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6:30 What is genomic testing?
13:52 The problem with current testing methods
17:05 Why looking at one gene isn’t enough
23:00 Should people be cautious of genomic testing?
29:39 The importance of microRNA
32:19 Will the Progene DX test be worth the cost?

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Chris Kresser: I’m Chris Kresser and this is Revolution Health Radio.

Hey, everybody, it’s Chris Kresser. Welcome to another episode of Revolution Health Radio. I’m really excited to welcome Dr. Ritchie Shoemaker back on the show for the second time as my guest.

Dr. Ritchie Shoemaker is a pioneer in understanding how low-dose biotoxin exposure, including toxic mold and algae, impacts our health and contributes to disease. He’s the author of eight books and multiple published academic papers. His latest book, Surviving Mold: Life in the Era of Dangerous Buildings, is a guide through diagnosis, treatment, remediation, and return to health. Dr. Shoemaker is currently retired, but continues to lecture throughout the US on chronic inflammatory illnesses that are caused by exposure to moldy buildings and other biotoxins.

If you’ve been listening to my podcast for a while or following my email list, you’ll know that this is a topic of great interest to me both professionally as a clinician because we’re starting to treat a lot of patients with CIRS, or chronic inflammatory response syndrome, and also personally because I recently discovered a mold issue in our home, and my entire family, my wife and our daughter, were all affected by that. We’ve since, fortunately, gotten out of that house, and we’re in a new house now, and we’re well along the path of recovery from that.

This is something that I’m really fascinated by, and it’s something we’re seeing a lot in our practice, so I wanted to ask Dr. Shoemaker to come back to particularly talk about some new genomic testing that is becoming available that quite dramatically improves our ability to diagnose this condition and get a lot more specific about how to treat it. So far, there have been some tantalizing developments in the world of genetic testing, promise that sequencing our genome would lead to personalized medicine and treatments, and I would say that so far that has mostly been a failure. I mean, there have been some ways that that has been helpful, but overall, it hasn’t really panned out the way that we thought it was going to pan out, and part of the reason for that is that genes only tell us what our predisposition is. They’re kind of like the imprint or the template, but if we don’t know what’s happening with gene expression, the genetic data is often of limited value, and that’s why the genomic testing is so exciting, because it’s telling us what’s happening in the genome in real time, and Dr. Shoemaker is going to explain more about that, so let’s dive in.

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OK, now back to the show.

Chris Kresser: Dr. Shoemaker, it’s great to have you back on the program. We had such a great response to our initial interview, and we’ve had so many people asking to have you back. I’ve been really looking forward to talking to you about genomics—or transcriptomics—as we’ll be discussing in more detail, so welcome back!

Ritchie Shoemaker, MD: Well, thank you. I think you’re my favorite person in the world to talk to on these computer things.

Chris Kresser: I’m flattered!

Ritchie Shoemaker, MD: I’m pleased you’re letting me talk to you twice.

Chris Kresser: Well, there’s so much to talk about, and that’s the thing: We’ve barely scratched the surface, and yet I think we’ve already managed to help a lot of people. I know we have patients coming to us in our practice, specifically mentioning the podcast that they heard, and it really flipped the lightswitch for them. They were able to identify themselves in all of the symptoms and signs that we were talking about, and I don’t need to tell you, because I learned this from you, how many people are being misdiagnosed and just missed out there with this condition.

Ritchie Shoemaker, MD: Now that we are seeing some new wrinkles that weren’t on your first podcast, we are also seeing the possibility that there is a toxin or some inflammatory compound made by organisms that like to stay in dental bone that was unknown, and hopefully within the next three weeks we will have the fairly sophisticated gas chromatography and mass spectroscopy done to look at these unusual organisms because this is uncharted territory. Golly, it’s like the old days where I was so excited to come in the office to see a fax report or some sort of computer thing of an HLA.

Chris Kresser: Right.

