Aaron Goodman: [00:00:00] You are listening to the Chemical Sensitivity Podcast. I'm Aaron Goodman. I'm a journalist, documentary maker and researcher, and I'm someone who's lived with multiple chemical sensitivity or M-C-S-M-C-S affects millions around the world. It's a condition that makes everyday life extremely challenging.

Fragrance, air fresheners, fresh paint, scented laundry products on someone's clothing, and a lot. More can trigger exhaustion, brain fog, muscle pain, rashes, and a wide range of symptoms. And yet, for all its impacts, MCS remains largely invisible. Most doctors dismiss it. Employers rarely accommodate it. Even friends and family struggle to understand.

This podcast aims to change that we dive into the latest research, share real stories, and explore how people navigate life with an illness. Many refuse to see. Now lately on the Chemical Sensitivity Podcast, I've been checking in with you the lister about how we could possibly take to [00:01:00] task researchers and clinicians who falsely, in my view, label MCS as a psychological disorder.

In speaking with guests on the podcast, I've gained some helpful insights into why this continues to happen. And I know how deeply painful this form of healthcare invalidation can be for people with MCS and other illnesses. Some researchers defend industries that cause harm. Other scholars are blinded by their own training and disciplines, and many researchers still sadly don't speak with people with MCS and involve us in their studies.

Why do we need research that challenges false claims when we know what's true? Credible research can influence how doctors respond to us and how and if they diagnose us. Research influences whether or not we're successful in requesting accommodations that we depend on. And it impacts [00:02:00] how others even loved ones regard us.

So when I came across Professor Beatrice Al's research about Gulf War illness and its ties to MCS, I quickly reached out to request an interview for the podcast, and I'll tell you why. Professor Goam is a professor in residence of medicine at the University of California San Diego in the United States.

Her research focuses on the health effects of environmental, chemical exposures, mitochondrial and bioenergetic dysfunction, adverse effects of medications such as statins and others, and multis symptom illnesses. Including Gulf War illness and MCS. This is the second time Professor Goam has been on the podcast and I found our new conversation to be complex.

Yet the material and information she shared is understandable and [00:03:00] deeply relevant and timely over decades. Professor Glom has worked closely with soldiers who served in the Gulf War in Iraq in 1990 to 91. These veterans were deployed mainly to the Persian Gulf region, to Kuwait, Iraq, Saudi Arabia, and beyond.

Gulf War illness is linked to exposures that occurred during that period to nerve agent prophylactics, like pyridostigmine, bromide or PB pesticides, oil well, fire, smoke, and other toxicants. Rather than combat injuries and many Gulf War veterans developed and continue to live with MCS through her decades of work.

Dr. Golum has uncovered that Gulf War illness is caused by cellular damage brought on by medication soldiers took. And [00:04:00] the chemicals they were exposed to specifically, and this is helpful for civilians with MCS, she says MCS is a result of the damage to part of our cells in our bodies, again, that are called mitochondria.

Mitochondria are the. Power plants of ourselves. They take the food we eat and the oxygen we breathe and turn them into energy so our cells and we can stay alive and active. Mitochondrial damage or mitochondrial disease, as Professor Golum says, created by toxins, medication, and compounded. By a genetic inability to process chemicals can lead to MCS.

My hope is that her research spreads and that more and more scholars understand her work. And so when we go to doctors and clinicians, [00:05:00] they can be on the lookout for mitochondrial damage, which can contribute to MCS, and I hope that soon. We will no longer be told that MCS is in our head. So in this episode, you'll hear Professor Gola go into detail about the connections between Gulf War illness and MCS, how through years of rigorous research and advocacy she led a campaign that secured official medical recognition for Gulf War illness transforming.

Decades of dismissal into validation and care for affected veterans. How MCS is clearly not a psychological condition, but an illness, again, affected by mitochondrial or cellular damage, genetics and chemical exposure. Hello again, professor Golum. Thank you very much for joining me. 

Beatrice Golomb: It's my pleasure. 

Aaron Goodman: Would you please just take a moment to [00:06:00] remind listeners about the importance of your research?

Why have you spent so much time looking at the impact of chemical exposures for Gulf War veterans? 

Beatrice Golomb: After the close to 700,000 US deployed veterans return from the Gulf in 1991, a good fraction of them were reporting development of chronic multiple symptoms and. A lot of people were saying it's not real, it's in your head.

And that we spoke to, to this day say that their biggest psychological scars are not from the things they experienced in the war, but from the way they were dishonored by many medical providers on their return. And the early reports that came out from the Presidential Advisory Committee and the Institute of Medicine, which is now called the National Academy of Medicine.

Basically used the following inappropriate reasoning standard for organic causes, meaning physiological causes like environmental factors. They said absence of [00:07:00] proof that it's responsible is proof of absence, whereas for stress. They basically said, well, gee, stress can cause lots of things, so it must be causing this.

So basically for stress, suggestion was construed as proof, like there was no requirement that the people that had more stress were more ill. There was no requirement that stress had led to a similar profile of chronic symptoms in previous settings. And indeed subsequent data found that stress is not an independent predictor of goal for illness.

So I was disturbed that these veterans who served donation honorably and put their lives on their line for the country. I came back with toxic wounds from the war, and this was not taken seriously. Mm-hmm. Mm-hmm. Our work was the first to show that the energy powerhouses called mitochondria are affected in Gulf War illness.

That the severity of Gulf War illness is tied to the severity of that energy deficit that. Although inflammation is elevated and effect goal for veterans on average, not in everybody, [00:08:00] the degree of elevation is not positively tied to illness severity. In fact, it's actually negatively tied to severity once you take into account the mitochondrial impairment and it is tied to drivers of what's called program cell death or apoptosis, and many other findings of that kind, including findings like that treatment with coq 10.

In a double blind randomized trial that is directed towards cell energy and oxidative stress, both alleviated symptoms compared to placebo, and then also significantly improved objectively measured physical function. We're doing a larger replication study of that right now. But those are some of the things that we found.

Aaron Goodman: So what kind of medication were people exposed to that led to MCS? I 

Beatrice Golomb: haven't specifically looked at the medications that led to MCS, but we know about the medicines that contributed to goal for illness severity, and about half of affected veterans in most of our Freddy's, between 40 and 60% depending on the study [00:09:00] of veterans with illness are chemically sensitive.

So they were given a nerve agent pretreatment pill. Istic mean bromide, a number of them were given ciprofloxacin, a fluoroquinolone agent that, mm-hmm. That our data and others data have tied to chemical and actually even electromagnetic sensitivity, and is also tied in existing literature to quote photos.

Sensitivity with ultraviolet light and quote, radio sensitivity, meaning medical radiation, so that's ionizing. Radiation and fluoroquinolones are also mitochondrial toxins, and they were given in some cases for bio warfare protection in the event that Saddam Hussein used his stockpile of weaponized anthrax, which did not happen.

Those are the main sort of drugs for which there's data. Tying them to goal for illness severity. Mm-hmm. Certainly there are other drugs like methyl, which is an anti-malarial that is tied to mitochondrial injury and persistent problems in [00:10:00] some people, often neuropsychiatric problems. But those were the main sort of drugs that were.

