Listen to Ep 05 where Dr. David Brady talks how chronic infections cause molecular mimicry in the immune system, problems with defining vague conditions like CFS and Fibromyalgia, evidenced-based approaches to viral infections & pain, and more...
Full Text Transcript:
Dr. Craig: You’re listening to Spoonie Radio, I’m your host Dr. Courtney Craig. My guest today is Dr. David Brady. He is a licensed naturopathic medical physician and a Board Certified clinical nutritionist. He has over 22 years of experience as an integrated physician and over 18 years in health sciences academia. He is currently the Vice Provost of the Division of Health Sciences Director of the Human Nutrition Institute and an Associate Professor of Clinical Sciences at the University of Bridgeport in Connecticut.
He maintains a private practice; Whole Body Medicine in Trumbull, Connecticut and Dr. Brady is also the chief medical officer for the supplement company Designs for Health. He is an internationally sought-after presenter and has appeared on the speaking panel of some of the largest and most prestigious conferences in the field.
Dr. Brady has published a multitude of peer-reviewed scientific papers and textbooks related to chronic pain, autoimmunity and functional gastroenterology. He is also a featured contributing author in several medical textbooks and his latest popular book for the general public is titled Dr. Brady’s Healthy Revolution: What you Need to Know to be Healthy in a Sick World.
Welcome to the show Dr. Brady.
Dr. Brady: Well thank you I appreciate you having me on and allowing me to do the interview.
Dr. Craig: Yeah, thanks so much for being here today to share your expertise to the ME/CFS community. And for those listeners who are not familiar with you or your work, I wanted to have you on the show today to really highlight your knowledge of the role of chronic infections, both in this condition as well as in autoimmunity and fibromyalgia.
So we will get to that later today but first I want to start by getting your opinion from your many decades of experience treating fatigue of all different types, how do we differentiate and diagnose different fatigue types? Have you found that chronic fatigue syndrome is its own entity or have you found there to be overlapping conditions and different subtypes of this condition?
Dr. Brady: Yes. It’s a complicated answer; I guess it’s a complicated question. I think first of all I will say up front I think my experience, my research publications things like that, I would be much more confident answering that from the perspective of fibromyalgia… than chronic fatigue syndrome, or CFIDS or any of those variants.
But I can’t say just globally that most of these diagnostic criteria that come out whether they are for chronic fatigue syndrome or fibromyalgia or many of these complicated chronic conditions, leave a lot to be desired. They are very inaccurate, they become these sort of cast nets I like to call them where it catches people with all kinds of different problems, different reasons for their symptoms and tries to lump them under one convenient diagnostic label when when you really look under the covers if you will, and you tease all of these different problems apart in these people that may share this common label whether it’s fibromyalgia, whether it’s chronic fatigue syndrome, or what have you, you will find a lot of diverse problems that people have. They are not the same condition from one patient to the next.
In fibromyalgia, which we will spend some time on, there is a definite condition involving central pain sensitization which causes global pain and fatigue, and a whole bunch of other stuff that we would consider the classic form of fibromyalgia that the literature is really talking about. But then there is a whole lot more people that are given the label of fibromyalgia, that really have other conditions that are not adequately being detected, understood, and addressed but result in the patient nevertheless getting this label of fibromyalgia. It doesn’t mean that there’s nothing wrong with them, it just simply means that it’s not the classic pain processing disorder that the medical literature is really talking about when they reference fibromyalgia.
The same thing really happens in the chronic fatigue bucket. You have all these people defined as or labeled as chronic fatigue syndrome but some of them have energy production mitochondrial, biochemical problems. Some have undiagnosed thyroid issues, some have toxicity issues, some have immune challenge issues that are causing fatigue – so there are lots of different pathways into these labels. Unless you find out why the patient is there at that label chronic fatigue or fibromyalgia; accurately, you will have a hard time stumbling upon the appropriate treatment because the treatments are inherently different depending on what’s actually really wrong with the patient if that makes any sense.
Dr. Craig: Absolutely, it makes a lot of sense. Now let’s get into this, chronic infections, especially the chronic and viral infections. So in chronic fatigue syndrome, we have found high incidence of things like Epstein-Barr, different types of mycoplasma, HHV-6…but these viruses are also ubiquitous in the general public. So what role do you think chronic infections like these have in the symptom presentation we see in chronic fatigue?
Dr. Brady: I think they play a major role in some people and they probably are not playing a significant role in other people who are also fatigued--have long-term fatigue. But I think it’s definitely an issue in play that needs to be looked at.