Ritchie Shoemaker, MD: Now I’m looking for what kind of endodontal organisms were found in a failed root canal. Good gracious.

Chris Kresser: Yeah.

Ritchie Shoemaker, MD: And it all ties together.

What is genomic testing?

Chris Kresser: Well, let’s talk about that because that’s really the subject of the show today. There’s a new test that you’ve been working on for some time now that is going to be of assistance to us as clinicians and to patients, I would say just anyone dealing with a mysterious undiagnosed chronic disease, but specifically people with chronic inflammatory response syndrome, which we talked about, post-Lyme syndrome, and chronic fatigue syndrome. This is the genomics or transcriptomics testing. Maybe you could just give us a brief overview or intro to what it is, and then we’ll dive into some more detail.

Ritchie Shoemaker, MD: One of the spinoffs from the last 15 years since the Human Genome Project was brought to light is just how little we knew about DNA back in my high school days and maybe even yours and how much more we’re seeing, and then to take one more step is the application to help people from our new knowledge about DNA and how DNA works and controls day-to-day life. It’s just opening doors that were previously sealed shut. This is the dawn of the new era.

I was interested the other day when a Time Magazine arrived. There on page two was an ad for genomics, and as you might expect, it was about cancer.

Chris Kresser: Right.

A new genomic test could have a major impact on how we diagnose chronic illness.

Ritchie Shoemaker, MD: Most of them are looking at DNA, looking for mutations that control cancer and, to a lesser extent, atherosclerosis, but the basic concepts of the integrity of science apply—whether it’s cancer or atherosclerosis or CIRS—that we can accumulate enough data—provided we have enough computing power and time for computing power—to look at just about any illness there is from new perspectives.

When you and I first started talking a couple of years ago now—time has gone by—the state-of-the-art was all proteomics. Looking at labs, and we had maybe 25 or 30 labs we could look at, and those were validated, and there must be a hundred or so that people used that weren’t so validated. Now we can look to see what are the mechanisms that control those lab abnormalities from DNA and then, vice versa, how some of these proteomic changes, especially with TGF-beta-1—that’s transforming growth factor beta 1—also tie to transcription factors in DNA. I think we’re in a situation, not necessarily of yin and yang—and you know more about that than I do—but you don’t know about genomics without knowing proteomics, and you don’t know about proteomics without knowing genomics.

Chris Kresser: Right.

Ritchie Shoemaker, MD: So our new company called Progene is some advertising way of saying proteogenomics.

Chris Kresser: Right.

Ritchie Shoemaker, MD: Both are together. The future is untapped in CIRS because nobody is paying attention to the fact that it’s not just one gene that controls this whole group of new sorts of knowledge. It is a group of genes. If you analyze a group, you have a much better chance to learn about the one.

Chris Kresser: Right, so this is a deeper layer here. We talked in the first episode about markers like C4A and TGF-beta-1 and MMP-9, and now we’re talking about the genomic or transcriptomic changes that happen that lead to the abnormal expression of these markers.

Ritchie Shoemaker, MD: That’s exactly correct. As usual, you are right on the button. But you know, I mentioned some of these organisms in the nose that are benign and don’t cause nasal symptoms and don’t cause headaches or sinus problems, but people don’t get better unless these things are eradicated because we’re now seeing the mechanism by which they make people worse is by acting on gene transcription. I think I mentioned this before. If a MARCoNS—multiple antibiotic resistant coagulase negative staph—that sits in the nose makes biofilm that’s from this little igloo that keeps it shielded from all the environmental influences—and our immune defenses, too—if this guy can release something into the environment to do whatever malicious things he wants to, you think there might be somebody sitting in the small intestine, doing that? How about the large intestine?

Chris Kresser: There’s plenty of room for biofilm formation there. Lots of surface area.