Given, and also there were vaccinations including the Anthrax vaccine, the first widespread use during a time when there was very lax FDA oversight of the production. And it was the exclusive time that Botulinum Toxoid vaccine was used in the military and a high level, high number of multiple vaccines where the other medications that were involved and in some studies have been tied to presence and severity of illness.

Aaron Goodman: Very interesting. So I know many listeners are very interested in finding supplements that can assist people with MCS. You mentioned coq 10. Do you want to talk about what role coq 10 may play in assisting with mitochondrial damage and MCS? 

Beatrice Golomb: Yep. So I don't really know how effective it is for [00:11:00] MCS, uh, but I can tell you what our findings are related to mitochondrial impairment and oxidative stress and MCS and how that would relate to coq 10.

And also I can mention other supplements that are broadly beneficial for mitochondrial antioxidation. Have shown benefit against injury from innumerable chemicals, as has coq 10. So let me sort of start by saying what I think is going on as a piece of the puzzle with chemical sensitivity and the fact that both in, in our Gulf War population and now we're also setting the people that were exposed to the.

Derailment and chemical release and burn in policy in Ohio in February, 2023, and we find that their illness profile, the ones that develop persistent symptoms is a match goal for illness. And also in that group, around half of those that meet those goal for illness criteria also report new chemical [00:12:00] sensitivity.

So that's a match there as well with a completely different group of chemicals. Among the things that led me to focus on mitochondrial impairment and gulf for illness are the following. So pretty much every chemical, no matter it's a chemical class or nominal mechanism of action. Produces part of its toxicity by damaging mitochondria and causing oxidative stress.

And I've heard doctors say multiple chemical sensitivity can't be real because people are responding to chemicals from completely different chemical classes with different mechanisms. But the thing is, mitochondrial injury occurs for pretty much every chemical, no matter what its mechanism. And also there's what are called gene environment interaction data so that people that have a genetic.

Variant of a M fund that detoxifies one of those exposures where their detoxification is impaired. Mm-hmm. If they also had the exposure, their almost rates are much higher. Mm-hmm. For [00:13:00] example, there was a 2015 study that these. Variants of enzyme called buterol. Tase involved in detox like PDB should be looked at because if there was a causal relationship, people that had genetically impaired detoxification should have higher rates of I if they took the pd.

Mm-hmm. And the evidence now shows that, so people who took the PD. If they have the usual variant of the detoxifying enzyme, they had about a 2.6 fold elevated risk of developing goal for illness. If they had the impaired detoxifying gene but didn't take pb, they have no elevated risk, which is ideal. It means they weren't predestined to be ill by their genetics acquired the exposure.

Mm-hmm. But if they had the PD and the impaired detoxification. It's a 40 fold elevated risk of illness. Mm-hmm. Which is obviously quite substantial. Mm-hmm. So back to that y mitochondria. So first off, like mm-hmm. Every chemical pretty much contributes to that. Mm-hmm. And different Gulf four veterans had very different chemical [00:14:00] exposures.

There was everything on the battlefield from depleted uranium to smoke from oil fires, to jet fuel to something called chemical agent resistant compound, or Kirk Paint. Impregnated uniforms, massive numbers of different exposures with different veterans experiencing different subsets of those, and yet the profile of illness from veteran group to veteran group remains consistent.

And so that suggests to me that again, this shared mechanism that can add and synergize across different chemicals was dominating the illness profile. Second feature was what are the nature of the symptoms that are elevated and pretty much goal four veterans have multiple symptoms spanning many different symptom classes, which is classic for mitochondrial impairment, but dominated by fatigue, brain, and muscle symptoms.

That is to say [00:15:00] fatigue, which is itself sort of low energy. Then symptoms, what are called post mitotic organs, meaning they're mostly done dividing that have high energy demand, brain and muscle. Mm-hmm. And so that's also classic for mitochondrial impairment. And then also there was variable latency to symptom onset.

There was a study that showed that like of these increased symptoms that these Gulf War veterans had, 40% of them emerged over a year after people had come back. That's also classic for mitochondrial impairment. The variable latency to onset is classic, and that's because the mitochondrial impairment begets more oxidative stress.

So mitochondria, the main source of the free radicals, the oxygen free radicals that cause oxidative stress, and there's some main target because most of those free radicals are made right there in the mitochondria. So mitochondrial, DNA and RNA and lipids and proteins are especially vulnerable. And then mitochondrial DNA also have less efficient repair [00:16:00] mechanisms than the regular Watson.

Quick double strand, DNA, that you inherit from both parents. Mitochondrial kind of like little colonies of bacteria in every cell. And in fact, the main theory of what mitochondria are is that that's how they originated. They have their own bacterial style DNA that is generally inherited only from the mother, but their DNA repair mechanisms are less robust.

Mm-hmm. Which is why as people get older, especially, you know, well into older age, there are sort of exponential rise in mitochondrial DNA needs. Mutations because once they hit a certain point, they cause more free radicals to be produced. Mm-hmm. In the process of energy generation. And that leads to more mitochondrial DNA damage and worse mitochondrial function, which leads to still more free radicals and so on.

And so in goal four illness, it looks like that's just happening at an earlier age. And in fact, many or most of the features of goal for illness look like accelerated aging. The conditions that they have at high rates are conditions that typically [00:17:00] rise with age, and then the symptoms or symptoms that typically rise with age, et cetera.

So those were some of the reasons why it looked like it had to be mitochondrial impairment. And indeed. Findings, that is mitochondrial impairment. Again, there are other objective markers that are altered, most of which can be explained by mitochondrial impairment and it's downstream mechanisms. And then back to CO two 10, you asked how does that help?

Yes. Well, CO two 10, it's, it's actually a co-enzyme in mitochondrial electron transport made by the body. Both production and transport are. Inhibited by things like statin, cholesterol lowering drugs, which block a step early in the pathway, and cholesterol also transports cozy Q 10, which is the reason why some people on statins get fatigue and muscle problems and cognitive problems, the same kinds of problems that Gulf four veterans get, that it's usually reversible because.

When you stop the statin, the coen on ketone level, which was the problem, [00:18:00] goes back up, which is different from the mechanism of mitochondrial impairment in Gulf War veterans. So it is a co-factor. There are data showing that essentially irrespective of the respiratory chain defect, meaning which particular problem in the mitochondrial.

Electron transport or energy production chain coincide Q 10 helps to bypass that defect, which is also why you take something like statins, which is basically withdrawing coq 10 and you're unmasking unquote mitochondrial problems. So all of us start out with mutations and deficits and so forth, but the hope is that they're covered by.

Adequate levels of antioxidants and energy supports and that there's adequate energy reserve. And in fact, that's what I think is the issue with chemical sensitivity. You have somebody that's been exposed to chemicals, their energy reserve has been cut, and their antioxidant defenses are [00:19:00] strained by existing oxidative stress from mitochondrial damage itself and or from other chemicals and exposures.

They're either perked close to the point where there's not enough energy to prevent symptoms or, or they're already on the steep part of the curve where each additional cut in energy or includes an oxidative stress produces more symptoms. I think that's why in Gulf War Veterans, it's generally the ones that develop Goal four illness.

