s the case, why wouldn’t I just mix some Nystatin with EDTA and swallow it? The answer is because I believe that using an antifungal nasally may confir some protective effect against nano sized biotoxins from getting into my brain via the olfactory system. Allow me to explain by looking at the olfactory system.
The olfactory system is what we use to smell. This system resides behind the bridge of your nose. It consists of really tiny hair-like structures (cilia) that project into the nasal cavity. Super tiny inhaled particles are dissolved by mucus produced by the olfactory bulbs that sit above the cilia. Cilia in contact with this dissolved material are attached to olfactory receptors and together they send electrical signals to the brain. These signals travel along nerves that run from the olfactory system into regions in the brain where the hypothalamus resides.
For a while now, I’ve learned that when the bridge of my nose starts to ache, it means I’m taking a mold hit. This happens within 10 minutes of being in a moldy building. Having learned about the olfactory system when I studied about MARCoNS, I always wondered if part of why I’m more susceptible to biotoxins may have to do with dysfunctional defense mechanisms in the olfactory system. After all, the body must have some way of prevent super small toxins from getting into my brain via my sense of smell. Maybe having CIRS means these defenses don’t work well?
Regardless, the bridge of my nose would continue to ache for the couple of days it took to reset using cholestyramine (CSM) and various anti-inflammatory supplements. In fact, I make mention of the fact that Dr. Klinghart had said that the olfactory system was a portal of entry for mold toxins in MARCoNS – Fungal Colonization. So along comes Dr. Berndtson talking along the same lines and I thought it might be time to see if there was any merit to these claims myself.
Dr. Berndtson gave his talk on nano-particles on Friday at the November 2015 Second Annual Conference: State Of The Art In Mold, Wet Buildings, & CIRS by Dr. Keith Berndtson. In his talk, Dr. Berndtson claims that it’s entirely possible that nano-sized mold biotoxins are traveling up into the olfactory bulb in the nose and subsequently finding their way into the brain. He states that these ultrafine particles (UFP) move from the olfactory bulb along the nerves to the parts of the hypothalamus in the brain responsible for making ADH, MSH, and VIP.
In support of this claim, Dr. Berndtson references a 1941 study by Howe & Bodian that Gregg Weatherman pointed out to him. In the study, the noses of chimps were exposed to polio virus. Polio virus is 30 nanometers (nm) in size. The study showed the olfactory bulbs and olfactory nerves are portals of entry into the central nervous system. I couldn’t find this older study but did find newer studies that confirm this finding. If you’re interested, just Google “translocation inhaled ultrafine particles”.
For example, in Translocation of Inhaled Ultrafine Particles to the Brain, the authors say, “Ultrafine particles (UFP), particles 100 nm, are ubiquitous in ambient urban and indoor air from multiple sources…We conclude from our study that the CNS can be targeted by airborne solid ultrafine particles and that the most likely mechanism is from deposits on the olfactory mucosa of the nasopharyngeal region of the respiratory tract and subsequent translocation via the olfactory nerve.” This is important because not only does it show that really small particles can get into a person’s brain via the olfactory system but it also gives us a sense of size. In the study the researchers used particles 100nm in size. This begs the question, how big are airborne biotoxins?
In his talk, Dr. Berndtson presents a graph showing the diameter and concentration of ultrafine particle (UFP) in water damaged buildings (WDB). In this graph, the bulk of the tiny biotoxins are 0.010 microns in size. A micron is one millionth of a meter and a nanometer is one billionth of a meter. Moving the decimal point to the right three places tells us that 0.010 micron = 10 nanometers (nm). That’s well under the 100nm particle size used in the study. As such, we can convincingly posit that small biotoxins are getting into the brain via the olfactory system. Using the nanometer scale to the right, you can understand why Dr. Berndtson said in his talk that you can fit 1,000,000 biotoxins across the width of a period.
Wanting to substantiate Dr. Berndtson’s graph, I went about figuring out how big some of the various biotoxins associated with moldy buildings were. Studies show there are over 500 mold fragments for every spore floating in the air. How big are those mold fragments? How big are mycotoxins? As noted early, Dr. Shoemaker says that for every one mycotoxin you’re exposed to, you will also be exposed to 1,000 beta glucans and 1,000 mannans. How big are they? What about Microbial Volatile Organic Compounds (MVOCs) that are responsible for the musty smell and exudate (guttate) water droplets that rise to the surface of mold and are then shed? How many of these mold inflammagens are under 100nm in size and are they finding their way into the brain?
