Why You Should Listen
In this episode, you will learn about recovering from Lyme disease.
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About My Guest
My guest for this episode is Dr. Dan Kinderlehrer. Dan Kinderlehrer, MD is a nationally recognized physician with expertise in the fields of nutrition, allergy, environmental medicine, Lyme disease, and the healing of mind-body-spirit as a unified whole. Dr. Kinderlehrer co-founded The New England Center for Holistic Medicine in Newbury MA and has taught extensively, including practitioner training courses at the Omega Institute, The National Institute of Behavioral Medicine, and the International Lyme and Associated Diseases Society. He created and organized the Lyme Fundamentals course which is presented annually at the International Lyme and Associated Diseases conferences. He is the author of several review articles in medical journals and the Lyme Times. His integrated medical practice in Denver, CO focuses on the diagnosis and treatment of tick-borne disease. Dr. Kinderlehrer is the author of "Recovery from Lyme Disease: The Integrative Medicine Guide to Diagnosing and Treating Tick-Borne Illness".
Key Takeaways
- How have the Lyme Wars between IDSA and ILADS changed?
- What is the role of epigenetics?
- Do Adverse Childhood Events (ACEs) play a role in the development of Lyme disease?
- What is Post Treatment Lyme Disease Syndrome (PTLDS)?
- How might treatment be approached after a tick bite?
- What are other means of transmission of Lyme disease besides tick bites?
- Which microbes play the biggest role in anxiety, depression, OCD, and neuropsychiatric symptoms?
- Do patients do better at higher altitudes or at sea level?
- What is the latest on Disulfiram for treating Lyme disease?
- What labs have been most helpful?
- What are some of the key treatment options for Lyme and co-infections?
- Might Bartonella play a role in SIBO?
- How is dysautonomia addressed?
- What is the role of MCAS in Lyme disease?
- How much does mold impact patients with Lyme disease?
- Which oxidative therapies have been helpful for Lyme patients?
- How important is limbic system retraining?
Related Resources
Interview Date
March 12, 2021
Transcript
Transcript Disclaimer: Transcripts are intended to provide optimized access to information contained in the podcast. They are not a full replacement for the discussion. Timestamps are provided to facilitate finding portions of the conversation. Errors and omissions may be present as the transcript is not created by someone familiar with the topics being discussed. Please Contact Me with any corrections.
[00:00:00.25] Welcome to BetterHealthGuy Blogcasts, empowering your better health. And now, here's Scott, your Better Health Guy.
[00:00:14.13] The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.
[00:00:35.22] Scott: Hello everyone, and welcome to episode number 141 of the BetterHealthGuy Blogcasts series. Today's guest is Dr. Dan Kinderlehrer, and the topic of the show is Recovery from Lyme Disease. Dr. Dan Kinderlehrer is a nationally recognized physician with expertise in the fields of nutrition, allergy, environmental medicine, Lyme disease, and the healing of mind-body-spirit as a unified whole.
Dr. Kinderlehrer co-founded the New England Center for Holistic Medicine in Newbury, Massachusetts and has taught extensively, including practitioner training courses at the Omega Institute, the National Institute of Behavioral Medicine, and the International Lyme and Associated Diseases Society. He created and organized the Lyme Fundamentals course, which is presented annually at the ILADS conference.
He is the author of several review articles in medical journals and the Lyme Times. His integrative medical practice in Denver, Colorado focuses on the diagnosis and treatment of tick-borne disease. Dr. Kinderlehrer is the author of “Recovery from Lyme Disease: The Integrative Medicine Guide to Diagnosing and Treating Tick-Borne Illness”. And now my interview with Dr. Dan Kinderlehrer.
Your passion in helping others with Lyme disease came from your personal experience with this difficult condition. Tell us about your personal journey and how that led you to your passion to help others and to write this book.
[00:02:07.17] Dr. Kinderlehrer: I was a healthy 46-year-old in the middle of the summer of 1996 when I suddenly came down with a high fever like 104 degrees, diffuse chills, shaking chills, bed shaking, teeth chattering kind of chills, and then severe drenching sweats, and severe muscle aches, and headache. It all lasted like two, three days, and then I was okay.
And I lived in Massachusetts. Certainly, it was Lyme territory. Had not seen a tick, which, as you know, was not uncommon; I had not seen a rash, I had no idea what it was. But after three days, I was okay, and I thought, well, I'm just going to attribute this to a virus and keep going. However, it didn't work out; the next week, I had another two days of chill, sweats, and aching.
