Medically speaking; Lyme disease does not exist in Australia. According to experts, Borrelia burgdoferi which is responsible for true Lyme disease is not found in Australia.
However, as a growing number of sufferers and their clinicians can attest; there is something which appears to be “Lyme-like” in origin which is affecting a large number of people.
Today, we are joined by Dr Mark Donohoe who shares his vast experience with patients with chronic illness and chronic fatigue which has led him to the conclusion that a wider discussion needs to be had about the presence of Borrelia in Australia. Together with Andrew they cover the many questions and controversies this topic raises.
Covered in this episode:
[00:40] Welcoming back Dr Mark Donohoe
[01:07] A broad overview of Lyme
[06:42] Why testing can be inconclusive
[12:04] Viral DNA stays with the host
[15:52] What about echidnas?
[17:24] Individual host susceptibility
[23:41] Psychological aspects to illness
[28:34] What interventions are necessary in these patients?
[31:09] Opinion on IV Vitamin C?
[34:38] Mark's final words on the future in this field…
Joining me in the studio is Dr. Mark Donohoe. GP of great renown with integrated medicine circles, and today we're gonna be discussing something which I am just on the very beginning of the learning cusp, and we're gonna be talking about Lyme disease controversies.
So I'd like to welcome Mark back to the studio. How are you?
Mark: I'm great. I think it's Lyme and Lyme-like diseases.
Andrew: Lyme-like, that's indeed it.
Mark: Borrelia burgdorferi. It was where it was first described, northeastern United States, and it is an acute illness post tick bite. There are classic signs of a target like lesion where the tick has bitten. There is an illness. There's a red ring around it, and so there are...
Andrew: Called the bull's eye mark, yeah?
Mark: Yeah, the bull's eye. And do not for a moment think that...
Andrew: But that doesn't always happen, right?
Mark: No, that's right, that doesn't always happen. I'm not talking to you as a person who's been heavily involved in the Lyme area. People keep describing me as "Lyme literate", and I am not in the sense that I have not gone into the depths that many of our doctors here in Australia have.
But the classic acute infection is a known pathogen identified, fits the Koch's hypothesis of causation, and there is not much doubt about that acute illness.
Andrew: But it wasn't identified for many years because it's extremely hard to grow.
Mark: It is.
Andrew: So this is one of those things...I mean, we could talk about this for ages. Is depending on what you test for is depending on the answer you get.
Mark: Yeah. You see what you believe you will see and you never see what you believe you won't see, right? So that if your eyes are closed, your eyes are closed. The problem is, what's the progression onto chronic inflammatory problems post-bite? Post classic Lyme infection?
Andrew: Now this is...we're still talking Lyme.
Mark: We're still talking Lyme. And so Borrelia burgdorferi, the identified tick, the classic thing we'd ask, "Have you been to upstate New York? Have you been in an area of the northeast United States where there are deer, and there are ticks?" And so in that confined area, I think medicine has no doubt about there being acute Lyme disease.
Whether it is one organism or whether they're a variance of that organism, that's, you know, in the area of medical uncertainty. There may be variations there. There is also not much doubt that a similar and related pathogen exists in Europe and in Germany, there are definitely cases of the acute Lyme disease.
Andrew: But that may or may not be Borrelia burgdorferi?
Mark: It probably is a variant of that, and so it...
Andrew: Borrelia, but not necessarily burgdorferi.
Mark: Yeah, the subspecies of what we're interested in.
In fact, the problem is, is it even necessary that it be a Borrelia? A Borrelia is a spirochete organism. Doctors always freak out over spirochetes because of syphilis. And so the history of syphilis and the spirochete and the damage that it could do the brains of people, that shadow hangs over us. And so forever we will think, “Mmmm, Spirochetes, possibly bad news and possibly things that are gonna get to the brain."
What then happened was there were a significant percentage of people who were developing long-term consequences following proven acute Lyme disease. And that smallish subset may have only been say 3%, 2% or 3% or 4%, but there was clearly something that was happening that some people went on with the illness. The difficulty was it's very hard to establish where that bug is, except at autopsy and maybe even not at autopsy.