Ritchie Shoemaker, MD: Yeah, and then the whole mechanism. How many years ago it was when we looked at cystic fibrosis and we all said the pseudomonas germs lived there because they’re resistant to antibiotics, and it wasn’t until we started seeing these pseudomonas organisms growing freely on perfectly cleaned bronchoscopes that we recognized that these guys, these bacteria, like certain econiches where they make their biofilm that prevents them from being killed by normal defense mechanisms.

Do the pseudomonas germs in cystic fibrosis release compounds like the MARCoNS do? Well, if so, we should be able to sort genomic results, looking with a next-generation DNA sequencer, that will give a fingerprint for a pseudomonas in some site, whether it’s blood or lung or urine or somewhere else, that would be distinctive, and what a step-up on prompt diagnosis. Imagine if you’re working in the ICU and you want to know about pseudomonas sepsis. You take one tube of blood, send it down to the lab for next-generation DNA sequencing that can do a thousand a day, and in 25 minutes, the computer is telling you you have a pseudomonas biofilm former and look out! Well, it’s not too farfetched. We already are there, we think, with some of the inflammatory response syndromes.

When I talk about mold—this is just for the sake of your audience—when we talk about wet buildings or water-damaged buildings, mold gets a lot of the publicity, but there are at least 30 different elements or items that are part of the agenda that create this mixed chemical exposure that all set off inflammatory responses. They all have their signatures, and they all sum together so that in the same next-generation sequencing—not of the future, but of today—we should be able to tell you in a very short period of time if you have a water-damaged building, and in fact, we can. We’re extending that to post-Lyme syndrome. We’re working on these unusual MARCoNS, but, Chris, it’s just going to be a matter of time before the same process of science—disciplined science—proceeds with peer review and publication and argument with colleagues, so something is going to come out of this fire that is honed just like the sword you see on the Marine guy on these basketball ads.

The problem with current testing methods

Chris Kresser: Yeah. I’m excited about it because, as a clinician who has been dipping my toe in this water for the past couple of years, that seems to be one of the biggest challenges. We see someone who has elevated inflammatory markers like C4A or TGF-beta-1 or MMP-9. We can do a kind of survey or history. We can learn about their environment. We can actually send someone out to their home to do some testing, but both my own personal experience with now, as you know, Ritchie, two different houses and an office and having kind of supervised several patients go through that experience, tells me that it’s not perfect. There’s no 100 percent certainty that you get going through that that you’re in a completely mold-free environment or even that it’s mold itself that’s causing the problem, so the ability to have another level of testing that can point to a specific cause in the elevation of these markers is really exciting, and I guess that’s what you’re saying that gene activation will tell us.

Ritchie Shoemaker, MD: Part of the difficulty in bringing these tests to clinical use has been the regulatory hurdles that are placed on new labs and new diagnostic tests. How do we know? How can we say? There have been some others before that I think have been a little bit misleading in terms of what genomics is and what it really means for health, but those hurdles have been passed. The testing itself involves a lot of reagents that are not free, so there’s an expense to getting these tests done, but now that some of these hurdles are over, it won’t be too long before I can be talking to someone like you and say, “Well, doctor, here are the results of your genomics,” and because I know you a little bit, the first question that you’re going to have is not, “What do my genomics show?” It’s, “What do my daughter’s show?”

Chris Kresser: Yeah.

Ritchie Shoemaker, MD: It gets to a face system and not a science system that says we can look at genes and predict the future, what the genes tell us and what’s going on when the blood was drawn, in blood.

Chris Kresser: Right.

Ritchie Shoemaker, MD: It doesn’t tell us what’s going on in the brain, however much we want to do that. We have to be doing the same approach to spinal fluid.

Chris Kresser: Right.

Ritchie Shoemaker, MD: And yet when one of your colleagues in your office has a patient who has pretty severe-looking Alzheimer’s-type features and Parkinson’s features and is living in a really wet place—the moldy of moldy—how do we know what she has?

Chris Kresser: Right. Or inflammatory bowel disease, right? That’s something that is often misdiagnosed when someone may have the underlying features of CIRS.