They're far more likely to be the ones that have chemical sensitivity because they're the ones that are already on the steep part of the curve. Cell energy isn't enough to protect against symptoms in the general state and or anti accident defenses are not sufficient to offset oxidative stress and that leads to symptoms.

Aaron Goodman: This is fascinating, complex, but fascinating. It really resonates. Are there any practical steps that people might do to reduce [00:20:00] oxidative stress and or support mitochondrial health? 

Beatrice Golomb: Yeah, there are a number of them and probably three supplements that have the strongest evidence of really broad benefit.

And again, there are studies for each of them showing protection, amelioration defense, mitigation of harm from myriad, different chemicals, radiation, et cetera, are cozy Q 10 itself. Mm-hmm. And then melatonin. Which people think of us for sleep. It actually, it's a really critical pre radical scavenger that also upregulates other antioxidants and an acetyl cysteine, which is the precursor for glutathione, which is another of the major important antioxidant.

Mm-hmm. Pathways, uh, glutathione peroxidase needs selenium, and so some people will also recommend adding some selenium together with. Other supplements in order to have that cofactor be present. Mm-hmm. [00:21:00] But those are with glutathione. 

Aaron Goodman: Glutathione, correct. The last one was glutathione. Yeah, 

Beatrice Golomb: glutathione is is produced from N-Acetyl.

You can get things like liposomal glutathione that may be assimilated. The reason a lot of people use the precursor NAC, is that glutathione is usually not. That well assimilated by the body that that's several amino acids that make up glutathione or pretty much n-acetylcysteine is the most commonly used thing.

I should mention that for n-acetylcysteine, there will be people that get worse. There are issues like people may have gene variants in like something for example called glutathione reductase, where they may have trouble. Making glutathione go back to the reduced form that serves as an antioxidant. So for NAC, I don't know if it's equal true for melatonin.

I haven't really looked that up, but for a lot of antioxidants, there will be a subset of people that rather than being made better, will be made worse. In the case of ENSs, I'm qan, it comes in both the ubiquinone [00:22:00] form, which has been on the market for longer and has a much more robust body of evidence showing that it protects against.

Many, many different things from headache to heart attack to cutting the risk of death in heart failure patients by over 40% compared to placebo, protects against fatigue and pain and lots of different things. Most of those data are with the ubiquinone form, and we did our first study with the ubiquinone form, even though there were a lot of people saying, oh, ubiquinol is better because it's the reduced form that can serve as an antioxidant.

My thinking was that's a nice theoretical claim. But there aren't the clinical data, and sometimes there will be a surprise, like either this is the thing you'd put in the pill to keep it in the reduced form is causing a problem or this or that. And indeed we later found that both for Gulf four veterans and for fluoroquinolone affected patients, a subset and minority subset, but a subset report getting better on ubiquinol, but [00:23:00] actually being made worse on ubiquinol.

So energy production. Excuses of the ubiquinone form, the oxidized form. And if the coq 10 inside the mitochondria is too heavily in the quote reduced form, the form that serves as an antioxidant will actually drive energy production backward, will harm energy production and paradoxically increase the oxidative stress inside the mitochondrion.

So we, we tend to. Not, this is not a recommendation, but mm-hmm. For people who wanna take kq 10, because my personal attitude is first, you know, harm and some people are made worse with ubiquinol, even though maybe some people will be made better with it, we tend to go with the ubiquinone form. And I should also mention that there are very wide differences in bioavailability for different products and.

Pro 10 is hard to make bioavailable. We used a specific [00:24:00] brand, actually the pharma nor Brand made in Denmark, uh, for our studies. And that's been used in a lot of the studies that have shown the different benefits. And I mentioned that because it's not really the case that all Ubiquinone has created equal and some of the most affected mitochondrial patients I know get tremendous benefit from.

That brand. And I think there are probably a couple of other good brands, but there are a lot that really just are not bioavailable and don't really do much of anything for some people. 

Aaron Goodman: And, and that brandd did you meant say? 

Beatrice Golomb: Pharma Nord, P-H-A-R-M-A, capital NORD. And I don't mean to be touting a particular brand, but for this supplement it's, yes, the quality control and bioavailability issue is so important.

Aaron Goodman: Yeah. Thank you so much. Uh, professor, I want to ask you about the connection between Gulf War illness and MCS for the general population, people who haven't served in the military, and so much of what you've shared resonates with me personally, [00:25:00] and I think it will resonate with others. For example, in my youth, I had methyl antimalarial when I Oh, interest worked overseas.

Oh, interesting. Yeah. I also was exposed to ci Permethrin. You mentioned Permethrin was in the clothing of people in the military. Yep. Yep. Multiple vaccines for working in, uh, the global south. Do you want to talk a little bit about, do you think your findings apply to civilians with MCS? 

Beatrice Golomb: I do think they apply to civilians with MCS.

With the caveat that, for example, the genetic finding that, that we may or may not get to talking about its relation to MCS is mostly gonna show up in samples of people that have been heavily chemically exposed. Because if you don't have a lot of mitochondrial oxidative stress to manage, then genetic management of mitochondrial, oxidative stress is not gonna show up as a factor.

So unless you've got a population with a lot of people that are chemically sensitive. [00:26:00] Ideally with people who are and are not chemically sensitive, both having had chemical exposures, then you can't really see how the genetics plays out in determining chemical sensitivity risk. The point of showing the genetic relationship is several fold.

Right now. When doctors put in a, a diagnostic code for chemical sensitivity, it's usually under the somatoform. Or somatic symptom disorder label, which basically means it's all in patient's heads. And that is a tremendous disservice to affected people. And it drives the belief that the problem isn't real and it's not really caused by chemicals.

And, and the thing is, it doesn't matter whether you have this particular genetic variant or not that promotes it. What this shows is that there is a pathway that involves. Mitochondrial oxidative stress management [00:27:00] that is implicated, but there may well be other genes that influence that pathway that people have, and the particular genetic finding that we have.

Doesn't call for a d. Management approach than just the knowledge that mitochondrial management of oxidative stress is implicated. I will say that there is a follow-up genetic thing that we really need to look at, and if you have people on your podcast that wanna help by participating in a genetic study, have them reach out to us.

The 

Aaron Goodman: research that you're doing is very important and will share a contact. In the show notes for people who want to reach out. And I wanna ask you, professor Glom, this year, I believe Gulf War illness finally received its own medical diagnostic code. Yes. Correct. I led 

Beatrice Golomb: that effort. 

Aaron Goodman: You were a big part of that effort.

And I 

Beatrice Golomb: led it. Yes. 

Aaron Goodman: Yeah. And so important, but do you wanna talk about [00:28:00] why it's important not only for folks with Gulf War illness, but. Potentially for people with MCS, because as you mentioned, when we go to. A doctor there isn't a diagnostic code and that's why we're told it's a psychological disorder. So what does this change perhaps for civilians?

Beatrice Golomb: I hope it leads the way for a broader understanding that just because a doctor doesn't happen to understand somebody's problems, just because they have multiple symptoms, just because one of their routinely conducted. Past doesn't show an abnormality with a given group of people doesn't mean the problem isn't real.