You mentioned Epstein-Barr virus but also cytomegalovirus, HSV, there’s a whole bunch more and there is probably a lot more that we don’t even know. But they’ve done systematic research trials on etiologies of chronic fatigue and fibromyalgia and many of them especially 10, 15 even 20 years ago were centering on viral infections being the main issue. That really was a rabbit hole that never really produced much compelling data in fibromyalgia.
It is much more prevalent I think in chronic fatigue syndrome particularly with the people with the classic story of their fatigue starting after a flu-like illness or clearly some sort of viral type of infection that challenged their immune system in the way that it ended up being dysfunctional in the longer term and they have sort of that CFIDS, Chronic Fatigue and Immunodeficiency variant type of fatigue where you can see changes in the lymphocyte subsets and you can find these chronic sort of a viral antibody titers being high and so forth.
I think in those types of patients, these smoldering or stealth types of infections are a major contributor if not a prime etiology. But I think that a lot of people who have the label “chronic fatigue syndrome” that their problems are entirely different and unrelated to viruses or any stealth infection.
Dr. Craig: Right. And from that subtype that does seem to have these chronic viral reactivations, the gold standard treatment right now is antiviral medication but the results that I’ve seen from my own experience and with patients that I consult with, the results are not promising. So what do you think is the issue with prescribing antiviral medications? Is this not the right approach? Should we instead be looking for more natural methods, looking at root causes?
Dr. Brady: Yeah. And some people may choose to try those and if they offer them significant benefit then great but if they don’t I wouldn’t keep taking them. They have a lot of toxicity profiles to them like they can be very hepatotoxic, they can be very expensive so if they are really not yielding obvious results I would not continue to do that… Because the antiviral drugs are not super specific to any of these organisms per se, they work on more generalized mechanisms and they tend to beat down symptomology and more overt or acute types of infections and not so much on these lower-level smoldering chronic types of infections.
I would favor the approach of trying to augment the body’s innate immune response against viruses and other pathogens whether that can be the use of natural killer cell up regulators, various mushroom fractions, shiitake, Reishi, all of those can be helpful; beta-glucan, larch extracts, things like that can be helpful for sure.
I also use lauric acid, something called monolauren (Immunotone; DFH) which is a form of lauric acid which particularly in the encapsulated viruses, it exposes them for your immune system to recognize when they previous to that would be stealthy.
Because it’s an interesting effect, a lot of these viruses…of course the viruses’ game is to get in your body, get into one of your cells, reprogram your own cells to replicate more viruses and then the viruses leave that cell in a process called “budding,” to move on and infect another cell. When they do so some of these viruses, in order to shield themselves or hide from the immune system, they drag some of the phospholipids or the fats from your own cell membranes around themselves. They sort of enveloped themselves in this phospholipid layer so that your immune system sees that layer of phospholipids around the viral particle and interprets that as being self, because it looks like your own cell membranes. So that’s how they hide from the immune system.
So some of these agents, like the monolauren form of lauric acid can emulsify this phospholipid layer around the viral particles and it won’t do the same thing to a vibrant living cells but it will do it to this sort of unsupported phospholipid layer around these viral particles and it could then expose them for the immune system to now recognize. So monolauren can be helpful. I’ve also had some pretty decent success using a water clustered silver called Silvercillin (DFH) that sort of works on about 7 or 8 different known mechanisms against viruses but it’s also antibacterial, antifungal. It can be very helpful in stealthy types of infections including even Lyme to some degree.
Dr. Craig: Interesting what you just described there with the protective coating around the viruses, makes me think of how bacteria become resistant and build biofilms. Is that kind of a similar process as that?
Dr. Brady: Well it’s similar and different in that in the viral situation it’s each viral particle organism coats itself with the phospholipid layer and then moves around the body sort of undetected. Where the bacteria tend to cluster in colonies and secrete different types of materials; proteoglycans and so form this sort of sticky layer of the biofilm that they live in, it’s sort of their colony if you will.
But so a lot of people are all about trying to use these different agents to dissolve biofilms including things like chelating agents and the like, because it can help disrupt them. The problem with that however is the good organisms live in a biofilm as well as the bad organisms live in a biofilm. So for instance trying to disrupt that biofilm in the G.I. tract, well you are disrupting where the good guys live too. So that’s still an area that’s kind of fraught with a lot of uncertainty and controversy to some degree.