It turns out this isn’t an easy question to answer. You have to actually know the molecular shape of the molecule you’re talking about and then know how to convert this into a physical size. This is done based upon the number and size of the atoms along with the type and angle of bonds between the atoms. Nevertheless, I found plenty of information in support of the contention that there are a lot of biotoxins under 100nm in size floating around in the air in water damaged buildings (WDB). Here’s some of what I found.
In Fungal Fragments in Moldy Houses: A Field Study in Homes in New Orleans and Southern Ohio, the authors say, “…large quantities of submicrometer-sized fungal and actinomycete fragments (ranging from 30 nm to 1 µm/1000nm) are released together with intact spores from contaminated surfaces. These studies demonstrated that the number of released fragments was always higher, up to 500 times, than the number of intact spores.” That’s good to know. Clearly there are a lot mold fragments well under the 100nm threshold in WDB. Most certainly, these fragments are coated with toxins (mycotoxins).
Speaking of mycotoxins, two common WDB mycotoxins are Aflatoxin from Aspergillus mold and Trichothecene from Stachybotrys mold. Now I may be serious about learning when it comes to CIRS, but not to the extent that I’m going to teach myself how to calculate the physical size of molecules. Instead, in Size Matters: How big are molecules? the author calculates the size of a molecule with as many or more atoms of a similar type to these two mycotoxins. If you look at the pictures of molecular structures above, you’ll see that this similar looking molecule to Aflatoxin turned out to be 1.6nm in size. That’s way under the 100nm sized particles that were shown to enter the brain. Although not definitive, it sure looks like damn near all mycotoxins are small enough to travel up the olfactory system and impact the hypothalamus.
Likewise, if you look at the molecular structure of Microbial Volatile Organic Compounds (MVOCs), these are fairly simple molecules. Clearly these along with nano-sized exudates are also small enough to find their way into the brain. Furthermore, I found some information that suggests endotoxins are also small enough being in the range of 50nm. At that point, I figured it was pretty clear that there is a long list of biotoxins that are small enough to find their way into the brain via the olfactory system.
So maybe coating the mucus and cilia of the olfactory system with an antifungal spray three times daily offers some sort of protection against super small biotoxins that are inhaled through the nose. Who knows; I’m just speculating based upon my symptoms. We do know these minuscule particles do get into the brain this way. However, if antifungals help protect against this is just me positing out loud.
Along these lines, I do sometimes wonder if the reason I was able to keep from crashing for as long as I did had to do with the way that I breathe. Early on, I learned to hold my breath at the first whiff of bad smells (using chemicals working on machines that go fast). On top of that, I’ve been a “mouth breather” for as long as I can remember – tend to breathe through my mouth especially when doing physical work. Given what we now know about biotoxins entering the brain via the olfactory system, these two defense strategies make sense. My advice for those with CIRS would be to breathe through their mouth if they think they’re in a moldy environment.
Derealization Caused by Inhaled Biotoxins
Interestingly, I’ve noticed that after taking a mold hit signaled by pain at the bridge of my nose, I will often experience derealization for a couple days while I recover from the insult. Given what we now know about biotoxins making their way into the brain via the olfactory (smell) system, this makes complete sense. Add to this statements made in the “Final Report of the New Jersey Comparative Risk Project” regarding the effects of Pfiesteria biotoxins on researchers. In Appendix 4, author, Tom Atherholt, states “Adverse human heath effects were first observed in laboratory personnel working with Pfiesteria cultures…Affected workers have complained of disorientation with a sense of depersonalization and of being compelled to continue and lacking an ability to recognize that something was wrong…”
That sure sounds familiar. Biotoxins make people freaked out and stupid. I know for myself that when I was in the throws of CIRS many years ago, I walked around in a perpetual state of derealization for about a year.
Wikipedia has a pretty good definition of derealization. They describe derealization as “an alteration in the perception or experience of the external world so that it seems unreal. Other symptoms include feeling as though one’s environment is lacking in spontaneity, emotional colouring and depth… Frequently, derealization occurs in the context of constant worrying or “intrusive thoughts” that one finds hard to switch off. In such cases it can build unnoticed along with the underlying anxiety attached to these disturbing thoughts…” What’s missing is just how unsettling the experience can be.