So the assumption was this was chronic Lyme disease or Lyme disease that made it to the central nervous system, which is certainly not an impossibility. We know spirochetes have made that journey before, and syphilis, the neurosyphilis was the devastating consequence, is a terrifying disease.
So that expansion happened for a smallish group of people. The problem as I see it is, once you see that can happen and you think, "Oh, does that explain all of my patients or does that explain all of the people? Can I call it neuroborreliosis?" Which you would think, you know, maybe happens to one in a thousand. Is it maybe 10% or 5% or is it a much higher percentage? Starts you on a journey, which is, I'm looking for a cause for all of these chronically ill people with severe neurological symptoms, neuro-inflammation, a whole lot of these…
I will go and do tests to find out if that bug is there. And the problem with the testing is it's very specific for an organism. It didn't travel well outside the kind of New York or the northeast of the United States, and the generally accepted test...
Andrew: Which seems weird.
Mark: Yes, I know but...
Andrew: It seems weird.
Mark: But that's not that weird. And so this is what I've come to understand. We have this thing of, you know, do we do PCR testing, western blot testing? We do all of these kind of testing. And you think, "Oh, well that must be a standardised test kit and it must give a black and white answer." And this kind of black and white, we want it to be Lyme disease or not Lyme disease. So the groups line up on either side. The infectious diseases specialists say, "No, we have no Borrelia burgdorferi here. There is no Lyme Disease in Australia." You've got on the other side...
Andrew: But that may be true.
Mark: It may be true.
Mark: And on the other side you've got doctors saying, "But we see something that is exactly like what they saw in the United States, and so it must be a Borrelia. And when we give antibiotics, these people improve quite dramatically so that must prove that it's an infectious organism."
Andrew: But that doesn't...that's an assumption, that's a correlation.
Mark: So each side is correct. So each comes from a different world view. One world view is, "I know Borrelia and I know how to identify it. Here's the laboratory I'll use. And when it gets so many bands on this testing, then that is a Borrelia and the person has probably caught it from overseas."
Andrew: But that...I just want to cover this off in my mind. And forgive me, forgive the listeners. I'm not just being a naysayer. I'm trying to make it more concrete in my mind, and that is; if the test is for Borrelia burgdorferi...is it burgdorferi?
Andrew: Yeah. If the test is for Borrelia burgdorferi, and Borrelia burgdorferi shows up certain bands on a test, how do they know that a Borrelia...
Mark: Non burgdorferi.
Andrew: ...X species...
Andrew: ...will have the same bands unless...
Mark: They don't. And so that's where the controversy has adequate room to expand.
Mark: And so I'm trying to keep myself uncommitted to either side. I have friends and people I went through university in infectious diseases who say, "There's never been a case in Australia, and these people are all idiots." I have friends in the infectious disease GP side of this that say, "How can they miss such an obvious thing that we are doing testing and it's showing, according to our criteria, that these people have a Borrelia-like organism?" And you call it now an Australian variant or you call it something different. And in that grey area of the differences you've got one side lining up saying, "Never, ever, none," and the other side saying, "It is very, very common and it may even be passed on."
Andrew: Why do humans do this?
Mark: Well, because simplistic answers tend to get more headlines than the complexity in between.
Andrew: That's right, yeah.
Mark: And this comes back to a previous discussion we've had. Ritchie Shoemaker used to be in that category of, "It is Lyme disease that is causing these problems." And when he expanded it out to, "Hang on, there is a pattern of disability, of illness, sickness, which is a chronic inflammatory response." You focus less on the bug and the specifics of what it does, and say, "There's something about each person's susceptibility. Why would everybody that's bitten with a Lyme-carrying bug not get the chronic disease?"
Because there's something about their inflammatory genetics, the HLAs that predisposes them to grind on and on and on in a kind of unending fight, and they get knocked down in the process. For true, you know, neuro-borreliosis, for things that get into the brain where people are really quite damaged, then the treatment is very, very difficult. It is high-cost, long-term, and it's done in a hospital, and it is a life-threatening disease. But we're not talking for the majority of these cases.