Dr. Craig: Yeah, we are still learning so much about the gut and the gut is really a major focus of interest in chronic fatigue syndrome research right now. And one thing I heard you say in a lecture that you gave recently a couple of months ago, is that we are not quite sure what happens first, is it the change in the microbiota in the gut that leads to the disease or does the disease causes the shift itself?
So I wonder if you could speak to that. It’s sort of like a chicken or the egg scenario.
Dr. Brady: Well in the case of autoimmune disease we have data. I personally don’t think for instance fibromyalgia, true classic fibromyalgia, is not a gut microbiome mediated disorder, it’s not inflammatory, it’s not autoimmune, it’s none of those things. It’s a central nervous system processing disorder. It doesn’t mean that there aren’t people that have classic fibromyalgia, the central nervous system processing disorder that also don’t have some gut issues related to the microbiome, it’s just not driving their global pain and fatigue.
But there are people who may have a label of fibromyalgia that don’t have classic fibromyalgia. They have something related to an autoimmune process or something that may be driven by the gut. But with autoimmunity, we know there are various triggers that may be presented by organisms that are in the G.I. microbiome that can cause an immune response which can through molecular mimicry cross-react to host tissues. In that situation, the data is pretty clear that the microbiome changes first and it drives the disease process versus the other way around.
For instance, we know through studies on organisms like Citrobacter freundii, Klebsiella pneumonae and others in rheumatoid arthritis and ankylosing spondylitis that those diseases by the way fit the pattern of most autoimmune diseases in that they wax and wane and they will get very symptomatic and you will be exacerbated and in bad shape and then for no apparent reason you seem to get better for a while and then you’ll get worse again.
And they’ve actually studied the composition of the microbiota in those types of subjects pretty extensively and have shown that when they are in a period of quiescence, when they feel good, their microbiome pretty much looks like—or the G.I microbiota more specifically—pretty much looks like everyone else who is healthy but when they are exacerbated, they have an overexpression of Klebsiella, Citrobacter and some of these patterns that are associated with molecular mimicry causing cross-reactivity to joint tissues where these antigen-antibody complexes will stick in the synovial linings of joints and they will get inflamed and you will drive that autoimmune inflammatory erosive destruction of the joints. When they are exacerbated, they have these bad bugs essentially. And they’ve looked at it sequentially to show that the microbiome shifts and then the disease exacerbates.
Now you might ask deeper questions like, “Why do those people who get RA or get ankylosing spondylitis, why are they susceptible to a shift or an overgrowth of Klebsiella and Citrobacter?” Or, “Why does someone with an autoimmune thyroiditis like Hashimoto’s or Graves, have a propensity to have an overgrowth Yersinia enterocolitica in the gut presents protein receptors on its surface that look like TSH receptors on the thyroid so your body makes antibodies to bind to that specific antigen and it gets confused and locks on to your TSH receptor.
Those are deeper questions that we just simply don’t have the answers to at this point. They have established not only that association but with some of these organisms, they’ve worked out this timing sequence where the shift in the microbiota occurs before the disease exacerbates. They have pretty firm data in the case of some of these organisms that it’s not just an association; that is actually causal, it’s driving the process. Probably some of the most compelling data in that is with p. gingivalis and rheumatoid arthritis.
If you have gum disease and overgrowth p. gingivalis and bad oral hygiene, that organism can secrete enzymes that lead directly to citrullination of host peptides and you can drive the rheumatoid addresses process directly from the p. gingivalis overgrowth.
Dr. Craig: That’s a really fascinating connection. A lot of people I know are not aware of that. So you bring up this idea of molecular mimicry and that can be triggered by bugs essentially but what other things can trigger this similar mechanism?
Dr. Brady: Oh foods, big time! Molecular mimicry is a simple concept, the details get complicated but the overall picture involves protein, something that’s foreign to you and you are genetically susceptible, in other words your immune system has a unique characteristic to react in a dramatic way to that environmental antigen and that environmental antigen, that protein or peptide, has a structural similarity. So it’s amino acid sequence is very similar or somewhat similar to a protein that’s naturally in the body or expressed on a body tissue. You can, when you are exposed to that protein, react to it in an exaggerated way which can result in loss of discrimination between the subtle difference between that environmental protein and the protein on your host tissue. At that point you cross over and you start an immune attack against a tissue with a similar protein. It’s easier if I give you a couple of examples.
Dr. Craig: Okay.