Being set apart from thoughts and feelings can really be distressing in part because you don’t know if you’ll ever be able to connect to Life as you had in the past. I also believe another component of this is the fight-or-flight response that gets triggered by the toxins. It wouldn’t be so bad if a person was completely out of it. Unfortunately, awareness around what is happening remains.
You’re aware of being abruptly cut off from feeling connected to your own mental and emotional life. If you’ve never experienced this, imagine having Alzheimer’s. This illness can cause strong feelings of depersonalization. Imagine not knowing who you are, who other people are, where anything is, and so on. In that state of mind, there’s just this moment without any ability to anticipate or make plans for the future. This is more extreme, but hopefully you get a sense of what I’m talking about.
In spite of this abrupt disconnect, what remains is the ability to reason, awareness itself, and the knowing that the ability to connect is gone. In the case of mold exposure, I’m aware that those parts that once made me integral with my day-to-day life are completely gone. There’s no way back. Even after having meditated for decades, I’ve yet to find a meditative way to get reconnected. All I can do is surrender and wait for the biotoxins to clear my body.
While experiencing depersonalization, I’ve learned to relax and remind myself that consciousness alone is the one constant and that my job is simply to bring love to whatever the situation is. It takes a level of fearlessness to relax into this level of forced detachment. In this disconnected state, it can be seen that part of what makes life enjoyable and worth living is being able to emotionally connect and interact with it.
Finally and from a Buddhist perspective, this unique state of mind is often heralded in as good news – the fruit of meditation. It’s considered good news because the ability to fool ourselves, to get caught up in drama, is gone. In this state, it is much easier to see that all the traits that a person considers “me” are very temporal. They’re here today and gone tomorrow.
Being relaxed and in this altered state, an interesting question to ask is “Who am I when my sense of identity falls away?” What’s left? What’s left of this individual called “me”? For myself, the answer is that consciousness alone remains and this consciousness is direct and immediate. It is not localized. Rather, one could describe it as being a sort of universal awareness that permeates all of Space. Well, that’s getting into it a bit. The main point is finding a way to be OK when reality shifts is really helpful for those with CIRS.
My Experience with Pharmaceutical and Do-It-Yourself Nasal Antifungals
For the remainder of this article, I’m going to talk about my experience using Sporanax and EDTA/Polysorbate 80 (Chelating PX) antifungals from ASL Pharmacy along with using the NasaTouch atomizer. I’m also going to cover what I believe is a much better and less expensive alternative to these pricey pharmaceuticals. As I’m doing this, I’ll describe the improvements I experienced and cover the specifics on how to mix up a comparable solution of antifungals for a fraction of the cost of pharmaceuticals.
Update May 2017
Given the already dubious benefit of using antifungals along with recent information about more and more resistant forms of MARCoNS possibly being linked to antifungal use (especially the “azoles“), I would think long an hard about whether you want to use antifungals particularly if you have MARCoNS.
Sporanax and Chelating PX – ASL Pharmacy
I started by trying Sporanax with the biofilm buster, “Chelating PX”, from ASL Pharmacy. Both the Sporanax and biofilm buster came in small clear plastic ampules. You can either administer one right after the other or, mix and apply them together. I chose the later because it took less time. This is to be done twice daily (BID).
Using Sporanox and EDTA in the NasaTouch initially helped with energy, greater calm, and a little better sleep. However, after two weeks, I started to experience increasing anxiety, gas, fatigue, an ear ache, and raw nasal passages. Foolishly, I also decided to start taking Sporanax capsules. This took me over the edge and after a really bad night of anxiety, I decided to switch to Nystatin nasal spray and forgo taking antifungals orally. I attribute most of my symptoms to being way to aggressive resulting in really messed up gut flora. Sporanax and Chelating PX are available from ASL Pharmacy by prescription only. Sporanax is a systemic antifungal.
900 Calle Plano, Suite M, Camarillo, CA 93012
Nysatin and Chelating PX – ASL Pharmacy
Due to strong reactions I was starting to have, I switched from Sporanax to Nystatin. Initially, I ordered Nystatin and Chelating PX from ASL Pharmacy. The cost was about $250 for one month! The Nystatin comes as a dry powder in capsules. For each dose, you empty a capsule of Nystatin in a small mixing jar with a lid and add in 15ml (about 1 tablespoon) of saline water. The saline itself is made up by mixing a premeasured packet of saline salt with distilled water. Once mixed, the Nystatin solution and Chelating PX are put in the NasaTouch and applied.