Vast majority are not the life-threatening. They're the grumbling, chronic, inflammatory, never well, never really recovering. C-reactive protein, as that marker of inflammation just in the highish end: five, six, and eight, somewhere around there.
So the GPs are saying, "We've got these problem patients that don't fit any known pattern." We've done tests that say it's similar to this type of thing that we know has gone on in America. We probably have an Australian variant of that Borrelia organism. And I'm not saying yes or no. I'm saying they have sufficient evidence to be going down that pathway and saying, "Here's the DNA testing that says it's very like that. Here's what we regard as the problem."
The missing thing has always been, "Where does the bug come from? Which ticks?" And I, like many people, you know, I'm a Sydney doctor, I've been watching for years as the northern beaches of Sydney, the Palm Beach, Whale Beach, Avalon, and then moving down to Newport, there's a kind of progression down where people are reporting tick bites and these long, prolonged illnesses. We as doctors focus on Rickettsia, Babesia. We focus on the things that we know that the ticks can and do carry, and we often see those positive. And for a non-Lyme doctor, that explains it. You know, a chronic Rickettsial infection doesn't need to have Lyme Disease or anything there. These are tough infections to get over.
Where the problem, I think, arises is I have for 30 years been in this area of say chronic fatigue syndrome. Which was originally chronic Epstein–Barr virus, which was originally chronic Coxsackievirus. That what you believe is the cause, you can't stop seeing it once you believe it. And so I have had to go through that transformation myself.
Andrew: And so this is something like I've seen in the industry for, you know, chronic fatigue, multiple chemical sensitivities, then...you know, there's this explosion of thyroid issues, there's an explosion of vitamin D issues, there's...
Andrew: And it seems like the next flavour of the month, and I think we've gotta be really, really, really cautious in just jumping on a bandwagon. You know, I've seen natural medicine practitioners trying to order hundreds of dollars of tests off GPs, and the GPs are going, "I'm not doing this."
Andrew: So I mean, we've got to be really cautious of what we...
Mark: Well, the measurement issue is a really big thing. Everybody needs to agree that the test says something is or something isn't present. Is the thyroid high or low? If an endocrinologist says, "The TSH of four doesn't bother me," and a GP says, "Well, a TSH of four does bother me." And that's a body struggling for more thyroid hormone. You get divergent views about what to do about that.
Andrew: Yeah, yeah, that's right.
Mark: When you have test results on infectious organisms we tend to do a swab and say, you know, "Does strep grow? Or do we get, you know, flu virus? What variety of flu virus?"
We tend to think of them as black and white tests, but they are anything but. There are a lot of antibodies which are carryovers from things that we have had way in our distant past. For herpes viruses, Epstein-Barr, cytomegalovirus, the herpes 1 and 2, once they're in you, they're with you for life. And so, of course, you have defences and antibodies against it. The question is, are they active or are they not active?
What we are learning as a fascinating story here that...I won't go into it too much. What we are learning is, we even have endogenous retroviruses called the HERVs, the human endogenous retroviruses. They form up to 10% of our entire genome. These are viruses that made it in...
Andrew: They're very in.
Mark: Yeah, these are viruses that made it into us. And one line of thinking about DNA is it's a construction of a bunch of viruses. Viruses are described as DNAs wrapped up in a lousy package that knows how to get to you. But the DNA has always been considered to be silent.
When a person gets chronically sick, the chronic fatigue syndrome, with a variety of different attributes. Is it Lyme? Is it Epstein-Barr? Is it Coxsackie? Is it, you know, the neuron leukemia virus? Every time we have the evidence that that is the ‘thing’, you know, the antibodies are high to that, it must be true. What we're seeing from De Meirleir's work is human endogenous retroviruses, the ones that are locked up and quiet and stable in our genomes, get active.
Andrew: Who was the word done by?