Dr. Brady: We know that, let’s say that someone has the human leukocyte antigen… or HLA presenting antigens on their immune cells or their T cells, the HLA DQ-8 or DQ-2 or both of them. And they eat gluten containing grains in the diet. Well unlike someone who does not have those presenting antigens, they may eat the gluten, they take it in, it comes through the intestines and their immune system may go, “Hey, this is a little weird, this gluten gliadin stuff. Mhm, seems a little weird but we’re not going to freak out about it.”
Well someone with that HLA pattern grabs that gliadin fragment and holds it out to their immune cells then says, “Hey, look at this, react to this. This is bad, this is not me.” They are having a much more dramatic presentation of that antigen to their immune system so that’s the genetic susceptibility; they are exposed to the antigen, they take it and waive the red flag with it. Their immune system engages. For instance we know gluten gliadin, antigen-antibody complexes have an affinity to bind to thyroid receptors and that can drive an autoimmune process against the thyroid. That’s why for instance people with overt celiac disease or at least that’s where the data is the strongest, have anywhere depends on the study you look at, anywhere from 10 to 20 times the rate of Hashimoto’s or Graves’ than people without celiac disease.
But people with non-celiac gluten sensitivity, I find clinically have much higher prevalence of autoimmune thyroiditis. So that’s an example of a food.
Another classic example of the food is with type I diabetes. Genetically susceptible children with immune responses or immune system presenting antigens that react to certain milk proteins bovine albumin peptides specifically, if they are given milk while they’re growing up, they hold out this protein to their immune system and start training the immune system, “This isn’t me, this isn’t good, I don’t want this in my body.”
And they transition at a certain point where they lose that discrimination between that bovine albumin peptide and some proteins that are expressed on the pancreatic cells that produce insulin. So they cross over and now instead of reacting to that milk protein they develop these antibodies against their pancreatic cells that produce insulin and they rapidly destroy them and take them out. And that’s why you have a perfectly normal kid who is fine one day, the next day falls down, passes out, gets taken to the emergency room and their glucose is 500. It happens very quickly and they just destroy their insulin producing cells and that’s an autoimmune molecular mimicry reaction in some cases to dairy proteins.
But it’s not the only way you can get type I diabetes. There is viral triggers, there is even data on triggers from insect bite venom so there is more than one way in. So like with autoimmune thyroiditis, I mentioned it could be driven by gluten but it could also be driven by the peptide on the surface of this Yersinia bacteria that can overgrow in some of these people’s guts and that protein looks like TSH receptors on the thyroid.
So once again, you can cross over so molecular mimicry just means one protein looks enough like another or if you are genetically susceptible and you waive that protein for your immune system to really react to, it will get so hyperreactive to it that it will lose its fine discrimination between the subtle differences between peptides and you get this cross over reaction.
So you need this perfect triad like if you read Alessio Fasano’s work, mainly in celiac and gluten sensitivity but it applies to all autoimmune disease, you need sort of these 3 elements to sustain an autoimmune process. You need exposure to whatever the offending environmental antigen is. You need a unique genetically determined immune response to that environmental antigen which generally is a more robust response than the average person. And then you generally not in all cases, but generally need a hyperpermeability or a leaky kind of degraded gut lining, particularly if you are reacting to environmentally derived proteins that are coming through the gastrointestinal mucosa and they include foods and bugs that grow in the gut.
So what is your most massive exposure to foreign proteins? It’s the food you eat and the bugs that are growing in your gut. So that’s why with any autoimmune process, we really don’t get hung up on the specific disease when we look at the overall approach. I don’t care if it’s MS or Hashimoto’s or rheumatoid arthritis or lupus, it really doesn’t matter; I am knocking down those 3 pillars. I want to know well, I have an offended environmental antigen coming in; do I have a genetically susceptible person?
So we check predictive autoantibodies or HLA patterns or whatever we need to to see is this a person that susceptible to this specific autoimmune disease and then we look at their gut health. We try to maximize their G.I. microbiota health; so we want all the good guys there, we want to hunt for any of the bad guys we know are associated with autoimmunity, and specifically the autoimmune disease that we suspect in that person because if they are clinical symptoms, maybe because of their family history, or maybe because of the predictive auto antibodies we found.
So we want to fix the gut lining and make it “less leaky” if you will. We can’t change the genes, we can’t change the susceptibility right now but we can try to get rid of the offending environmental antigen by killing the bug in the gut, by knocking down the stealth chronic viruses that may be at play or by doing an immune compatibility test with the food that they are eating and taking out the foods that their immune system doesn’t play nice with.