And again and again, we've seen the same thing, whether it's fibromyalgia or chronic fatigue syndrome, multiple chemical sensitivity goal for illness, we we see that there are a group of people who say the problem isn't real. It's all in their head. They're just malingering. And yet they continue to say this even [00:29:00] after there's abundant evidence showing.

Problems. And in each of those cases, mitochondrial problems and other soul energy impairment problems are part of it. There's mitochondrial problems and also long COVID mitochondrial problems documented in fibromyalgia and also. There are studies showing that, and these are not uncorrelated by the way, showing that patients with fibromyalgia have reduced capillary in their muscle, meaning they have fewer blood vessels, meaning that some of those cells have, don't have easy access to.

To the oxygen and the glucose and the other energy substrates. There's ischemic muscle pain, meaning not enough energy to the cells that arises very easily when there's not enough blood flow. And on top of that, you have impaired mitochondrial function in chronic fatigue syndrome. There's analogous data showing that a good chunk of people have reduced total body blood volume.

So when you go to the doctor, [00:30:00] they measure like your hemoglobin and your hematocrit, which is the red blood cells and oxygen curing capacity per blood volume. But if the total blood volume is low, then that doesn't show up. That hematocrit and oxygen curing capacity may look normal, but that's again, per volume.

And if you're down like a liter of blood out of five or six liters, then that. Oxygen curing capacity is actually inadequate and will contribute to driving things like fatigue. I think it's not an accident that mitochondrial impairment shows up in these problems because doctors are basically trained in organ-based physiology, like it's either a lung problem or a heart problem, or a kidney problem, or a liver problem.

Mitochondrial problems don't fit an organ based system, cell energy is needed for every cell in the body. More energy is needed for highly energy demanding organs like brain, and muscle and heart, but all organs need. And [00:31:00] so mitochondrial impairment can cause symptoms in all organs, and those symptoms vary a bit from person to person, and there are a lot of reasons for that.

There's something called quote heteros, which means that those colonies of bacterial mitochondria. Have different mutations, and those mutations may go to some organs so that people can start out with different vulnerability and different organs. And then on top of that, we talked about medications and other exposures.

Those can have a tropism, meaning can preferentially go to some organ like the liver or the kidney or the skin, making that part of the body then become more vulnerable in that person so that, so different people in mitochondrial disease in general and in. Environmentally triggered mitochondrial disease in specific the patterns of illness.

On a group level are consistent, but individual to individual, different people will have different ones of the symptoms that are characteristic. And again, doctors aren't used to thinking in that way. [00:32:00] And there is a legacy that comes from Freud back in the era where neurology and psychiatry hadn't yet divided up, where he had this basically delusional idea.

That a lot of different medical problems were in patients' heads, and it's basically the same kind of thinking that has come down through history. There never was any positive evidence that psychogenic illness ever produces persistent symptoms in anybody. It was a made up idea that took hold and has had a persistent legacy.

To this day, when I entered medical residency, I remember seeing a list of the causes of low back pain and top on the list was psychogenic. And then miraculously when ergonomics came in, somebody figured out that people had transitioned heavily to office jobs and didn't understand the ergonomics, and then people began understanding ergonomics and it miraculously, it fixed all those neuroses.

So these ideas that when there's a problem where you don't [00:33:00] have something you can measure. There seemed to be a good chunk of people who choose to believe that the patient is responsible for their problem, and I think that's unconscionable. I think it's a violation of Hippocratic Oath. Our data on Gulf War.

Veterans suggest that those damaging attitudes not just cause emotional distress in the patient, but they also affect things like return for care and following provider. Directions, which makes sense because they erode trust in the provider and then that can affect both continuity of care and also effective care for their other health problems.

So these are very damaging attitudes. They were never justified and they need to be stamped out. 

Aaron Goodman: I'm, I'm so grateful to you for talking about that. At some point the researchers. And clinicians who continue to put out this false argument that multiple chemical sensitivity is a psychological disorder.

Mm-hmm. You think they owe us an apology? [00:34:00] 

Beatrice Golomb: Yeah, I do think so, but I don't know what that exactly brings you, but most of them all, they need a revision in their attitude. In a lot of the settings where these problems emerge that are classed by some people as mass hysteria or psychogenic. Settings where there's a party with a financial stake, chemical injury settings, drug adverse effect settings.

Those are settings where there's a powerful wealthy party that has an interest in denying that their product bears a role, and I think that may be a reason for the persistence of these concepts. In medicine because that seems to be the primary place where these continued to take hold. 

Aaron Goodman: You're talking about the military industrial complex, right?

And the chemical industry. And the pharmaceutical industry. What's bigger than those chemical 

Beatrice Golomb: industry, the pharmaceutical industry for people with electro [00:35:00] sensitivity. There's the utility industry, there's big data, there's big telecom, all of those things. 

Aaron Goodman: Professor Golum, are you continuing to encourage younger researchers to.

Follow this path. 

Beatrice Golomb: It's not an easy path to follow in research because there's not really a separate body of funding, and so that is challenging. People typically go where the money is because that's how you have and maintain a career, and so that's a big challenge. We actually have some amazing additional preliminary data on chemical sensitivity.

Related both to the mitochondrial things and related Actually the membrane effects. The membrane 

Aaron Goodman: effects. Membrane effects, 

Beatrice Golomb: yeah. Yeah. So like it turns out, membranes are the barriers of the cell, but they also have critical roles in the energy process, and it looks like both of those are turning out to be really important, and we're struggling to figure out where can we go to get.

The resources to take the next step. And that's a big challenge, I will say. And that is, I think a reason, like a lot of [00:36:00] the things I have, the areas that I've embarked on have been areas where not a lot of scientists spread because there hasn't really been a will to fund them. And that is an issue. And the good news is, for a while there was this pot of goal for illness funding that.

Has been very fruitful in helping with chemical sensitivity because chemical sensitivity was a big part of Gulf illness, but I think we've paid more attention to than anybody else. We've got also a paper showing that patients with higher chemical sensitivity ratings also have higher rates of actual adverse effects to many drugs and chemicals.

The more kind of acknowledged adverse effect issues are also elevated. So it's hard for me to exactly encourage students to go somewhere where. It's not really clear if they can have a sustained career, but I would encourage people to reach out to your Congress people [00:37:00] to NIH, et cetera, and encourage them to advance funding in this area.

And if people happen to know philanthropists that have an interest in this kind of area, that is often a place where initial important work can happen as well. 

Aaron Goodman: How is it for you as a researcher taking on this work and not. Seeing other people doing it? 

Beatrice Golomb: Yeah, that's a, an interesting question and I guess because I've always felt like I'm a patient advocate and I pick areas where it feels like the need is greatest, where there are a lot of people suffering and there are not a lot of doctors and scientists trying to help them.

I'm on the outside trying to move the needle. But on the other hand, it's really worthwhile work, and when we get letters like the ones we've gotten recently from Gulf four veterans who are so appreciative about the ICD code, that's the kind of thing that really makes it all worthwhile. 

Aaron Goodman: Thank you so much for taking time and I hope it's okay if I reach out again in the future as your research continues and I will share the contact for your research.

Thank you so [00:38:00] much. 