Mark: Kenny De Meirleir.
Andrew: Kenny De Meirleir.
Mark: Yeah. Kenny is well-known in the chronic fatigue syndrome community over here. De Meirleir published a paper on chronic fatigue syndrome: activation of human endogenous retroviruses.
This comes back to also work done in Australia with HIV people where autoimmune disease was being turned off by the use of anti...of retroviral, anti-retroviral agents. We're discovering that we have bugs within, bugs that we carry with us, which are viral DNA. Which we've always assumed to be just historical carry overs, little fossils that are stuck in the DNA, that are making a rise again.
This comes back again to where does chronic inflammation arise? Something maybe like a tick bite, a Rickettsial infection, a Lyme disease, a Borrelia, these may be the agents which start a process, which some people cannot turn off. And I think that there's pretty good evidence that the treatment of the Australian Lyme disease with the antibiotic courses, with the things that we believe would kill the bug, don't do the job that they're meant to do at anything like the rate that you would expect from an infectious disease. You don't expect half of the people with pneumonia that you give, you know, ceftriaxone to or something like that, you don't expect half to die. You expect 99% recovery rates when you have the right drug for the right infection. And yes, syphilis was difficult to treat and yes, some bugs are harder than others. But when you get effect rates that are lower than 50% you start to think, "Well, there's a placebo component of that. There is also an anti-infectious component."
Andrew: Or at least something harder, I mean, let's look at Helicobacter, I mentioned this in another podcast. I mean, Helicobacter pylori isn't treated with one drug, is it?
Mark: That's right. Well, here's the point. Sometimes the antibiotics do things you don't expect. A lot of tetracyclines are immunosuppressants. What they do is turn off the inflammatory response in a way that is very, very interesting. You can give them to rheumatoid arthritis patients, the rheumatoid seems to get better. Does that mean a bug caused the rheumatoid? No, but it may mean the bugs that it treats are components of that, and immunology settles down as a result. So my take on this is neither side is perfectly right. There probably is...
Andrew: I think it's just really early days.
Andrew: But I do make the point that like...and I was a skeptic. I gotta say I was real skeptic of this. But now they found a Borrelia species in an echidna, one, one echidna. That echidna most probably didn't go to Lyme, Connecticut. So the naysayers in Australia, the virologists, the esteemed virologists that say Borrelia therefore doesn't exist in Australia because we've only found in one, mate, it’s here! Just because you've only found it in one doesn't mean it's not in more echidnas and more diverse range of species.
Mark: There's steps to go. The basic research, which friends of mine are doing and I absolutely would support this to the hilt. Is go looking for where the vectors are and do they have the bug.
Andrew: Yeah. Bitten by an echidna!
Mark: And so the finding of a Borrelia subspecies in an echidna is of interest but isn't proof of pathogenicity. There’s a lot of further work to be done for that particular variant of Borrelia.
Andrew: But it is proof that that genus, at least, exists outside Connecticut.
Mark: Yeah. You would be surprised if Borrelia and Borrelia relatives were stuck in one particular area of the world anyway. So there will be variants, and there is usually...it is usually true that high pathogenicity starts in a place where pathogenicity and human contact are both high. There has to be something for the survival and the transmission of that bug so...
Andrew: Which is an interesting argument with Ebola virus, but anyway...
Mark: Yes, yes, I know.
Andrew: It’s a converse thing, but anyway…
Mark: I do note, and the world of infectious diseases is not as simple. A Pasteurian view of one bug, one disease, it worked beautifully when we had, you know, Mycoplasma pneumoniae and where you're given an antibiotic and the person who was going to die gets better.
That's powerful, powerful plays on the mind of the population and of doctors. When it worked to keep people alive through World War II, that would otherwise absolutely, certainly have died. You know that you've got a way of attacking the microbes that are really there to take us out, you've got a way of bringing them under control.
Andrew: But they're there to take us out once they reach a certain...
Andrew: A certain load dependent on the virulence of that genus and species.
Mark: And dependent upon...
Andrew: And the host.
