Mold expert, Keith Berndtson, MD shares tips about treating and preventing mold toxicity.
Mike Mutzel: Fantastic. Let’s open up a can of worms on mold and mold toxicity. We’re talking before we start…
Dr. Keith Berndtson: Now there’s a great need to do it. People often want to know how I got into this. And back in 2007 when I opened this practice, a patient walked in with this book called “Mold Warriors” by some guy named Ritchie Shoemaker. And you know, I finally got around opening it and reading a little bit, and began to feel like I was drinking from a fire hose because there’s so much information in it—a lot of path of physiology, but also getting into the patients’ stories and legal ramifications; and implications for agricultural practice, construction practice; remediation, inspection, and cleaning; and all that kind of stuff. So I wondered what I got myself into, but I’ve then subscribed to the newsletter from Surviving Mold, his website, which now gets about 3 million hits a month, and built up my confidence to start taking these patients on. Even at that point, I was kind of at the lower end of the learning curve. But what’s important to understand here is that this is not just about mold toxicity. Back in 1973, when there was a OPEC Embargo and there were long gasoline station lines and so forth, there was a premium on conserving energy, and so builders decided they would step up and they would start building homes that were pretty tightly sealed that you could trap heat and save money during the winter and all that.
Dr. Keith Berndtson: But creating conditions were moisture had nowhere to go. The buildings weren’t breathing the way they used to, and so we started to have more of what’s called “sick buildings syndrome,” which in the beginning wasn’t very well understood and kind of got laughed at the room and a lot of grand rounds and that sort of thing. But now we know much more that under certain recurrent moisture conditions or after water intrusion events—roofs leak, leaks under sinks, flooding of course, flooded basements—that molds can get a leg up. And all molds need to grow is moisture and cellulose; dust contains cellulose, so they pretty much have growing conditions almost anywhere where there’s been enough moisture. So it’s very important to discover these intrusions and remediate them quickly because within 48 hours, you’ve got mold growing. And not all molds are toxin producers, either; but the ones that are have genes that code for toxins that they use to defend themselves when they pick up stress signals, and that could be running into manmade chemicals in the dry wall or whatever. They make spores that carry toxins. When things dry up, the spores go dormant; but when the moisture returns, they become active, they could be spitting out toxins. And heavily water-damaged buildings, it’s not just mold toxins, there are other inflammogens—microbial, volatile organic compounds, manmade volatile organic compounds—they all enter the mix; there are fungal fragments, bacterial fragments. So anybody can get pretty sick in a building like that. But in what’s commonly referred to as “mold toxicity syndrome,” about one in four people carry these HLA genes; HLA means it’s on chromosome 6, and it has to do with the part of the immune system that presents antigens from one cell to another, processes those antigens first, and begins this process where you can acquire a coordinated cellular and antibody response against something like this should you come across it again.
Dr. Keith Berndtson: But in one in four people, there are now 12 genes that have been identified—12 HLA genotypes—that render people susceptible to poor clearance of toxins made by living things, or biotoxins. In the category of biotoxins, molds account for 80 percent of the clinical problem; but bacteria can generate toxins, parasites, fungal strains, that might colonize mucous membranes—also capable of producing toxins that are nasty. Candida albicans, for example, has been shown to make something called “gliotoxin;” it’s called “gliotoxin” because it can find its way into the microglia of the brain and disrupt things. And we know that many of the mold toxins that have been described are cytotoxic as well; they can arrest cell cycles, they can arrest mitosis, they cause oxidative stress, they cause ribosomal stress—so they’re bad actors. And I fear one of those four, or one in four, was a hard time clearing these things; you become sick over time. You might not, on your first exposure, and in many people it seems to require a priming event of some kind, like a major stress, or an accident, or a bout of mono, or something like that. And once that’s happened, the next time, now that your immune system is primed to martial a big response—next time you’re exposed to biotoxins, it’s going to start to cause this inflammation, because the complement system, which is part of the innate immune system, is genetically programmed to respond dangers in molecular patterns that we’ve been exposed to over the eons through our ancestors—and most of them come from microbes. There’s one complement protein called “C4-A;” this is the activated form of “C4” that seems to specialize in responding to toxins made by living things. So when you’ve got these toxins on your body and you’ve got the genes that make it hard for you to clear them, C4-A is responding to this again and again and again like it’s seen it for the first time, and when that happens, it initiates a cascade of downstream inflammation that ropes in a bunch of other markers, but not C-reactive protein, not the classic markers of inflammation that we see.