Beatrice Golomb: Yeah. Thank you for your interest in the area 

Aaron Goodman: you've been listening to, the Chemical Sensitivity Podcast and the host and podcast creator Aaron Goodman. The Chemical Sensitivity podcast is buy and. For the MCS community, the podcast is generously supported by the Marilyn Brockman Hoffman Foundation and listeners like you.

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I.

Aaron Goodman: You are listening to the Chemical Sensitivity Podcast. I'm Aaron Goodman. I'm a journalist, documentary maker and researcher, and I'm someone who's lived with multiple chemical sensitivity or M-C-S-M-C-S affects millions around the world. It's a condition that makes everyday life extremely challenging.

Fragrance, air fresheners, fresh paint, scented laundry products on someone's clothing, and a lot. More can trigger exhaustion, brain fog, muscle pain, rashes, and a wide range of symptoms. And yet, for all its impacts, MCS remains largely invisible. Most doctors dismiss it. [00:40:00] Employers rarely accommodate it. Even friends and family struggle to understand.

This podcast aims to change that we dive into the latest research, share real stories, and explore how people navigate life with an illness. Many refuse to see. Now lately on the Chemical Sensitivity Podcast, I've been checking in with you the lister about how we could possibly take to task researchers and clinicians who falsely, in my view, label MCS as a psychological disorder.

In speaking with guests on the podcast, I've gained some helpful insights into why this continues to happen. And I know how deeply painful this form of healthcare invalidation can be for people with MCS and other illnesses. Some researchers defend industries that cause harm. Other scholars are blinded by their own training and disciplines, and many researchers still sadly don't speak with people with MCS and involve us in their [00:41:00] studies.

Why do we need research that challenges false claims when we know what's true? Credible research can influence how doctors respond to us and how and if they diagnose us. Research influences whether or not we're successful in requesting accommodations that we depend on. And it impacts how others even loved ones regard us.

So when I came across Professor Beatrice Al's research about Gulf War illness and its ties to MCS, I quickly reached out to request an interview for the podcast, and I'll tell you why. Professor Goam is a professor in residence of medicine at the University of California San Diego in the United States.

Her research focuses on the health effects of environmental, chemical exposures, mitochondrial and bioenergetic dysfunction, adverse [00:42:00] effects of medications such as statins and others, and multis symptom illnesses. Including Gulf War illness and MCS. This is the second time Professor Goam has been on the podcast and I found our new conversation to be complex.

Yet the material and information she shared is understandable and deeply relevant and timely over decades. Professor Glom has worked closely with soldiers who served in the Gulf War in Iraq in 1990 to 91. These veterans were deployed mainly to the Persian Gulf region, to Kuwait, Iraq, Saudi Arabia, and beyond.

Gulf War illness is linked to exposures that occurred during that period to nerve agent prophylactics, like pyridostigmine, bromide or PB pesticides, oil well, fire, smoke, and other toxicants. Rather [00:43:00] than combat injuries and many Gulf War veterans developed and continue to live with MCS through her decades of work.

Dr. Golum has uncovered that Gulf War illness is caused by cellular damage brought on by medication soldiers took. And the chemicals they were exposed to specifically, and this is helpful for civilians with MCS, she says MCS is a result of the damage to part of our cells in our bodies, again, that are called mitochondria.

Mitochondria are the. Power plants of ourselves. They take the food we eat and the oxygen we breathe and turn them into energy so our cells and we can stay alive and active. Mitochondrial damage or mitochondrial disease, [00:44:00] as Professor Golum says, created by toxins, medication, and compounded. By a genetic inability to process chemicals can lead to MCS.

My hope is that her research spreads and that more and more scholars understand her work. And so when we go to doctors and clinicians, they can be on the lookout for mitochondrial damage, which can contribute to MCS, and I hope that soon. We will no longer be told that MCS is in our head. So in this episode, you'll hear Professor Gola go into detail about the connections between Gulf War illness and MCS, how through years of rigorous research and advocacy she led a campaign that secured official medical recognition for Gulf War illness transforming.

Decades of dismissal into validation [00:45:00] and care for affected veterans. How MCS is clearly not a psychological condition, but an illness, again, affected by mitochondrial or cellular damage, genetics and chemical exposure. Hello again, professor Golum. Thank you very much for joining me. It's my pleasure. Would you please just take a moment to remind listeners about the importance of your research?

Why have you spent so much time looking at the impact of chemical exposures for Gulf War veterans? After the close to 700,000 US deployed veterans return from the Gulf in 1991, a good fraction of them were reporting development of chronic multiple symptoms and. A lot of people were saying it's not real, it's in your head.

Beatrice Golomb: And that we spoke to, to this day say that their biggest psychological scars are not from the things they experienced in the war, but from the way they were dishonored by [00:46:00] many medical providers on their return. And the early reports that came out from the Presidential Advisory Committee and the Institute of Medicine, which is now called the National Academy of Medicine.

Basically used the following inappropriate reasoning standard for organic causes, meaning physiological causes like environmental factors. They said absence of proof that it's responsible is proof of absence, whereas for stress. They basically said, well, gee, stress can cause lots of things, so it must be causing this.

So basically for stress, suggestion was construed as proof, like there was no requirement that the people that had more stress were more ill. There was no requirement that stress had led to a similar profile of chronic symptoms in previous settings. And indeed subsequent data found that stress is not an independent predictor of goal for illness.

So I was disturbed that these veterans who served donation honorably and put their lives on their line for the country. I came back with toxic [00:47:00] wounds from the war, and this was not taken seriously. Mm-hmm. Mm-hmm. Our work was the first to show that the energy powerhouses called mitochondria are affected in Gulf War illness.

That the severity of Gulf War illness is tied to the severity of that energy deficit that. Although inflammation is elevated and effect goal for veterans on average, not in everybody, the degree of elevation is not positively tied to illness severity. In fact, it's actually negatively tied to severity once you take into account the mitochondrial impairment and it is tied to drivers of what's called program cell death or apoptosis, and many other findings of that kind, including findings like that treatment with coq 10.

In a double blind randomized trial that is directed towards cell energy and oxidative stress, both alleviated symptoms compared to placebo, and then also significantly improved objectively measured physical function. We're doing a larger replication [00:48:00] study of that right now. But those are some of the things that we found.

Aaron Goodman: So what kind of medication were people exposed to that led to MCS? I haven't specifically looked at the medications that led to MCS, but we know about the medicines that contributed to goal for illness severity, and about half of affected veterans in most of our Freddy's, between 40 and 60% depending on the study of veterans with illness are chemically sensitive.

Beatrice Golomb: So they were given a nerve agent pretreatment pill. Istic mean bromide, a number of them were given ciprofloxacin, a fluoroquinolone agent that, mm-hmm. That our data and others data have tied to chemical and actually even electromagnetic sensitivity, and is also tied in existing literature to quote photos.

Sensitivity with ultraviolet light and quote, radio sensitivity, meaning medical radiation, so that's ionizing. Radiation and fluoroquinolones are also mitochondrial toxins, and they were given in some cases for bio warfare protection in the event [00:49:00] that Saddam Hussein used his stockpile of weaponized anthrax, which did not happen.