Mark: The variable susceptibility of the host.
Mark: So nobody ever doubts that people wounded in battle with shotgun and dirt getting into wounds, they're compromised full stop. The bug that finally is the thing that takes them out is just one of many that can line up. And so you do get a bug being blamed for the entire illness, which is really a complex mixture of susceptibilities.
Remember we talked about Ritchie Shoemaker's chronic inflammatory response. If you've got say 5 %to 7% of the population highly susceptible to chronic inflammation, that bug can be the tipping point. The tick bite becomes the event which catches our attention.
But I made the mistake myself of seeing 18, 17-year-olds doing their high school certificate getting glandular fever, developing just the same chronic inflammatory response, profoundly disabling joint aches and pains. There was no doubt about the catastrophe that went on. But I forgot early on to ask the question, "Why would that happen just in the HSC year?" What is it about their diet, lack of sleep, studying, you know...
Mark: The hormones that are raging around the place. There is a context to every bug.
Andrew: And stress.
Mark: And my honest feeling, I've said this and I've made enemies on both sides of the fence here, my honest feeling is there's something about susceptibility. This is not a thing that's going to rage through the population taking on the blood supply or water supply or anything like that. There's a susceptibility issue. There's an opportunity with a host, and then to our...it's upon us to be able to separate and not just create random fear.
If people are fearful that they have been infected with something that could do enormous damage and maybe even eat away their brain, their stress levels go extremely high, and it's unethical for doctors to play on that and say, "Therefore a barely proven treatment is going to be what I administer to you with a less than 50% chance of recovery." I don't think that that's a good look for medicine.
We should have the discussion between the groups saying, "There is something Borrelia-like. It does trigger really severe disease." Many of those people get better with antibiotics in the way that we use them, but many, many do not.
Andrew: Don't, yeah. And this to me, it's sort of...it smacks of the...as you say that, you know, the host immunity and what I like to call resilience.
Andrew: It seems to be importantly to do with whatever these multitude of insults are happening at the moment. You mentioned the teenagers, right, with the hormones, with the viral load, with...
Mark: With the study, loss of sleep, eating junk food.
Andrew: It seems to be, you know, the stress is such an important factor in so many of these chronic, debilitating, diseases but it seems to be their resilience of that. For instance, another person with exactly the same load seems to recover well.
Mark: Sure. The vast majority of high school certificate people who do get glandular fever don't disintegrate and fall into chronic ill health that lasts them 10 years.
So there is something about the host. There may well be something about co-infection, and this is an argument of the Lyme doctors, is it is not necessarily just one.
Andrew: One bug, yeah.
Mark: But if you get Babesia, Bartonella, or if you get Rickettsia, if there are multiple pathogens, you're no longer in that ballpark of what's the one bug that did it. The opportunistic side of that infection is multiple things at the one time. It can mean that one of those bugs makes it free.
Andrew: It’s another knock, yeah.
Mark: I have a favourite with Epstein-Barr. What people forget is Epstein-Barr invades what's called naïve B cells, so immune cells, B cells that have not yet been given a job. The Epstein-Barr gets into those. We thought it was about 5%, now the research says 95%.
Mark: What does that mean? It means you've got little circular piece of DNA in a cell that is yet to be given its job to do. When that cell finally gets given a job, and it's again something common like say candida or streptococcus or something like that, and it clones itself and replicates, it's replicating that virus at the same time. So the trick of Epstein-Barr appears to be not just to get on the nasopharynx, but those lymph nodes are replication of the virus. So it's riding on the back of a very active healthy young person's immune system and makes it… it interpolates itself.
Is that a problem? Not if the person's really healthy. If their diet is high in, you know, omega-3s and they've got a good variety of foods and they're sleeping well, we do that over and over. Those naive B cells become active, the virus is looked after, it goes back into jail, and you're good for another couple of years. For a person worn out, dragging their feet, that virus becomes their archenemy, and we do see this with what's called early antigen studies. They should only be there for the first part. They keep bouncing back time after time in these people.