Switching to Nystatin alleviated the issues I was having with Sporanax. In general, Nystatin and EDTA have helped significantly. I no longer experience a heightened alarm reaction every few minutes as a result of changes in environment or abrupt sounds. Also, I’m able to tolerate some exposure to mold in buildings that would have been very problematic in the past. Energy and focus are improved.
DIY Nystatin and EDTA
Given the exorbitantly high cost of Nystatin and Chelating PX from ASL pharmacy, I decided to make up a comparable solution for a fraction of the cost. I called ASL Pharmacy and spoke to a pharmacist who confirmed that the Nystatin pills contained fillers like xylitol and gelatin (Hypromellose). The capsules are labeled 50,000 IU. The pharmacist said the 50,000 IU capsules contained 50,000 IU of active Nystatin and that it had an approximate weight of 22mg. I then weighed the material in one capsule at 365mg. In other words, there is about 343mg of filler in each capsule.
I went on to mention to the pharmacist that I’d read that some Nystatin solutions contained 100,000 Units per milliliter. I asked the pharmacist if she thought this was the same as 100,000 IU. The answer was yes. Given that the ASL prescription is to inhale one capsule containing 50,000 IU of Nystatin twice daily, this works out to inhaling the same amount of active Nystatin.
At the source below, a 100 MU bottle contains 100,000,000 (one hundred million units) IU of active Nystatin. This equates to 1,000 nasal spray doses at 100,000 IU (two 50,000 IU capsules)! ASL Pharmacy charges around $250 for 30 doses at 100,000 IU including the EDTA biofilm buster. The 100 MU bottle of Nystatin costs $88 as of March 2016.
Nystatin USP Powder 100 MU
[PNY980-100] $88.00 – as of March 2016
Nystatin USP Powder 500MU
[PNY980-500] $155 – as of March 2016
Important: Make sure to buy “oral” and not “topical” Nystatin.
I generally only take one 50,000 IU capsule daily. Using a scale, I discovered that a “smidge” measuring spoon filled level with Nystatin is about 22mg, the equivalent dose to an ASL capsule. Don’t worry about being that exact. For example, the typical oral dose of Nystatin for treating Candida in the gut is 500,000 to 1,000,000 IU three-times daily. So long as you use the smidge measuring spoon, it’ll be close enough.
Note: Nystatin powder should be refrigerated between 36 and 46 degrees F (2 to 8 degrees C) and protected from light in a dark container. I wrap mine in aluminum foil. If you do this, the shelf life should be 36 months.
Regarding a biofilm buster, EDTA binds to the metals used by the microbes to create biofilm. The pharmacist said a 2ml ampule of Chelating PX solution contains 15mg of EDTA along with a surfactant. This works out to about 1/2 of a smidge spoon of EDTA. Personally, I use about 1/4 (200mg) of a capsule – way more than 15mg. In talking with my doctor, he suggested I could use more. In other words, like Nystatin, using a little more isn’t going to hurt and may help.
The final addition is a touch of Burt’s Bee shampoo as a surfactant. Chelating PX has a surfactant to break up the surface tension of the Nystatin-EDTA solution so it evenly coats the inside of your nose. In fact, a solution with 1% Johnson’s baby shampoo has been used to treat chronic rhinosinusitis. I like Burt’s Bee shampoo because it doesn’t have the chemicals in Johnson’s.
After placing one tablespoon (15ml) of saline water, the Nystatin, and the EDTA into a mixing jar with a lid, I put a very thin film of Burt’s Bee shampoo on a fingertip – less than the size of a pea. I touch the surface of the solution for a second. I know I’ve made contact with the solution when the sheen of Nystatin and EDTA quickly disperses. The surface of the solution immediately becomes clearer. After screwing on the cap and shaking for 30 second, the solution with have a little foam around the perimeter of the jar. When the solution is applied, there may be a very faint taste of the shampoo. You don’t need a lot.
Instead of buying an expensive NasaTouch machine, you can use a spray bottle. It may not atomize the solution as well, but personally, I think it’s almost as good. Tip your head down horizontally while keeping the spray bottle vertical. Aim at the back of your head – not toward the top of your nose. Inhale gently while spraying. That’s it.