Let me ask you this, though, just to play devil’s advocate. You see one gene up and one gene down, and you get the tube of blood drawn, and that’s what you see in the results, but what about the next moment, if the gene is up and another one is down? How do we know what we’re seeing is a clear and reliable signal?

Why looking at one gene isn’t enough

Ritchie Shoemaker, MD: I think we know pretty well that one gene at one time doesn’t tell us anything at all, not just about illness, not just about predictions for the future. There was an editorial or a lead article in the Journal of the American Medical Association that came out, my copy got here today, and that point is being underlined. We used to think that breast cancer genes, one gene up, one gene down, would tell us. Well, that turns out to be overstated. The complexity of breast cancer genes is a reason that you can’t look at one gene alone. Similarly we saw the same thing with hemochromatosis.

Chris Kresser: Yeah.

Ritchie Shoemaker, MD: You and I order these blood tests, and we get a few gene reports, and aha! You’re a carrier! That’s why your ferritin is high! But the issue is that if we don’t look simultaneously with one gene up and one gene down at factors that are known to regulate—or lack of regulate—one gene up or one gene down, we can’t interpret what that one gene means. We add to the strengths of the analysis, we add to the point of being clinically useful by being able to understand that for a given process, say, innate immune activation, there are about 1700 of 25,000 protein-coding genes that we have seen to be abnormal, and some of those are not very commonly up or not very commonly down, and if we winnow away and cull out the genes that are of a lower frequency, we get into a group of about 675 genes for women and about 575 for men that are highly variable, but highly present in patient with a given illness after patient after patient after patient.

I would have thought that we would have seen differences sorted by HLA. Actually we don’t. It’s not nearly the same strength. I would have thought C4A was a big player. It’s not. That’s more peripherally related. Th1 with MMP-9 is closely related to these problems. The best one is TGF-beta-1 and then some of these multiple antibiotic resistant coagulase negative staphs. So trying to look at 25,000 genes, and we haven’t even talked about the non-protein-coding genes. Oh, boy. Who knows about them?!

Chris Kresser: So we’re not talking about a single gene, single effect. We’re talking about a pattern where you can see multiple genes and their presence or lack of presence, and it’s more like a fingerprint, something that you would use diagnostically.

Ritchie Shoemaker, MD: I’m getting goosebumps because you get it, and you’ve gotten it almost from the get-go. That really does give us the advantage. I can’t tell you how much I wanted in November at the ILADS meetings to get up and say, “Here’s the genomics of post-Lyme syndrome, y’all. Stop doing all the stuff that you’ve been doing, and get on the program,” and I think we’re going to meet that timetable. We have it for mold, we have it for some other things.

But then the other issue is that what we also have seen is that there are some illnesses that are thought to have something to do with inflammation, and I’ll just speak from my own personal problems with obesity. Geez. How many people acquire leptin resistance as part of their CIRS? A lot. About a third of the people with weight problems are leptin resistant, so if you really go to saying inflammation underlies these problems, what about diabetes? What about obesity? But the big one is not cancer. We’re not there yet. It is with atherosclerosis and then to a second level of security is Alzheimer’s. These different illnesses do have genomic patterns that we’re looking at every day, and it’s just a matter of getting them published.

Chris Kresser: Mm-hmm. So if we’re using a group of genes—let’s call it a fingerprint—how many are we talking about before we can get to a threshold of diagnostic accuracy that is actionable clinically?

Ritchie Shoemaker, MD: Well, you don’t have the luxury, when you do next-generation sequencing, of only getting a few genes. You get 22,000 or 25,000.

Chris Kresser: Right!

Ritchie Shoemaker, MD: And the computer will determine, out of the 1700 whether it’s 675 or 657 or 800 because there’s a lot of variation that people have. But we think that it’s in the hundreds of genes and not in the teens of genes.