Dr. Craig: Yeah, there’s a little bit of research now that is starting to emerge in the chronic fatigue world that’s showing a high preponderance of celiac and non-celiac gluten sensitivity in this population but we need a lot more research. Because I certainly think that it’s playing a major role and I think we are getting a similar, not classically autoimmune, but similar process is going on particularly with gluten and gliadin peptides.
Dr. Brady: We could be very careful looking at research and saying, “Okay well we’re seeing the literature showing some gluten or non-gluten celiac sensitivity being more prevalent in people with chronic fatigue syndrome therefore this causes chronic fatigue syndrome; no I see that all over the fibromyalgia literature as well.
And the problem is, these subjects being studied that supposedly have fibromyalgia or chronic fatigue syndrome, have all kinds of different problems. They are not the same problems and you can’t lump them together under one convenient label and say because many of them have a certain issue that that is the driving issue because the data and the research is so dirty, you can’t even make heads or tails of it because these have become catch-all bins for people with all kinds of different chronic metabolic, biochemistry abnormalities, endocrine problems, I mean… toxic issues, you name it, they are thrown in these big bins. So when people study people in those bins, they are really studying people with all kinds of different problems trying to come up with a common conclusion. It’s insanity!
Dr. Craig: It really is.
Dr. Brady: It doesn’t make sense, yeah.
Dr. Craig: The diagnostic criteria we have is so inadequate and then there is so many different types of diagnostic criteria, whether you are in the US or in Canada or the UK, the research is really a disaster, I would agree with you on that.
Dr. Brady: Yeah, chronic fatigue just means; okay you are fatigued for what more than 3 months or 8 months, it depends on the diagnostic criteria. But fatigue is a vague symptom that can be caused by a lot of different things. So to try to find one universal cause or etiology for something as vague as chronic fatigue, you’re never going to find it because someone could be chronically fatigued because they are anemic and they are not oxygenating their cells, or they could be chronically fatigued because they are hypothyroid, or they can be chronically fatigued because they have mitochondrial uncoupling and energy production issues at the biochemical level based on their genomic variability and the way they produce certain enzymes, or the quality of the enzymes, or oxidative stress to their mitochondria or what have you, and just giving you a couple of examples.
They can be chronically fatigued because they have mercury toxic burden which is down regulating the conversion of their T4 to T3 thyroid hormone. Okay, so I just gave you like 4 or 5 reasons why you can be fatigued.
Dr. Craig: And there are many more, many more.
Dr. Brady: You have 5 people that have been fatigued for more than 3 months with those 5 different problems, they all could meet the diagnostic criteria for chronic fatigue syndrome. So you take them all, you do the diagnostic criteria, you tell them all they have chronic fatigue syndrome and then you study all 5 of those and then you find all these different things in them but they’re really all have different problems. The true thing to do is to have really well-trained clinicians who can tease all this apart and not just look for the overt disease but look at the nuances of their metabolism, their biochemistry, their toxic load or the microbiota, all these other things and try to find out what it really is and don’t get so hung up on calling it a label.
If someone has chronic fatigue because they have sort of undiagnosed non-overt but significant, symptomatically hypothyroidism because they have a conversion disorder of T4 to T3 or they have T3 resistance syndrome; do they have chronic fatigue syndrome? No, they have hypothyroidism. You know what I mean?
Dr. Craig: Right.
Dr. Brady: Find it, fix it and then call it hypothyroidism! Don’t call it some basket sort of label. And I find this happens so much in fibromyalgia I want to scream! And it leads to a lot of misinformation for people who may have these symptoms. It leads to misinformation all the way up into the health care provider.
Let me give an example in fibromyalgia, open your yellowpage books or do a Google search right now and look at practice ads or practice websites for physical therapists, chiropractors, massage therapists, any of those physical medicine people and you will find on almost every one of those, “We treat fibromyalgia. We have all this success with fibromyalgia.” Even though if you look in the medical literature, fibromyalgia, the true classic fibromyalgia is a problem where people do not process sensory information coming into their nervous system properly and they interpret things that should not be interpreted as pain. as pain—it’s called allodynia, they really have central allodynia.
They have failure of descending inhibition to shut off the sensory information so it doesn’t overload the nervous system. They interpret things that should be even light touch as pain. And the dysfunction is in the central nervous system. It involves the limbic system, it involves the descending anti-nocipceptive system. It involves the HPA axis and aberrant stress physiology and involves all kinds of neurotransmitter abnormalities including low central nervous system serotonin, high substance P, but is not a problem of the muscles. The muscles are normal! The soft tissues are normal. They study them every which way but loose; there is no hypertonicity, there is no trigger points, there is no metabolic crisis in the muscle, the mitochondria are working so it’s not a peripheral disorder.