What does it mean? They're fighting something else. We're seeing the Epstein-Barr and say, "Oh, it's got to be Epstein-Barr." We're putting all our effort into how do we kill Epstein-Barr virus, whereas you go back to first principles, what else is there that we could've done?
And that to me is a bigger answer. If there's other easier to hit infections, if there's gut parasites, if there are things that we can do with diet, sleep, and lifestyle. Host repair is absolutely as good as injury to the pathogen.
Mark: You never get rid of every last pathogen but you can...
Andrew: Do you necessarily want to?
Mark: No, you probably don't but you can't anyway. The lesson that we've learned is getting 99% reduction would be great, but that's still billions of the bugs that are left behind. And if the host is compromised, they'll make their way back again.
Andrew: So I have to ask. I remember years ago and I've brought this up in previous podcasts, a conversation that you had with a psychiatrist, I think? Where that psychiatrist was vehement. They were stoic saying, stoically saying, that chronic fatigue sufferers had somatisation, and you were saying, "No, they're not."
Andrew: So regardless of the reason, regardless of the reality, how great do you think the requirement, the need, the utility of psychological tools for recovery of physical illness is? i.e., and I'm going to say cognitive behaviour therapy, I know you'll say mindfulness.
Andrew: But how important...
Mark: Well, it's "mindful CBT" now.
Mark: The big thing is mindful CBT. And so everything in psychology aggregates whatever else was the good thing.
Andrew: So how important, how useful is that?
Mark: It's...I've become used to the fact it's critical.
However, here's the clinical pearl. People...there's one good study on chemical sensitivity. People found psychological intervention for support and recovery from the illness highly valuable. People found psychological interventions that blamed their illness on a psychological condition, not only unhelpful but felt sicker.
Mark: Our tendency to want to break it up into is it somatisation or is it real is our problem. Deep down people say, "Oh, we have a psychosocial, you know...we're very cool these days." But deep down doctors still have this, "Is it in your mind or is it actually real?"
And so we put people out to psychologists. The best psychologists now will say, "Yes, I'll do CBT," and they don't. CBT is funded, it's kind of evidence-based. And as we found in the chronic fatigue studies done in the United Kingdom where CBT was introduced, when people went back and said, "Why did CBT work there?" the question was, what did doctors do? Doctors did what they believed was cognitive therapies but there was no training in it. Doctors did what doctors did, which is they encouraged people to be active, they encouraged people to not be defeated by the disease.
A good clinician is a big part of the recovery of another person, even if they do nothing. Even if all they can do is reassure and say, "You are going to make it through this and you can bring this to your mind, you can bring what are symptoms and bring it to the mind and defeat those symptoms," for one group of people, that works really well. They tend to be the rational type people. For people who are more poetic, it doesn't work all that well, will say, "Oh, that's not how I deal with things."
So my problem with CBT is, you can construct trials of CBT responders that work for almost anything. You can say heart attacks, you can say anything you like because the mind is powerful. But if you think of that as the alternative to Lyme, Epstein-Barr, if you think of that as the alternative to a good diet, that is way off track. That is just yes, we can get the person over the next hurdle, which is, how does a person recover after chronic illness, and that's really important.
Andrew: And this is where I'm like...given that it seems to be largely empirical at least at this stage, what do you find are the most useful tools for those people who appear to be suffering a Lyme-like disorder in Australia?
Mark: Well, I have to say one thing. I obviously don't see the successes of the doctors that treat Lyme disease. So the people who they claim are better, the percentages, I cannot dispute that. It may be that 80% of people walk into their surgeries and come out well and I only see the other 20%.
Mark: I tend to see the people for whom the treatment was ineffective and/or who responded adversely to the antibiotics in the course of treatment.
It is a really complicated course of treatment. Burrascano's regimen and the filling of that regimen is incredibly fiddly. And in my experience in medicine, when things are incredibly fiddly, it's not the answer.
The simplicity of a concept and a conceptual framework like Shoemaker's of you are highly responsive to these types of inflammatory disorders, how do we undo that response to the inflammatory disorders I find far more elegant.