I tried to ignore it, but then it occurred for the third time, and I went to see a colleague of mine. And he examined me; he said, oh, guess what? Your spleen is enlarged. Ran some tests and said, oh, you're positive for Lyme disease. And I'm like great, I'll take antibiotics for a few weeks and I'll be fine, that's not what happened. I got worse. And what got worse initially was my sleep.
I went from being an Olympic sleeper to waking up earlier and earlier so that I was getting like two hours of sleep a night and anxiety. The anxiety, it was not something I had really ever experienced, that it was like this nine out of ten sense of impending doom total overwhelm, wanted to hide under the covers except even under the covers that I just felt like oh my god, something terrible is happening. No connection with what was happening in the outside world.
After a month of this, we did another blood test; it was still very positive, it was even more positive in the Western blot for Lyme disease. I've been on antibiotics for over a month at that point. And I call up an expert in this, so-called expert I've been advised not to name, but his name you would know it very well. And he was at Tufts New England Medical Center at the time, he's now at Mass General. And he authored the initial paper on Lyme disease in the United States; he was the first author.
Okay, so he was very courteous. You know this was back in 1996; back then, doctors could call doctors, and they would get a callback, you know. Now no, I don't know, it's not so easy to connect. But I gave him a call, and he very courteously listened to my presentation, and he said, well, you don't have Lyme disease. And I said why not, he said well because if you had Lyme disease, you'd be better by now.
I said, well, what about the tests? They were like slam dunk. He said, well, they were wrong; they're false positives. I said, well, what do I have then? Something else. Well, it's very interesting. The next thing I did was I called up a colleague in upstate New York, who I knew was treating people with Lyme. And I had not been treating people with Lyme.
And I presented my case and told him what happened when I talked to this so-called expert, and his response, which I'll never forget, was welcome to the Lyme wars. Well, you know this so-called expert; he was categorically wrong when he said I didn't have Lyme disease. I clearly had Lyme disease; there was no question. But he was also correct when he said I had something else, which was Babesia. Now, if I took my history now, any decent Lyme doctor taking my history now would say, oh, you got Babesia.
You have high fever, chills, sweats, and an enlarged spleen to boo; you know you got Babesia until proven otherwise. Eventually, I ended up with Bartonella as well. I suspect the Bartonella came from another tick attachment. But most of my symptoms were neuropsychiatric. I did have fatigue; I had these awful sleep problems. I did have some muscle aches and so on. But what was so debilitating was severe anxiety, sometimes panic attacks, severe depression.
I was suicidal; it was very hard getting through the day. And eventually, thankfully, I did recover with a lot of help and over a long period of time. Of course, during that time, I came to find out that infectious disease doctors know nothing about this illness. And that they're very few Lyme literate physicians. And I said, wow, I want to devote myself to treating people with this.
Hopefully, to prevent them from going through what I went through because it was terrible, it was really terrible. So that was the source of my passion; you know, how can I help people get better from this awful experience.
[00:07:42.10] Scott: It's interesting that you were dealing with this in 1996; that happens to be the same year that I had my known tick exposure, that led to my Lyme disease and Babesia and Bartonella. So lots of overlaps there.
You mentioned the Lyme wars, and so we could do a whole podcast on this, but just kind of at a high level. The Lyme wars between ILADS and the IDSA, those have been ongoing for many years. Do you think that things have improved at all in terms of making broader access to care available for those with Lyme disease?
[00:08:17.01] Dr. Kinderlehrer: I think it's shifting; it still has a long way to go. So just for your audience, the Lyme wars can be broken down to the Infectious Disease Society of America, who claim that Lyme is easily diagnosed, easily treated. Ten days to three weeks of antibiotics, you're good. If you're still sick, it's something else.
And then there's ILADS and physicians like myself and people like yourself, who say not so easily diagnosed, not so easily treated, frequently complicated by co-infections and other downstream effects of inflammation by the time it's properly diagnosed, and can take long-term treatment. There it is, there's your two distinctions.
One step in the right direction is when the infectious disease doctors acknowledge that at least 10 to 20 percent of people who are treated for acute Lyme disease continue to have chronic symptoms because initially, they wouldn't even acknowledge that. They said, oh, those are just the aches and pains of everyday life. Well, now they're acknowledging no, they're not, it's something more like post-COVID syndrome, which is interesting, isn't it?
And that these people are perhaps more debilitated than those with congestive heart failure. So, unfortunately, the designation they have for that is post-treatment Lyme disease syndrome, PTLDS. And like you, I abhor that designation; I don't use that designation because it suggests that the Lyme is no longer there.