Those are the main sort of drugs for which there's data. Tying them to goal for illness severity. Mm-hmm. Certainly there are other drugs like methyl, which is an anti-malarial that is tied to mitochondrial injury and persistent problems in some people, often neuropsychiatric problems. But those were the main sort of drugs that were.

Given, and also there were vaccinations including the Anthrax vaccine, the first widespread use during a time when there was very lax FDA oversight of the production. And it was the exclusive time that Botulinum Toxoid vaccine was used in the military and a high level, high number of multiple vaccines where the other medications that were involved and in some studies have been tied to presence and severity of illness.

Aaron Goodman: Very interesting. So I know [00:50:00] many listeners are very interested in finding supplements that can assist people with MCS. You mentioned coq 10. Do you want to talk about what role coq 10 may play in assisting with mitochondrial damage and MCS? Yep. So I don't really know how effective it is for MCS, uh, but I can tell you what our findings are related to mitochondrial impairment and oxidative stress and MCS and how that would relate to coq 10.

Beatrice Golomb: And also I can mention other supplements that are broadly beneficial for mitochondrial antioxidation. Have shown benefit against injury from innumerable chemicals, as has coq 10. So let me sort of start by saying what I think is going on as a piece of the puzzle with chemical sensitivity and the fact that both in, in our Gulf War population and now we're also setting the people that were [00:51:00] exposed to the.

Derailment and chemical release and burn in policy in Ohio in February, 2023, and we find that their illness profile, the ones that develop persistent symptoms is a match goal for illness. And also in that group, around half of those that meet those goal for illness criteria also report new chemical sensitivity.

So that's a match there as well with a completely different group of chemicals. Among the things that led me to focus on mitochondrial impairment and gulf for illness are the following. So pretty much every chemical, no matter it's a chemical class or nominal mechanism of action. Produces part of its toxicity by damaging mitochondria and causing oxidative stress.

And I've heard doctors say multiple chemical sensitivity can't be real because people are responding to chemicals from completely different chemical classes with different mechanisms. But the thing is, mitochondrial injury occurs for pretty much every [00:52:00] chemical, no matter what its mechanism. And also there's what are called gene environment interaction data so that people that have a genetic.

Variant of a M fund that detoxifies one of those exposures where their detoxification is impaired. Mm-hmm. If they also had the exposure, their almost rates are much higher. Mm-hmm. For example, there was a 2015 study that these. Variants of enzyme called buterol. Tase involved in detox like PDB should be looked at because if there was a causal relationship, people that had genetically impaired detoxification should have higher rates of I if they took the pd.

Mm-hmm. And the evidence now shows that, so people who took the PD. If they have the usual variant of the detoxifying enzyme, they had about a 2.6 fold elevated risk of developing goal for illness. If they had the impaired detoxifying gene but didn't take pb, they have no elevated risk, which is ideal. It means they [00:53:00] weren't predestined to be ill by their genetics acquired the exposure.

Mm-hmm. But if they had the PD and the impaired detoxification. It's a 40 fold elevated risk of illness. Mm-hmm. Which is obviously quite substantial. Mm-hmm. So back to that y mitochondria. So first off, like mm-hmm. Every chemical pretty much contributes to that. Mm-hmm. And different Gulf four veterans had very different chemical exposures.

There was everything on the battlefield from depleted uranium to smoke from oil fires, to jet fuel to something called chemical agent resistant compound, or Kirk Paint. Impregnated uniforms, massive numbers of different exposures with different veterans experiencing different subsets of those, and yet the profile of illness from veteran group to veteran group remains consistent.

And so that suggests to me that again, this shared mechanism that can add and synergize across different [00:54:00] chemicals was dominating the illness profile. Second feature was what are the nature of the symptoms that are elevated and pretty much goal four veterans have multiple symptoms spanning many different symptom classes, which is classic for mitochondrial impairment, but dominated by fatigue, brain, and muscle symptoms.

That is to say fatigue, which is itself sort of low energy. Then symptoms, what are called post mitotic organs, meaning they're mostly done dividing that have high energy demand, brain and muscle. Mm-hmm. And so that's also classic for mitochondrial impairment. And then also there was variable latency to symptom onset.

There was a study that showed that like of these increased symptoms that these Gulf War veterans had, 40% of them emerged over a year after people had come back. That's also classic for mitochondrial impairment. The variable latency to onset is classic, and that's because the mitochondrial impairment begets more [00:55:00] oxidative stress.

So mitochondria, the main source of the free radicals, the oxygen free radicals that cause oxidative stress, and there's some main target because most of those free radicals are made right there in the mitochondria. So mitochondrial, DNA and RNA and lipids and proteins are especially vulnerable. And then mitochondrial DNA also have less efficient repair mechanisms than the regular Watson.

Quick double strand, DNA, that you inherit from both parents. Mitochondrial kind of like little colonies of bacteria in every cell. And in fact, the main theory of what mitochondria are is that that's how they originated. They have their own bacterial style DNA that is generally inherited only from the mother, but their DNA repair mechanisms are less robust.

Mm-hmm. Which is why as people get older, especially, you know, well into older age, there are sort of exponential rise in mitochondrial DNA needs. Mutations because once they hit a certain point, they cause more free radicals to be produced. Mm-hmm. In the [00:56:00] process of energy generation. And that leads to more mitochondrial DNA damage and worse mitochondrial function, which leads to still more free radicals and so on.

And so in goal four illness, it looks like that's just happening at an earlier age. And in fact, many or most of the features of goal for illness look like accelerated aging. The conditions that they have at high rates are conditions that typically rise with age, and then the symptoms or symptoms that typically rise with age, et cetera.

So those were some of the reasons why it looked like it had to be mitochondrial impairment. And indeed. Findings, that is mitochondrial impairment. Again, there are other objective markers that are altered, most of which can be explained by mitochondrial impairment and it's downstream mechanisms. And then back to CO two 10, you asked how does that help?

Yes. Well, CO two 10, it's, it's actually a co-enzyme in mitochondrial electron transport made by the body. Both production and transport are. Inhibited by [00:57:00] things like statin, cholesterol lowering drugs, which block a step early in the pathway, and cholesterol also transports cozy Q 10, which is the reason why some people on statins get fatigue and muscle problems and cognitive problems, the same kinds of problems that Gulf four veterans get, that it's usually reversible because.

When you stop the statin, the coen on ketone level, which was the problem, goes back up, which is different from the mechanism of mitochondrial impairment in Gulf War veterans. So it is a co-factor. There are data showing that essentially irrespective of the respiratory chain defect, meaning which particular problem in the mitochondrial.

Electron transport or energy production chain coincide Q 10 helps to bypass that defect, which is also why you take something like statins, which is basically withdrawing coq 10 and you're unmasking unquote mitochondrial problems. So all of us start out with [00:58:00] mutations and deficits and so forth, but the hope is that they're covered by.

Adequate levels of antioxidants and energy supports and that there's adequate energy reserve. And in fact, that's what I think is the issue with chemical sensitivity. You have somebody that's been exposed to chemicals, their energy reserve has been cut, and their antioxidant defenses are strained by existing oxidative stress from mitochondrial damage itself and or from other chemicals and exposures.