Chris Kresser: OK. You mentioned before, 675 genes for women and 575, or thereabouts, for men. I don’t think it would come as any surprise to most men out there that women are more sophisticated than us! But now we’re seeing it genetically, as well! Tell me about that.

Ritchie Shoemaker, MD: Well, in chronic fatigue syndrome, there’s probably been more work looking at gender differences and incidence of cases, and there are all kinds of ways to look at bias, but I think that most people in this field would acknowledge that chronic inflammatory response syndromes are seen more commonly in women than men, and with the same level of exposure, it’s more common to see women having problems than men having problems. Is that just because women access physicians more? Are they more sensitive? Are they more attuned to their bodies? Or is there a fundamental difference in genomic response based on gender? That’s a question that’s tantalizing. Our data says yes.

Should people be cautious of genomic testing?

Chris Kresser: Yeah. All right, so let’s just address, maybe, some of the criticisms or thoughts that some people who are listening might have when they hear this show. I mean, I myself have been critical of some of the genomic testing that’s been offered so far and some of the predictions that were being made based on those results, to the point where it even seemed unethical, and there’s been a debate about that, as you know. Showing someone, “Hey, you have this gene. Your risk of Alzheimer’s is 30 percent higher,” and then they become completely stressed out and worried, and maybe it’s a self-fulfilling prophecy to some extent. What do you say to people who might be cautious about this kind of testing on that basis?

Ritchie Shoemaker, MD: The first level of response is to simply say that transcriptomics is looking at genes that are being expressed. That means there’s action involved with these genes. It is far fewer genes that are expressed compared to genes that are present, and simple presence is not enough to show gene expression and gene activation. Some of the tests based on single-nucleotide polymorphisms have made an assumption that presence translates into the genes being active, but we know that’s just not true, and because we don’t know about regulation of gene activity just because of its presence, then we have a second layer: Even if there is expression, how do we know that the regulation of the gene activity is understood?

The third and final layer goes to what people are calling epigenetics, and there’s such an explosion in the literature on epigenetics, it’s hard to keep up, but it looks like some of the long non-coding RNAs—what used to be called junk DNA—are ones that actually live with proteins without a nuclear membrane, in the nucleus itself, that regulate regulation of DNA. You heard me right. I’m not repeating myself on purpose. If we look at gene abnormalities that could be contributing to illness, some of those are turned on or turned off. There are mechanisms like microRNA and who knows what else that have already been shown to regulate genes, but regulation of regulation is the final concept of how you get to this all-powerful BINGO sitting at the end of the world, telling our genes to be turned on, yes or no.

When someone who is skeptical—and all people, I think, should be skeptical of something that’s new and novel. This is new and novel. It’s based on FDA approval of the results that come from this next-generation DNA sequencer. It’s based on the process of medicine that’s already survived multiple court challenges. It has been admitted for years in one way or another, but what we want to know is, if you showed presence of a gene, did you simultaneously show the microRNA that controls the mRNA getting out of the nucleus, and did you show the ribonucleoproteins that control microRNA and mRNA both?

If all three are present, then I think you can make some assumptions that not only was the science good, it was thorough, as best we know now—tomorrow is a new day—but if we see all of those, then some of the skepticism starts to fade because if you have skepticism that’s based on ignorance—and unfortunately, especially in litigation, we see a lot of that—that is inappropriate. Skepticism based on science is real and is worthy of time, not just speculation on a rainy Sunday afternoon, but the issue for people listening to this broadcast is, are we at a level of sophistication with next-generation DNA sequencing that we can give reasonable probability of illnesses, yes or no, and that answer is clearly yes for a few. We’re working on more.

There’s one more piece, and I have a feeling you probably would have gotten to it, but if we look at a group of genes, activation or lack of activation is one level of analysis, but what if we look at the physiologic pathways that these genes partake in? Now we’re looking at what the clinicians want, because what is wrong with people are abnormal physiologic pathways. The DNA may be saying what’s going to go on with these pathways, but what’s abnormal that has to be fixed can be delineated to a very high level of certainty, and here’s where the biggest bang for the buck is going to come the quickest.