What I can tell you and I can't prove this categorically, but the evidence certainly supports it. Is that those people who continue to be symptomatic after treatment for acute Lyme disease and have this "PTLDS" syndrome, they all have co-infections, and then they have all sorts of other downstream issues. I actually think the biggest difference between those who do just fine after getting their ten days to three weeks of antibiotics and those who go on to chronic symptoms is co-infections, which have become more the rule than the exception.
And there are studies that suggest probably 85 percent of people who get Lyme also get co-infections. So that's sort of it in a nutshell, that there is some movement. But I still have patients who have to go to the emergency room for something, and they say, well, I have chronic Lyme disease. And the doctor starts yelling at them, there's no such thing as chronic Lyme.
I had a patient, an interesting story this patient, I'll make it brief. He was in his 20s; he graduated college, he wanted to be a professional hockey player. But he ended up getting whacked in the head; he had a TBI, a traumatic brain injury. He was cognitively impaired; he wasn't going to be playing hockey anymore. But someone, I don't remember how or why someone had the bright idea of having him tested to Lyme, it was positive, and he came to see me.
And I said, gee, I don't know what's causing your impaired condition, is this related to your brain injury, or is this related to the bugs? But let's treat the bugs, and let's see what happens. And he had a whole bunch of downstream issues, too, endocrine disruption and mold and this and that. We treated him; he was fine, and then guess what?
He went to medical school, and now he's a third-year orthopedic resident. But when he was in medical school, the point of the story, he was a fourth-year medical student, and I said to him it's just three years ago. I said to him, so what are they saying about Lyme disease on the wards? He said they think it's a joke, they just laugh, they think it's just false.
[00:12:09.08] Scott: Yes, sadly, I agree. I don't know that the Lyme wars between ILADS and IDSA have necessarily gotten much better. What has gotten better is ILADS has grown in size over the years. I remember my first ILADS conference in 2006, there were maybe 75 people, and now I think it's probably closer to a thousand at these ILADS related events.
So that's certainly a big shift and very positive. One of the things that you talked about in the book that caught my attention was zinc deficiency, and you talk about how that can be epigenetically passed down to future generations.
And so I often see people that have low Alk Phos that you give them zinc, you give them minerals, and it just doesn't really seem to move the needle very much. And so I'm wondering does that imply that we need to address the more mental, emotional trans-generational issues or inherited issues to be able to actually utilize the zinc that we might be supplementally consuming.
[00:13:14.06] Dr. Kinderlehrer: Okay. So I was using the zinc as an example of epigenetic transmission. And you probably know Jeffrey Bland, right? Probably 30 odd years ago, he gave a talk where he described this experiment where they took rats, they made them zinc deficient. And, of course, they had immune deficits, that's what they'd expect.
And then the next generation of rats from that group also had immune deficits, no big surprise. But when they repleted the zinc in their diet, they still had immune deficits. And it took two generations, and two generations later, there were still some immune deficits but much less. So this was my introduction to epigenetics.
The amazing thing about the internet is I could go online and find that study that Jeff Bland had described 30 years ago. Okay, so in epigenetics, what we're talking about is not changing the DNA, we're not using CRISPR or something like that to actually modify DNA. That takes millennia of natural selection. But there are proteins that sit on top of the DNA, and they turn the DNA on and off, that's the epigenetics.
And there are so many different stressors, thousands of different stressors that can alter the epigenetics and immediately get transferred to the next generation. So now I'm going to just broaden what you're talking about beyond zinc. Because I think in the past 100 years, there have been so many epigenetic stresses that have accumulated from one generation to the next. So we could start with 100 years ago, look at the difference in diets.
Look at the mineral depletion in the soil; look at all the sugar that people are now eating. Then look at all the chemicals that have been added to our diets, not to mention the air pollution and the water pollution. All the xenobiotic agents that were exposed to that weren't even known to man a century ago. And these are each one like RoundUp.
They've been demonstrated to cause epigenetic changes. And then guess what? That gets passed on to offspring. And so we're talking about cumulative stuff, and this even applies to emotional trauma. PTSD can get passed down to offspring because of these epigenetic changes. Obesity can be passed down to offspring, one generation to the next.
Not going back thousands of years. And so what's happened now is we're seeing other epidemics besides Lyme disease, and I think there's a commonality to it. That these epigenetic changes have resulted in significant immune dysfunction, neurological instability. And we could broaden it because most of it results in some degree of autoimmunity.