However, having said that, that I only see the failures, the responses are easier to manage because the person's left the antibiotic world and left the Lyme disease world to say, "What else can I do?" It may even be that Lyme was only 20% or 30% of why that person was sick, and what all I have to do is clean up the allergies, get the diet right and get to work with other things.
So from my perspective, it is particularly parochial. I see it as success of what I do on the back of whatever those Lyme doctors have done.
Mark: Well, it's the basics of getting back to diet. What do you do...how do you respond to different foods? Are there other pathogens? Get the stool test done. Stool tests are often missed out by Lyme doctors simply because they're focused on the organism.
And so understanding what's going on with zonulin, gut permeability. Those are important factors for me, and I fully understand that if I start a person who's actually got a Lyme-like illness on those, I will be probably very ineffective. So I do admit that I run on the back of failed treatment courses coming to me. At least one thing's out of the way. They no longer are going to be going down that Lyme pathway or antibiotic pathway.
I think, though, my advice on every side of this is the discussion still needs to be done. We have to not have AB variance. It's not everybody has Lyme or nobody has Lyme. It is, there is a Lyme-like organism that shows up partial test results. That everyone kind of agrees is a little bit like it, but not quite the thing. And it's part of the entire host response that sees that get out of control. It's not everyone that gets it. And once we start that discussion and we start to think, "Well, what's the complexity? What's the time series? What's the person's story?" then it's very difficult to get back to what the specialists love, which is randomised control trials of 100 people, all identical, having the same antibiotic.
Andrew: Do you think that'll ever happen?
Mark: I don't think it will, but that...there is a feeling in medicine that the RCTs, the concept of controlling all variables has had its day. And it's powerful for saying, does the drug work and is the drug safe? And when you've got one dimension, a randomised control trial is not a bad way of saying with 95% certainty this is unlikely to have happened by chance.
Where it's complex is nutrition, lifestyle, diet, teenagers kissing each other, getting viruses, eating poorly, having stress, and then the genetics of those people and the family history. You cannot randomise that because all the variables of interest are the life story of the person. So a controlled variable trial can answer one small question with high accuracy. It is not meaningful for the majority of what we have to handle in general practice or in naturopathic practice. And because of that, all randomised control trials do is guide us to, "Here's a thing that in these circumstances works well. Are you, my patient, like the people in that trial? And if you're not that is not applicable to you. And if you are, this might be a very useful piece of information."
Mark: Yeah, I'm a big fan of it, and I haven't done it for a while.
But there is, you know, there's an epochal story from my own practice. I started in '83. In '84 I became interested in the vitamin C. I was seeing allergy, I was seeing immunology, I was treating infections, I was doing a lot, and a core group of people just refused to get better. And that 30 or so people kind of dominated my practice. I heard about Ian Brighthope, got the intravenous vitamin C from Biological Therapies, and I started running them in, and half of my patients got so dramatically better so quickly.
Andrew: On what dose? Are we talking 30, 50 grams?
Mark: Well, yeah, I was...30 to 45 grams, sometimes even up to 60.
But I was new, I was keen. I was sure this was something worth trying, and I can never get that out of my mind, that naiveté has a benefit. You believe that the stuff is working. What do we know about placebo responses? It's not the patient's belief in the treatment. It's the patient's belief in the professional and the professional's belief in that treatment.
So the highest placebo response is, if I believe vitamin C is going to help and the patient believes me, then it does the help. It's not whether they believe in vitamin C. So what happened was I got a huge proportion of my practice who had been difficult to treat a lot better very quickly. And to me I just said, "Oh, that's magic. Why did I not know about vitamin C? It's good for everything."
Mark: I started introducing it as first line treatment, and it was ridiculously ineffective. People just got sore veins, they didn't feel any better. And it took a lot of reflection to realise that all the spadework done before that didn't seem to do any good for them was in fact essential. You’ll remember a guy called William Vader?