Chris Kresser: Let me break this down a little bit because I think it’s a really important point, and I want to make sure that everyone listening gets this. When we look at some of the tests offered through 23andMe, for example, of single-nucleotide polymorphisms, and one of the trends that started happening as a result of those tests is people will run the test, run their results through something like Genetic Genie, and they’ll see that they’re heterozygous for MTHFR C677T. They have a SNP in this one gene, and then they start taking a boatload of supplements based only on having that SNP in that gene. There are a lot of problems I have with that, but one of the main ones is that that is a highly prevalent SNP. Something like 30 percent of the population has that, but the penetrance is low. Just knowing that the SNP is present doesn’t tell us anything about how it’s actually affecting the person.

The level that you’re talking about with this testing is not just the status of the gene, but how that gene is expressing, if it’s expressing, how it’s being activated. But not only that, the next level from there is what specific inflammatory markers and other biomarkers is it showing up in that we can track over time as we do our intervention as proof or objective markers for the progress that we make instead of just guessing, essentially, which is what’s happening with a lot of these single-nucleotide polymorphism tests.

The importance of microRNA

Ritchie Shoemaker, MD: I think you are right on the button. If you think for a minute about what I mentioned without definition—I apologize—microRNA, these are about 18 to 20 nucleotides. They’re not coding for a protein. They’re part of the junk DNA. Remember, the junk DNA idea. Ninety-eight percent of the DNA that was found in 2002 was not protein coding, therefore junk. But microRNA, I call it the tollbooth operator. It’s kind of at the junction of the nucleus and the nuclear membrane with the cytoplasm and says, “They shall not pass,” or “They may go.” mRNA carries the reverse message of DNA, and if you are making a protein, that mRNA has to get out of the nucleus and get into the cytoplasm, but in order to do so, it has to go through that tollbooth.

MicroRNAs are regulatory in the sense that each one of these compounds will knock out from 10 to 100 and some people say 1000—miR-155 might be the thousandth—but it can knock out these particular genes that are trying to be transcribed and trying to be made into proteins, but the microRNA says, “No. We are not going to let you out of the nucleus.” So the poor DNA is getting the signal to make an mRNA like crazy. It says, “Give me more adiponectin so I can fix the weight problem,” and the microRNA sits at the nucleus and says, “No, adiponectin, you’re not going to get out,” so the weight problem gets worse and worse and worse.

Then people have been coming along and say, wait a minute. Why are we worrying about getting adiponectin transcribed? Why are we working on the DNA when, in fact, what we can do is create a compound—and here’s a good one—an antagonist of microRNA, what’s called an antagomir? There’s one for your crossword puzzle. The antagomirs cost about $6 to make, they knock out the microRNA, so therefore it lets the gene transcription fulfill its single duty, and you will make a protein.

I think we’re going to see a lot of treatments with antagomirs coming through. I know right now there are some very interesting working going on with cardiomyopathy and then hepatitis C. Hepatitis C is a very expensive disease to treat. $6 a day is kind of a bargain.

Is the Progene DX test worth the cost?

Chris Kresser: Absolutely. Well, speaking of bargains and cost, one of the biggest criticisms that some people have about this type of investigational approach is that it’s more expensive. My response to that is, well, if I can do some extensive testing up front now and prevent diabetes in someone, a disease that can cost upwards of a quarter of a million dollars to treat over the course of a patient’s lifetime, then I see that as a bargain. This test that we’re talking about here, the Progene DX, it’s going to be available from your website, Surviving Mold.com, very soon. It’s not a cheap test. It’s about $1750, so tell me why this could actually be cost-effective for a patient who is dealing with chronic illness and who is worried about how they’re going to apply their health dollars.