The perception of pain is in the peripheral tissues but the problem is the central. So the solution or the therapy has to be directed to the central mediated issues, not the periphery. Which means if you really have classic fibromyalgia you can massage it all day long, you can electromuscle stim it, you can ultrasound it, you can manipulate it, you can pull it, you can tug it, you can stretch it, you can burn it, you can do whatever you want to do the muscles, it’s not doing a damn thing other than torturing the patient!
Dr. Craig: Right.
Dr. Brady: And I am not saying those kind of providers don’t help a lot of people who come in and say, “I have fibromyalgia.” They do! The problem is the person who said, “I have fibromyalgia,” probably had myofascial pain syndrome with true triggerpoints or problems in the peripheral tissues, in the muscles, they didn’t have classic fibromyalgia. And the provider doesn’t know enough to know that they didn’t really have fibromyalgia, they had myofascial pain syndrome. So what do they propagate? They propagate the myth that by doing these things to the peripheral tissues you can cure or help fibromyalgia which is not true so it just allegates. And the healthcare providers are just as culpable, actually more culpable in perpetuating the misinformation about these disorders.
Dr. Craig: Absolutely. So what is your approach than to pain relief and fibromyalgia if everything is happening in the brain?
Dr. Brady: Well, my first approach in fibromyalgia is to find out what does the person who just came in and told me they have fibromyalgia really have. That’s the key. I don’t mean to say that in a tone that someone would interpret me to say that I think most people that say they have fibromyalgia really are just making it up, that they just don’t have anything, it’s all in their head, I am not saying that at all. I am saying I think that the vast majority of them come in and say, “I think I have fibromyalgia,” have real problems. The problem is, they don’t all have truly what is classic fibromyalgia which is central allodynia and a central pain processing disorder.
I find in talking to colleagues who do a lot of work with fibromyalgia in clinical practice, I think, I don’t have any firm data behind this but in my personal estimation, of the people that come into my practice and say, “I am here because I have fibromyalgia,” and this includes people who diagnosed themselves from going on WebMD to people who their neighbor told them they have fibromyalgia, to people who their family practitioner or their chiropractor or acupuncturist told them they have fibromyalgia to someone who was actually been at the rheumatology Center in an academic ivory tower academic center; all of those people come in and I would say 70%-75%, I actually find something else that is the reason for their fatigue, their achiness, their brain fog and all of that. I find that most of them have not had a complete medical workup, they have not had all the ruled out blood work that should be done, not only conventional blood work but more integrative nutritional, functional kind of studies done.
Fibromyalgia should be a diagnosis of exclusion; there is no fibromyalgia factor lab test. There is no test that tells you, yes or no someone has it. You have to use laboratory studies, you have to use physical examination, you have to use history and you have to find out, does it really meet the criteria for classic fibromyalgia? And most of those folks, most of them, the vast majority are female, they truly have a global pain. By that I mean they hurt everywhere.
They don’t hurt just in their low back and their glutes and their traps, they don’t hurt just in their left leg and their neck, they hurt everywhere, it’s not discriminate by location, it’s global which means if you challenge them or you do things to them, putting pressure into large muscle groups, they hurt everywhere, not just a couple of places.
So they have to hurt everywhere, they are usually female, they almost always have concomitant issues which include at least mild depression, anxiety, even panic attack, insomnia, unrefreshed sleep, they have irritable bowel syndrome, very, very commonly and they often not always but often have some history of significant stress during upbringing and the formation of the nervous system. When the nervous system is still very neuroplastic, they were under stress, they felt unsafe, they felt threatened, they felt abused, something was going on. They usually have really not great family environmental circumstances when they were very young, maybe often times a parent including more so the father is alcoholic, maybe yell a lot, maybe physically abusive, those are very common stories to get.
But it can happen later in life after trauma. It could be significant trauma experienced by the patient whether it’s significant physical trauma in an accident, it could be a rape situation, an abuse situation, abusive relationship, whatever but stress and changes to the nervous system based on stress resulting in this sort of hypervigilant, over-processing of sensory information. They are in this hypervigilant, waiting for the next shoe to drop in the nervous system and it spills over into widening the receptive areas of pain or fields of pain and causes dysfunction deep in the nervous system in which you have to address there. And that involves some degree of stress mitigation.