They're either perked close to the point where there's not enough energy to prevent symptoms or, or they're already on the steep part of the curve where each additional cut in energy or includes an oxidative stress produces more symptoms. I think that's why in Gulf War Veterans, it's generally the ones that develop Goal four illness.

They're far more likely to be the ones that have chemical sensitivity because they're the ones that are already on the [00:59:00] steep part of the curve. Cell energy isn't enough to protect against symptoms in the general state and or anti accident defenses are not sufficient to offset oxidative stress and that leads to symptoms.

Aaron Goodman: This is fascinating, complex, but fascinating. It really resonates. Are there any practical steps that people might do to reduce oxidative stress and or support mitochondrial health? Yeah, there are a number of them and probably three supplements that have the strongest evidence of really broad benefit.

Beatrice Golomb: And again, there are studies for each of them showing protection, amelioration defense, mitigation of harm from myriad, different chemicals, radiation, et cetera, are cozy Q 10 itself. Mm-hmm. And then melatonin. Which people think of us for sleep. It actually, it's a really critical pre radical scavenger that also upregulates other [01:00:00] antioxidants and an acetyl cysteine, which is the precursor for glutathione, which is another of the major important antioxidant.

Mm-hmm. Pathways, uh, glutathione peroxidase needs selenium, and so some people will also recommend adding some selenium together with. Other supplements in order to have that cofactor be present. Mm-hmm. But those are with glutathione. Glutathione, correct. The last one was glutathione. Yeah, glutathione is is produced from N-Acetyl.

You can get things like liposomal glutathione that may be assimilated. The reason a lot of people use the precursor NAC, is that glutathione is usually not. That well assimilated by the body that that's several amino acids that make up glutathione or pretty much n-acetylcysteine is the most commonly used thing.

I should mention that for n-acetylcysteine, there will be people that get worse. There are issues like people may have gene variants in like something for example called [01:01:00] glutathione reductase, where they may have trouble. Making glutathione go back to the reduced form that serves as an antioxidant. So for NAC, I don't know if it's equal true for melatonin.

I haven't really looked that up, but for a lot of antioxidants, there will be a subset of people that rather than being made better, will be made worse. In the case of ENSs, I'm qan, it comes in both the ubiquinone form, which has been on the market for longer and has a much more robust body of evidence showing that it protects against.

Many, many different things from headache to heart attack to cutting the risk of death in heart failure patients by over 40% compared to placebo, protects against fatigue and pain and lots of different things. Most of those data are with the ubiquinone form, and we did our first study with the ubiquinone form, even though there were a lot of people saying, oh, ubiquinol is better because it's the reduced form that can serve as an antioxidant.

My thinking was that's a nice theoretical claim. [01:02:00] But there aren't the clinical data, and sometimes there will be a surprise, like either this is the thing you'd put in the pill to keep it in the reduced form is causing a problem or this or that. And indeed we later found that both for Gulf four veterans and for fluoroquinolone affected patients, a subset and minority subset, but a subset report getting better on ubiquinol, but actually being made worse on ubiquinol.

So energy production. Excuses of the ubiquinone form, the oxidized form. And if the coq 10 inside the mitochondria is too heavily in the quote reduced form, the form that serves as an antioxidant will actually drive energy production backward, will harm energy production and paradoxically increase the oxidative stress inside the mitochondrion.

So we, we tend to. Not, this is not a recommendation, but mm-hmm. For people who wanna take kq 10, because my personal [01:03:00] attitude is first, you know, harm and some people are made worse with ubiquinol, even though maybe some people will be made better with it, we tend to go with the ubiquinone form. And I should also mention that there are very wide differences in bioavailability for different products and.

Pro 10 is hard to make bioavailable. We used a specific brand, actually the pharma nor Brand made in Denmark, uh, for our studies. And that's been used in a lot of the studies that have shown the different benefits. And I mentioned that because it's not really the case that all Ubiquinone has created equal and some of the most affected mitochondrial patients I know get tremendous benefit from.

That brand. And I think there are probably a couple of other good brands, but there are a lot that really just are not bioavailable and don't really do much of anything for some people. And, and that brand did you meant say oid? Pharma Nord, P-H-A-R-M-A, capital NORD. And I don't mean to [01:04:00] be No, no. You know, touting a particular brand, but for this supplement it's, yes, the quality control and bioavailability issue is so important.

Aaron Goodman: Yeah. Thank you so much. Uh, professor, I want to ask you about the connection between Gulf War illness and MCS for the general population, people who haven't served in the military, and so much of what you've shared resonates with me personally, and I think it will resonate with others. For example, in my youth, I had methyl antimalarial when I Oh, interest worked overseas.

Oh, interesting. Yeah. I also was exposed to ci Permethrin. You mentioned Permethrin was in the clothing of people in the military. Yep. Yep. Multiple vaccines for working in, uh, the global south. Do you want to talk a little bit about, do you think your findings apply to civilians with MCS? I do think they apply to civilians with MCS.

Beatrice Golomb: With the caveat that, for example, the genetic finding that, that we may or may not get to talking about [01:05:00] its relation to MCS is mostly gonna show up in samples of people that have been heavily chemically exposed. Because if you don't have a lot of mitochondrial oxidative stress to manage, then genetic management of mitochondrial, oxidative stress is not gonna show up as a factor.

So unless you've got a population with a lot of people that are chemically sensitive. Ideally with people who are and are not chemically sensitive, both having had chemical exposures, then you can't really see how the genetics plays out in determining chemical sensitivity risk. The point of showing the genetic relationship is several fold.

Right now. When doctors put in a, a diagnostic code for chemical sensitivity, it's usually under the somatoform. Or somatic symptom disorder label, which basically means it's all in patient's heads. And that is a tremendous [01:06:00] disservice to affected people. And it drives the belief that the problem isn't real and it's not really caused by chemicals.

And, and the thing is, it doesn't matter whether you have this particular genetic variant or not that promotes it. What this shows is that there is a pathway that involves. Mitochondrial oxidative stress management that is implicated, but there may well be other genes that influence that pathway that people have, and the particular genetic finding that we have.

Doesn't call for a d. Management approach than just the knowledge that mitochondrial management of oxidative stress is implicated. I will say that there is a follow-up genetic thing that we really need to look at, and if you have people on your podcast that wanna help by participating in a genetic study, have them reach out to us.

The research that you're doing is very important and will [01:07:00] share a contact. In the show notes for people who want to reach out. And I wanna ask you, professor Glom, this year, I believe Gulf War illness finally received its own medical diagnostic code. Yes. Correct. I led that effort. You were a big part of that effort.

Aaron Goodman: And I led it. Yes. Yeah. And so important, but do you wanna talk about why it's important not only for folks with Gulf War illness, but. Potentially for people with MCS, because as you mentioned, when we go to. A doctor there isn't a diagnostic code and that's why we're told it's a psychological disorder. So what does this change perhaps for civilians?

Beatrice Golomb: I hope it leads the way for a broader understanding that just because a doctor doesn't happen to understand somebody's problems, just because they have multiple symptoms, just because one of their routinely conducted. Past doesn't show an abnormality with a [01:08:00] given group of people doesn't mean the problem isn't real.