Ritchie Shoemaker, MD: The question that I have to ask myself at the end of the day is, what are we giving to people when it comes to medical information? Is the information good or not? Back when we could only get MMP-9’s done on a cash basis, Esoterix, which was later bought by LabCorp, would do the test for $65. Back when I would try to get TGF-beta-1 levels done, I could only get it done on a cash basis, $65. Back when I was getting HLA tests done, $450, and yet people who are looking at the importance of those illnesses found that the money was worth it because it gave them information they couldn’t get anywhere else.

If we look at a battery of proteomic tests, and if you’re paying cash for those, it’s not unusual to spend $1000 to $5000, depending on how many you get. And we see the same thing is true when tests are being sold for Lyme disease and tests sold for mold problems and all that, but you know, the value of the test is basically what science underlies it.

There are some lab results that I get from people, and they say, “Oh, did you see my labs from XYZ?” And I say, “Yes. In fact, I read some of those when I put them at the bottom of the canary cage?” And they go, “You did what?!” And I say, “This test is not worthwhile.” And they go, “But I spent $300 for it!” And I say, “You wasted $300.”

That’s the state of the art. How can we show that the testing results with genomics is worth this much money? What we will be able to generate are results that are exactly reliable for this point in time, but we also will house that information under NIH guidelines in an international pool database that lets us go back six months later, a year later, five years later, and reassess at that time in the future and see what we really missed with Mrs. Jones or Mr. Smith. The issue is that this point in time of genomics becomes archived for all human population eventually to use, so there is an investment in the future, in addition to the investment at the time.

But having said all that, what’s it worth to that lady who is taking Parkinson’s drugs, who is not better at all, to know that her Parkinsonism is actually due to an injury to the caudate nucleus from her CIRS due to mold exposure? That happens and that’s real. The treatment for that lady might be something like VIP. We would never give that to a Parkinson’s disease patient all along. I mentioned antagomirs. We’re opening the doors to new therapy.

Maybe it’s a too-long-winded answer, but we have investment in accuracy and integrity of science now and in the future, and we have the ability to look at drug effect. Before and after is the easy way, and when you do before-and-after studies, you don’t have to repeat a lot of the analyses, so the pair is actually less expensive than two times the $1750 or whatever it is.

Just thinking about that cost for a minute, when I went on the internet just the other day to look to see what other labs are charging. $3000 to $5000 to $10,000 is what people are paying just for the genomics without the interpretation, without the pathway analysis, and without the fingerprints. It’s one thing to say, “This car is $50,000, and for me, I can’t afford that,” and someone else says, “Well, the Maserati is $450,000.” Well, I can’t afford that either.

Chris Kresser: Right!

Ritchie Shoemaker, MD: The real issue is that if we take a Maserati and make it available for a Ford price, which is what we’re doing, I think we have something pretty good.

Chris Kresser: Yeah, and if you’re that patient that’s been diagnosed with Parkinson’s, which is an incurable, progressive disease, and then you learn that you actually have a condition that’s caused by living in a water-damaged building, that can be treated effectively using a protocol that has been validated in clinical settings, that’s something I would definitely happily pay for if that were me or any kind of family member. You have a tube of my blood, Ritchie, and I’m eagerly awaiting seeing the results and definitely curious to see how my daughter has been affected by this recent mold exposure.

I mean, the truth is this test will be out of reach for some people, and there’s a whole discussion to have around that that we’re not going to have right now about our healthcare system and what our health insurance dollars are actually paying for versus what we would like them to pay for. Hopefully we’ll see progress and change in that realm soon, but we can only change so many things at once, and there are only so many battles that we can fight. As a clinician and as someone who has struggled with CIRS myself and with my family, I’m definitely glad that this test will be out there, and I look forward to learning how to utilize it as a clinician.