And when we look at bugs like we're dealing with Lyme, we're not dealing so much with invasion of a microbe, we're dealing with a weird reaction to a microbe that's resulting in systemic inflammation. And particularly, neuro-inflammation. And I really think that part of the Lyme epidemic is not just that these ticks are spreading for lots of reasons, because we're living in suburbia, and now we have climate change, and the ticks are hooking on the birds and goings all sorts of places where they couldn't exist previously because it was too cold.
So yes, we're seeing Lyme disease in every state in the union. But including Alaska, right? But we've changed, and our resistance to infection has changed. Our reaction to these infections have changed. So coming back to your original question, how do we deal with this? I think we're talking about major changes in lifestyle that the chemical-laden society we have created in the past century, it has been terrible. And one other piece of this that I feel is very important is the breakdown in community and extended families. You know we're told that sexual abuse is actually going down now; I certainly hope it's true.
But a century ago, if there were awful things happening in the family, that kid could go next door to his aunt, his uncle, to her grandparents, or whatever. There were safe people around. But we've seen the breakdown of these extended families and communities to nuclear families and then single-parent families. Now tragically homeless families, and there's not that safety that was available back then. In other words, I think that trauma is much worse.
I don't know if you've ever read Bessel van der Kolk's book; The Body Knows the Score, very interesting. So he works with people who've had really significant trauma in childhoods. And he was in the Boston area when I was there, and I heard him talk, and he said something very interesting, two things. One is these people have a lot of physical problems, and the other thing he said is the one issue, the one parameter that makes a big difference in whether they can heal or not is, was there one safe person.
You know could they access a sense inside them that ah, they can relax now, they're safe. Where their limbic system wasn't going haywire, and their bodies weren't hyper-vigilant. So I found it really interesting because I was seeing the same patients he was, but I was seeing him from the other end. They would come to me with the physical complaints.
So this is like 20 to 40 years ago, I'm seeing these very environmentally ill people. So these are the ones you know in the extreme, they're living in the main woods. And if someone within a mile has perfume on, they have an asthma attack. They're down to three different foods, and they can only wear cotton linen, severely sensitive people.
Back then, it's not so much true now, but back then, those severely environmentally ill people, a high, very high percentage of them, had a history of sexual abuse trauma, really tragic, challenging childhoods. And it made so much sense to me. Because the whole sense of immune system is boundary function is connected to our sense of safety in the world. If we don't feel it's safe in the world, and we don't know who's safe and who's not safe and what's an appropriate boundary because it's been invaded inappropriately.
Our immune system, our physiology respond the same way. It's not safe; we become hyper-vigilant in our nervous system and in our immune systems. Our immune systems don't know is eating this safe or not, is smelling this mold-safe or not. And this chemical safe or not, and these people become highly reactive. Okay, so the point is that we're losing safety; we really are. And it's really sad and tragic. Again, coming back to your original question. I think we need a wholesale change in how we live, I really do. Unfortunately, we Americans traditionally have treasured the independent go-it-alone John Wayne kind of whatever.
Where I don't need anybody, I can certainly stay at home and order whatever I want from Amazon, including food. And really, sadly, COVID-19 has not helped. But now, I think the technology we have has really hurt us; it has really hurt us. I think if we went back to a full-scale acknowledgement of our interdependence, and then it's changing our priorities.
Clean air, clean water, an inhabitable planet. Something where we're respecting what everybody needs, just not our personal needs. I think it's just basic being kind and human, rather than worried about oneself, worried about oneself and getting what we need, and basically self-serving. Which is understandable, given the way we're growing up now.
[00:22:48.22] Scott: I actually love that you mentioned Bessel van der Kolk, he's someone that I'm hoping to have on the podcast. So if anyone listening has a connection that might be able to help facilitate that, that would be great.
Some promote the use of doxycycline after a tick bite. It really, from my understanding, does fairly little for the co-infections like Bartonella and Babesia. Is doxycycline an adequate approach to avoiding chronic Lyme disease after a tick exposure?
[00:23:19.17] Dr. Kinderlehrer: Okay. In 2001, Nadelman had an article in New England Journal of Medicine which was about the morning-after pill. In which his study suggested that if someone had a tick attachment, and they took 200 milligrams of doxycycline within 72 hours, then they were much less likely to get Lyme disease.