So everything from-- It could be meditation, could be yoga, it could be prayer, it could be guided imagery, deep breathing, heart rate variability, some of those kind of practices that usually involve some sort of counseling or processing out of these long-term psychological things sort of driving this stress response in their brain combined with looking at the biochemical side.
So we will use things to modulates and correct their stress response often they are hyper-catecholamine producers and excretors so we can look for catecholamine metabolites… Use things to calm down there central nervous system and upregulate the things that calm them.
So we can use GABA-nergic botanicals, things like valerian, passionflower, melissa but we use a lot of calming neurotransmitter precursors, L-theanine, we use phosphoditylserine. We will actually use direct neurotransmitters like PharmaGaba to hit the GABA-nergic pathways, but we really rely heavily on modulating the serotonin pathways including using things like 5-hydroxy tryptophan and other serotonin precursors. (NeuroCalm; DFH)
And if necessary, medications that work on those pathways. So the SSNRI’s, Selector Serotonin Neuroepinephrine Re-Uptake Inhibitors, or the GABA-nergic, the GABA receptor agonists, gabapentinoids, things like that can be helpful if you need to resort to medication.
On the other side the other 70%, we have to figure out what do they really have? Do they have an organic medical condition that should be diagnosed and treated? Are they anemic? Do basic bloodwork. Do they have some kind of inflammatory condition? Do they have any significant organ dysfunction? Do they have a metastatic cancer situation that’s not diagnosed? Do they have MS? Do they have an autoimmune process? Is it an inflammatory arthropathy? Those things can easily be determined in the laboratory.
But then when you get to the more functional stuff, you need people trained in more functional, integrative types of models of medicine so you can turn to organic acid analysis to look at mitochondrial energy production, nutritional insufficiencies on biochemical pathways. You can look at stress metabolites so you can look at cortisol and catecholamine metabolites and try to correct the aberrant stress response and the HPA axis, that’s very, very important.
You can look at the thyroid from a much more granular perspective looking well beyond the classic TSH, T4 level for overt hypothyroidism but look for more subtle forms of thyroid function problems; look for toxicity, heavy metals, shifts in the microbiota and G.I. problems, all of that stuff needs to be run down. And then finally you need to make sure it’s not truly a peripheral musculoskeletal this order.
Is it myofascial trigger points or myofascial pain syndrome? Is it a hypertonic situation because of a postural distortion? Is it a scleratogenous referred pain kind of pattern or some sort of dermatomal pain pattern because of discopathy or a facet syndrome or something like that?
So you really have to just tease your way through the whole thing and fix what you find and not just accept that they have fibromyalgia so I’m going to use this because I heard it’s good for fibromyalgia, it just doesn’t work. You’re going to be shooting blind when you do that.
Dr. Craig: Right, there is so much data that needs to be collected and like you said, most of these patients are not getting a thorough assessment which is really a great disservice to both fibromyalgia and chronic fatigue patients I would say.
What you just described there I found interesting, and many listeners might find it controversial but, what you basically were describing is these different triggers in a fibromyalgia patients’ life and it sounds like maybe there is an epigenetic mechanism at play. I don’t know, has the research supported that at all? What role fo you think the supporting methylation has in there as well?
Dr. Brady: I don’t know if I can really intelligently answer what specific role methylation has but I can tell you that the studies suggest that there is a genetic component to the disorder and a genetic susceptibility that we know for instance that some people when they are stressed, particularly when their nervous system is in its learning sort of developmental phase, that some people can undergo significant amount of stress and they end up without any long-standing dysfunction in the nervous system should that stressor go away.
Other people, that’s not the case. The people who tend to have the long-standing aberration in the central nervous system’s behavior after these stressors, particularly the younger that occurs to them the worst apparently, that does run in families. And we know that it’s much more prevalent in females.
Now some of that may be because females just maybe, their brains work a little different than males in the way they respond to stress. We see neurotransmitter responses that are different males to females and you can see it in behavior. I mean it’s not politically correct I know to stereotype anymore or to say that women are different than men but guess what, they are. And just watch the news for instance, how many times lately have you seen a female when they are stressed or have some sort of posttraumatic stress issue walk in somewhere with a high-powered automatic rifle and start shooting match numbers of people? They don’t do that! Men do that!
Men act out violently when their nervous system has certain aberrations, created by significant stressors, women don’t do it. They act in different ways, they get classic fibromyalgia, pain disorders and fatigue, they get IBS. They compensate in different ways. And I might add much healthier ways than men do. But there is no doubt that they react differently; men don’t get IBS, they don’t get fibromyalgia. I’m not saying say never; but it’s rare. Women never do the kind of things that I just talked about that is unfortunately these days not that uncommon to see when males are under super stress.