Ritchie Shoemaker, MD: When I was in practice—I retired at the end of 2012—for every new patient that came—and some were very critical of my policy—I charged people $100 each before they were seen. It was a mandatory fee, and some people didn’t think that was right, but nonetheless, that went into what I called an indigent fund, and we used that to pay for people who had been disabled or injured to the point that they lost their home, they lost their job, they lost their family, they lost their bank account—they lost everything—and we could help out. And we did, with about $20,000 to $50,000 every year, depending on how much money we raised for the nonprofit group that made that charge.

Chris Kresser: Right.

Ritchie Shoemaker, MD: The same approach is also being applied to the cost of the genomics test. When the test is run through the Surviving Mold website, a significant donation, up to $200 per test, is put into a research pot that will be administered by Surviving Mold, that will be able to pay for genomic tests and other things similar to that in the future. We all hope that things can be reduced in cost, and I think that that’s going to happen as newer generations of the next-generation sequencer come. It used to be that this was a test that cost $25,000 to run one sample, and one sample a week was all they could do, and now we’re talking about doing a thousand a day. There are machines out there, and of course, you need million dollars to have one of these machines. You probably have two by now, Chris.

Chris Kresser: That’s phase two!

Ritchie Shoemaker, MD: The issue is that this is where the future is going to be. Someone might reasonably say, “All right. I’ll wait until the price comes down.” New demand for this, that, and the other, and then you wake up in the middle of the night and say, “Wait a minute. Here’s something reliable that I could be using now.” That’s a decision that only you can make.

I’m reminded about some of the interest in one of the viral causes of chronic fatigue syndrome, and Judy Mikovits certainly has talked more about XMRV and some of the problems that she faced with that test, but when word got out that here was a test for chronic fatigue syndrome—you could get an ELISA test and a culture, and it was about $1200—the labs were overrun with demand because people were sick and wanted to know. Even though the test was quite expensive, there was a bunch that went into that.

We hopefully learned from the bad examples that came out of that and the lessons of XMRV by publishing first and then making sure that the publications had been verified by others. That’s where we are. That’s why you’re seeing so many genomic studies. There’s genomics online that came out from Hopkins not long ago. It doesn’t look at all the genes that I would have necessarily liked, but it’s at least a step in the right direction. Other folks are recognizing that this is the kind of knowledge you can’t get anywhere else.

Chris Kresser: Yeah, and if I think of the amount of money that I spent doing down rabbit holes and barking up the wrong tree over the 10 years it took me to recover my health and get back to a place where I could function in the world, it’s orders of magnitude higher than $1700, unfortunately, for me!

I just want to be clear to everyone listening: I don’t have any financial stake or interest in this lab. I’m just a clinician trying to figure out the best tools to use for my patients and also even with myself and my family, in this case. Hopefully this information has been helpful.

Dr. Shoemaker, it’s always a pleasure to have you on the show. It’s always a fascinating conversation, and we’ll definitely have you back for part three because I know the next thing that people are going to want to talk about is, OK, we have all this great information. Now what do we do with it, and how do we fix it? That can be part three.

Ritchie Shoemaker, MD: I hope that what you’re going to call that is “The Genomics of Brain Injury and Brain Repair.”

Chris Kresser: Well, there you go. You just called it that for me, so that’s what we’ll call it! Sounds good! OK, Dr. Shoemaker, have a great day. Thanks again for joining me.

Ritchie Shoemaker, MD: You’re very kind. Thank you for your excellent questions as always.

Chris Kresser: All right, take care.

That’s the end of this episode of Revolution Health Radio. If you appreciate the show and want to help me create a healthier and happier world, please head over to iTunes and leave us a review. They really do make a difference.

If you’d like to ask a question for me to answer on a future episode, you can do that at ChrisKresser.com/PodcastQuestion. You can also leave a suggestion for someone you’d like me to interview there.

If you’re on social media, you can follow me at Twitter.com/ChrisKresser or Facebook.com/ChrisKresserLAc. I post a lot of articles and research that I do throughout the week there that never makes it to the blog or podcast, so it’s a great way to stay abreast of the latest developments.

Thanks so much for listening. Talk to you next time.

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