Mark: William had a metaphor, which to me is perfect, a boat with five anchors.
Mark: You pull up four of them, nothing's happened and you think, "God, that was a useless four anchors to pull up." You pull up the fifth one and the boat gets moving. Intravenous vitamin C was the fifth anchor.
Mark: And people got moving. But when it was the first anchor the other ones, the unmanaged, diet, lifestyle...
Andrew: But it was still one of the anchors.
Mark: Yeah. All the rest of them had not been dealt with, so magic doesn't really happen. The individual story is still important. You get the basics right and then you toss in the big guns, and I still to this day...the most amazing things I've seen are intravenous vitamin C for acute glandular fever, it works like magic.
I have seen people get over glandular fever in three to four days and be really well by one week. If I had a magic trial to do, it would be to get every HSC student who is going...gets glandular fever, and within 24 hours of the diagnosis use an intravenous vitamin C and you...
Andrew: But you don't do it once? You might have to do it two or three times.
Mark: You do it a number of times, but the very first occasion is quite dramatic.
So vitamin C is a very, very interesting product, and it's coming back as antiviral, and yeah, and Ian Dettman just did this discussion of “Here's the evidence for the antiviral activity”. It's potent. But it has to be administered while the virus is replicating.
The virus has a brief window of time where it replicates and we don't know, and then we get clinical illness. If you don't hit it very quickly at that point, intravenous vitamin C struggles the same as anything else.
So if I had one trial to do it would be all HSC students from two schools. One group all get vitamin...intravenous vitamin C, the other group all don't get intravenous vitamin C.
Andrew: But the variable is the curriculum and the tuckshop.
Mark: Yes, you don't want to do Mossman and another suburb.
Mark: Oh, the senate inquiry?
Andrew: The senate inquiry...
Mark: Yeah, the senate inquiry got called off because of the, you know, the double dissolution and the... And so they've left that in abeyance. There was a lot of BS that went in from both sides of that inquiry, and bluntly I think no one's going to restart it. I really don't think anyone's gonna restart that inquiry.
I think the next step is going to be someone needs to not have a war going. There needs to be a common ground between people with knowledge of infectious diseases of pathology, of the differences between different types of testing, and then there needs to be an awareness around the table that not everything is Lyme and not everything isn't Lyme.
What are we seeing? And if Shoemaker's framework provides one way of thinking about it, what's host response versus pathogen, I think that's a useful starting point. I think dragging in the oldies like me that remember every pathogen's had its day. Lyme disease has a very expensive and difficult to manage form of treatment, which is frankly dangerous. You do not want to unnecessarily use antibiotics which will breed resistance. The last thing we need is community resistance in the way that we developed it in hospitals simply because everyone runs out with long courses of ineffective antibiotics.
So there are reasons that we should do it from public safety. There are reasons we should do it to find out what is it about maybe 30%, 50% of people who get better. There's something in there, but we do not do well with a war where everyone sort of just shouts at each other. I think the next step is that conversation and I don't know how we get there.
Andrew: Not withstanding massive issues with cautions of what you think you see...
Andrew: I certainly believe that the issues of Lyme-like disease in Australia, like we are at the tip of the iceberg and it's only yet to develop.
Mark: That I would agree with.
Andrew: Yeah. So I look forward to definitely podcasting with you and bringing that sort of information in the future to our listeners.
Mark: I think we should bring in a couple of the Lyme doctors and the detractors. The problem that I did have is my infectious diseases friends, their answer was, "Could we have this discussion? Was…I'm not having a discussion with idiots." And that arrogance of the specialists also needs to be addressed. The generalising of the general practitioner needs to be addressed. They're talking different languages. The common language needs to be what's the care of these people with the chronic illnesses that the infectious diseases specialist can't identify and the GPs can? And to the patient's benefit that conversation's got to be cooperative rather than antagonistic.
|Dr Mark Donohoe|
|Dr Richie Shoemaker | Surviving Mold|
|Dr Kenny De Meirleir|
|Prof Ian Brighthope|
|Dr Ian Dettman|