So there are definite differences and I think some of that is genetic susceptibility. It doesn’t mean that genes drive the whole thing, it means that genes, genetic susceptibilities put in the right environmental circumstances result in certain outcomes.
Dr. Craig: Fascinating! I could pick your brain, Dr. Brady, all day but we are running out of time. But before we go, I want to know what you are working on next.
Dr. Brady: Well I am anticipating some time by the end of next year, probably about a year from now, having a book, a new book out on fibromyalgia and global pain syndromes, really directed toward the layperson, toward the mass audience so that they can better understand some of the things I have been talking about on the interview today so that they can be their own advocates and really make sure that they get good full workups and differential diagnosis to find out; is their problem really truly fibromyalgia in the classic sense? And If that’s the case, do the right treatment but if not, find out what is actually causing their symptoms. Because if they are just dealing with providers who are just accepting that they have a fibromyalgia without really confirming it and a lot of the treatments are drug based treatments; SSNRI’s, other drugs that are centrally acting and that you don’t want to be taking if you really don’t have that problem, You’re not going to get benefit, you’re just going to get the side effects.
So I have taken this case to the professionals by writing a lot of these concepts in professional medical journals aimed at all different kinds of providers from primary care physicians to naturopathic physicians, you name it but I really think it’s time to take the story in an entertaining digestible way to the masses because that’s the only way it’s going to make a major impact.
But for those of you who want information you can just visit my main website is www.DrDavidBrady.com. And there is an “Articles” tab and you will find a bunch of different papers on fibromyalgia and some of them have some really nice diagrams or algorithms in them. One of them actually a couple of them have the same algorithm just on trying to work your way through this label of fibromyalgia for the practitioner and it spits it off into classic fibromyalgia, what we call pseudo-fibromyalgia or a false label of it and then we break that up into different categories so you might want to take a look at that.
One of the papers from JMPT, I think it’s a paper that goes back to 2006 but at the end of that there’s actually a full-fledged diagnostic algorithm for physicians to work through this.
There is an interesting interview that was done with myself and one of my publishing partners Dr. Mike Schneider at the University of Pittsburgh that was published in the Townsend Letter that I have on the website that really talks about a lot of the issues that I did today.
And then finally for those folks who really have significant persistent fatigue whether they have been put in the chronic fatigue camp or the fibromyalgia camp, I would encourage them to look on the website called www.cell-fuel.com.
It’s a project by myself and the physician colleague of mine Todd LePine who is a medical physician, used to be at the Canyon Ranch up in the Berkshires in Massachusetts but now he is part of the Utltra Wellness Center with Dr. Mark Hyman.
And we’ve put together sort of a program to educate people and to have them try some things to push their mitochondrial function and energy production. And this can really help a lot of folks that have the chronic fatigue label or the fibromyalgia label for a myriad of reasons why they may be put in that label category. Mitochondrial function and problems with mitochondrial energy production at the biochemical level is somewhat of a common core problem if you will throughout a lot of these different folks no matter what the original etiology is so that can be very helpful.
So on that website there is a lot of good resources. There is a free e-book you can download there as well and a free newsletter you can get so I would encourage people to take a look at that.
Dr. Craig: Great, and once this episode is transcribed I will certainly include links to all of that wonderful information for those who like to read the text of the interview as well.
Well thank you so much I have learned a ton from you, not just today but through my whole experience at University of Bridgeport and every time I have heard you speak I always learn something new so I definitely appreciate you taking the time out of your schedule to record this with us today.
Dr. Brady: Well it’s my pleasure, I always appreciate the opportunities to get the story out because I really care for and I have compassion for all the people out there who get told they have chronic fatigue syndrome and or fibromyalgia. And especially if they are struggling to find some relief, some solutions and I think… Frankly I think they are owed better care than they are getting from the healthcare providers out there. I think the healthcare providers have an inexcusable lack of true understanding of these disorders and that’s unfortunate but we are trying to change it.
Dr. Craig: Yeah, absolutely. Myself included and that’s really the purpose of this whole podcast, is to raise understanding, look outside of the box a little bit, and bring hope to a lot of people that are dismissed unfortunately and I’ve had the same experience with my own chronic fatigue journey.
All right, thanks for tuning in today to Spoonie Radio; thank you again Dr. Brady.
Don’t forget, to our listeners to go to iTunes and Subscribe so you never miss a show. And until next time this is Spoonie Radio signing off.