And again and again, we've seen the same thing, whether it's fibromyalgia or chronic fatigue syndrome, multiple chemical sensitivity goal for illness, we we see that there are a group of people who say the problem isn't real. It's all in their head. They're just malingering. And yet they continue to say this even after there's abundant evidence showing.

Problems. And in each of those cases, mitochondrial problems and other soul energy impairment problems are part of it. There's mitochondrial problems and also long COVID mitochondrial problems documented in fibromyalgia and also. There are studies showing that, and these are not uncorrelated by the way, showing that patients with fibromyalgia have reduced capillary in their muscle, meaning they have fewer blood vessels, meaning that some of those cells have, don't have easy access to.

To the oxygen and the glucose and the other energy [01:09:00] substrates. There's ischemic muscle pain, meaning not enough energy to the cells that arises very easily when there's not enough blood flow. And on top of that, you have impaired mitochondrial function in chronic fatigue syndrome. There's analogous data showing that a good chunk of people have reduced total body blood volume.

So when you go to the doctor, they measure like your hemoglobin and your hematocrit, which is the red blood cells and oxygen curing capacity per blood volume. But if the total blood volume is low, then that doesn't show up. That hematocrit and oxygen curing capacity may look normal, but that's again, per volume.

And if you're down like a liter of blood out of five or six liters, then that. Oxygen curing capacity is actually inadequate and will contribute to driving things like fatigue. I think it's not an accident that mitochondrial impairment shows up in these problems because doctors are basically [01:10:00] trained in organ-based physiology, like it's either a lung problem or a heart problem, or a kidney problem, or a liver problem.

Mitochondrial problems don't fit an organ based system, cell energy is needed for every cell in the body. More energy is needed for highly energy demanding organs like brain, and muscle and heart, but all organs need. And so mitochondrial impairment can cause symptoms in all organs, and those symptoms vary a bit from person to person, and there are a lot of reasons for that.

There's something called quote heteros, which means that those colonies of bacterial mitochondria. Have different mutations, and those mutations may go to some organs so that people can start out with different vulnerability and different organs. And then on top of that, we talked about medications and other exposures.

Those can have a tropism, meaning can preferentially go to some organ like the liver or the kidney or the skin, making that part of the body then become more [01:11:00] vulnerable in that person so that, so different people in mitochondrial disease in general and in. Environmentally triggered mitochondrial disease in specific the patterns of illness.

On a group level are consistent, but individual to individual, different people will have different ones of the symptoms that are characteristic. And again, doctors aren't used to thinking in that way. And there is a legacy that comes from Freud back in the era where neurology and psychiatry hadn't yet divided up, where he had this basically delusional idea.

That a lot of different medical problems were in patients' heads, and it's basically the same kind of thinking that has come down through history. There never was any positive evidence that psychogenic illness ever produces persistent symptoms in anybody. It was a made up idea that took hold and has had a persistent legacy.

To this day, when I entered medical [01:12:00] residency, I remember seeing a list of the causes of low back pain and top on the list was psychogenic. And then miraculously when ergonomics came in, somebody figured out that people had transitioned heavily to office jobs and didn't understand the ergonomics, and then people began understanding ergonomics and it miraculously, it fixed all those neuroses.

So these ideas that when there's a problem where you don't have something you can measure. There seemed to be a good chunk of people who choose to believe that the patient is responsible for their problem, and I think that's unconscionable. I think it's a violation of Hippocratic Oath. Our data on Gulf War.

Veterans suggest that those damaging attitudes not just cause emotional distress in the patient, but they also affect things like return for care and following provider. Directions, which makes sense because they erode trust in the provider and then that can affect both continuity of care and also effective care [01:13:00] for their other health problems.

So these are very damaging attitudes. They were never justified and they need to be stamped out. I'm, I'm so grateful to you for talking about that. At some point the researchers. And clinicians who continue to put out this false argument that multiple chemical sensitivity is a psychological disorder.

Aaron Goodman: Mm-hmm. You think they owe us an apology? Yeah, I do think so, but I don't know what that exactly brings you, but most of them all, they need a revision in their attitude. In a lot of the settings where these problems emerge that are classed by some people as mass hysteria or psychogenic. Settings where there's a party with a financial stake, chemical injury settings, drug adverse effect settings.

Beatrice Golomb: Those are settings where there's a powerful wealthy party that has an interest in denying that their product bears a role, and I think that may be a reason [01:14:00] for the persistence of these concepts. In medicine because that seems to be the primary place where these continued to take hold. You're talking about the military industrial complex, right?

Aaron Goodman: And the chemical industry. And the pharmaceutical industry. What's bigger than those chemical industry, the pharmaceutical industry for people with electro sensitivity. There's the utility industry, there's big data, there's big telecom, all of those things. Professor Golum, are you continuing to encourage younger researchers to.

Follow this path. It's not an easy path to follow in research because there's not really a separate body of funding, and so that is challenging. People typically go where the money is because that's how you have and maintain a career, and so that's a big challenge. We actually have some amazing additional preliminary data on chemical sensitivity.

Beatrice Golomb: Related both to the mitochondrial things and related Actually the membrane effects. The [01:15:00] membrane effects. Membrane effects, yeah. Yeah. So like it turns out, membranes are the barriers of the cell, but they also have critical roles in the energy process, and it looks like both of those are turning out to be really important, and we're struggling to figure out where can we go to get.

The resources to take the next step. And that's a big challenge, I will say. And that is, I think a reason, like a lot of the things I have, the areas that I've embarked on have been areas where not a lot of scientists spread because there hasn't really been a will to fund them. And that is an issue. And the good news is, for a while there was this pot of goal for illness funding that.

Has been very fruitful in helping with chemical sensitivity because chemical sensitivity was a big part of Gulf illness, but I think we've paid more attention to than anybody else. We've got also a paper showing that patients with higher chemical sensitivity ratings also have higher rates [01:16:00] of actual adverse effects to many drugs and chemicals.

The more kind of acknowledged adverse effect issues are also elevated. So it's hard for me to exactly encourage students to go somewhere where. It's not really clear if they can have a sustained career, but I would encourage people to reach out to your Congress people to NIH, et cetera, and encourage them to advance funding in this area.

And if people happen to know philanthropists that have an interest in this kind of area, that is often a place where initial important work can happen as well. How is it for you as a researcher taking on this work and not. Seeing other people doing it? Yeah, that's a, an interesting question and I guess because I've always felt like I'm a patient advocate and I pick areas where it feels like the need is greatest, where there are a lot of people suffering and there are not a lot of doctors and scientists trying to help them.

I'm on the [01:17:00] outside trying to move the needle. But on the other hand, it's really worthwhile work, and when we get letters like the ones we've gotten recently from Gulf four veterans who are so appreciative about the ICD code, that's the kind of thing that really makes it all worthwhile. Thank you so much for taking time and I hope it's okay if I reach out again in the future as your research continues and I will share the contact for your research.

Aaron Goodman: Thank you so much. Yeah. Thank you for your interest in the area you've been listening to, the Chemical Sensitivity Podcast and the host and podcast creator Aaron Goodman. The Chemical Sensitivity podcast is buy and. For the MCS community, the podcast is generously supported by the Marilyn Brockman Hoffman Foundation and listeners like you.

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