Dr. Keith Berndtson: Things that aren’t familiar to many people, like they were to me when I first learned about these things—like TGF-beta1, MMP-9. There are three types of hormones in those regulatory neuropeptides that are made in the hypothalamus; they get roped into this problem. One is called “antidiuretic hormone” or “vaseopressin”; it tells the kidneys to conserve water, and so when it’s not getting synthesized and when we measure it, it’s often undetectable.
Dr. Keith Berndtson: That means the kidneys are not getting the message to conserve water, and you are getting dehydrated; and if you get dehydrated enough, you become symptomatic—you’re thirsty, you’re drinking water like a fish, but you’re peeing it out in about the same rate so you’re not gaining on it. At some point, if the osmolality, the electrolyte concentration, goes up high enough, you may become a static shock machine.
Dr. Keith Berndtson: And so that’s actually one of the symptoms that could provide a tip-off that something like this is going on. So antidiuretic hormone. And then, there’s something called “MSH (melanocyte-stimulating hormone)”—I know everybody gets tripped up on that one because they name these things whatever they find it doing when they first discovered it.
Dr. Keith Berndtson: But in the immunology literature, alpha-MSH is viewed as a field general coordinating immune defenses from mucous membranes in the body. So the respiratory tract, the gut, the urinary tract, and the skin is also involved here. So we know that synthesis of MSH is actually not a synthesis issue. MSH is bound to something called “POMC (proopiomelanocortin),” and when leptin (which you know plenty about) binds to its hypothalamic receptor, it initiates downstream pathway activation, including a process that would cleave POMC from MSH to free up MSH.
Dr. Keith Berndtson: Well, and POMC gets cleaved in to melatonin and beta-endorphin. So if that’s not happening because the leptin receptor’s partially blocked by pro-inflammatory cytokines, then your risk for not sleeping as well, for having your pain feeling amplified, and not having this field general coordinating mucous membrane defenses for you.
Dr. Keith Berndtson: And then, the other one is called “basal reactive intestinal polypeptide.” So those are the three regulatory neuropeptides that can get involved in this chronic inflammatory response syndrome that we call “CIRS.” Chronic does start with the hard C, CIRS is a soft C, but if we use the hard C, it would be curse, and that just seems like piling on.
Mike Mutzel: Right.
Dr. Keith Berndtson: They’re sick enough already.
Mike Mutzel: Sure.
Dr. Keith Berndtson: So basal active intestinal polypeptide is a really big player. I mean, it’s considered a master regulator of immune function and a master regulator of blood flow distribution in the microcirculatory regions of the body. When VIP is approaching the undetectable range, it’s not uncommon for these patients to have unusual shortness of breath, air hunger at times, and at some point they get chest pains because they’re trying to breathe so hard just to oxygenate. And what we find is that when TGF-beta1, which I mentioned earlier, is active enough, it can start causing remodeling in the areas that are inflamed; and if it’s airborne toxins, the first place where inflammation starts is in the lungs and in the bronchial tree. So what TGF-beta has to do is remodel, and that often results in a little bit of fibrosis.
Mike Mutzel: Wow.
Dr. Keith Berndtson: The fibrosis involves the arterials in the lungs so they narrow, and that puts increased pressure on the right side of the heart, which is trying to take this deoxygenated venous blood and send it back through the lungs, so that again, in the left side of the heart, and then back up, and around the horn. So what happens when you’ve got this back pressure is really it becomes an acquired form of pulmonary hypertension, and this is a new understanding of a form of pulmonary hypertension that is theoretically reversible, and in practices in most cases, reversible.
Mike Mutzel: Wow.
Dr. Keith Berndtson: Because people go online and read about pulmonary hypertension, and it almost reads like a death sentence.