Well, it was a terrible study; it had major flaws. His endpoint was at four weeks. Did you have a rash or not? There was no long-term follow-up. And there were still some cases in the treated group that did develop Lyme disease. In other words, I don't believe in the morning-after pill. But if we extend that and say if you get a tick attachment and you live in a Lyme endemic area, I'm going to suggest to get treated.
But treat as if you have the infection, not a prophylactic treatment, but a curative treatment. So I'm going to treat for at least four weeks, four to six weeks within my antibiotic, but then the question is, what do you treat with? Well, if we were going to be treating for Lyme, Babesia, and Bartonella and throw in Mycoplasma, we're talking at least triple antibiotics to someone who's healthy, and we don't even know if they got infected if there was actual transmission from this tick attachment, right?
What I recommend first of all is not doxycycline so much; for one thing, to get really adequate blood levels, you have to push the dose. And you push the dose, and it's much more likely you're going to get gastric problems, really common GI upset. But also I live in the southwest now, it is sunny all year long. And more than half the people develop photosensitization. I mean, develop second-degree burns if they're exposed to the sun while they're taking doxy.
So I'm not a big doxy fan. And I usually recommend that people take some combination of a cephalosporin and a macrolide. So something like Cefuroxime and Clarithromycin as a good drug, and understand as you're pointing out mainly we're hitting Lyme that way. And we're not hitting the co-infections that way. But what I also recommend is waiting a couple of weeks and then getting tested for the co-infection. I don't think if prophylactically, we can justify giving people triple antibiotics.
So mainly, I'm just preventing the Lyme. Or maybe I am, maybe I'm not; as you know, once you have Lyme plus co-infections, it's much harder to treat the Lyme. But I'm going to treat Lyme disease for four to six weeks; I'm going to have people check-in if they develop any symptoms.
And then, on the basis of symptoms, I may say, oh, I really think you have Bartonella or Babesia or whatever, and now we're going to add to your regimen. And if I can get them to do it, I'm going to also test them for the co-infections and wait a couple of weeks after the tick attachment to do that.
[00:26:46.14] Scott: And just to be clear, so the waiting a couple of weeks is waiting for the testing, but you're starting the Borrelia focused agents right away, not that we're waiting to start overall treatment until that two-week period. So tick bite starting treatment two weeks in, you're testing for co-infections and then adjusting the therapy based on those results and clinical presentation.
[00:27:07.19] Dr. Kinderlehrer: Thank you, yes. And I should mention that by treating for Lyme disease early, we're going to abrogate or prevent the antibody response, which is what we pick up on the test. So we're going to get a false negative test for Lyme disease by virtue of testing it early and appropriately. And patients have to be aware of that, that if they get tested for Lyme disease down the line, it doesn't mean they didn't have it or might not even still have it.
[00:27:37.17] Scott: Many call Lyme disease a tick-borne infection, but it's clear that there are other means of transmission, other insect factors, pregnancy, possible sexual transmission with Borrelia and even co-infections.
What are some of the ways through which you believe Lyme disease complex, and when we say complex, we're including the co-infections in addition to the Borrelia. What are some of the ways that you believe Lyme disease complex might be acquired?
[00:28:03.22] Dr. Kinderlehrer: Well, I think you nailed it, to be honest. Besides the tick factor, there are isolated cases; I've seen isolated cases where people swear they got it from a horsefly or a mosquito. We know that the spirochetes do inhabit other insects; why wouldn't they? The question is, how good are they transmitting it.
And there are these isolated cases, no big studies that I know of, that suggests it can be, at least to some degree, transmitted by other insects. But we don't have any hard data on it. There's no question at all that Lyme, Babesia, and Bartonella can all be transmitted in utero; a pregnant mother can give it to the fetus, sadly. When I have mothers who are being treated for these infections, we keep them on antibiotics throughout the pregnancy.
And they've done very well, and there's data on this, that women who are not on antibiotics do not do nearly as well, and the kids do not do as well, and they have more miscarriages. So all those bugs can be transmitted that way. The really big question is can sexual relations result in transmission. As you know, Syphilis is a spirochete, Lyme is a spirochete.
Syphilis is sexually transmitted, can Lyme be sexually transmitted. There's almost like two camps on this one; some say yes, some say no. I have to tell you, in seeing no one but tick-borne infections for 20 years, I've yet to see a case where I'm convinced there was sexual transmission. But of course, people are living in the same environments; they have similar exposures.
So how do we say they got it from sex versus they got it because they also had a tick attachment. And yes, I'm very aware of studies where they have shown spirochetes in vaginal secretions, as well as in semen of infected patients. It still doesn't prove it can be transmitted. I don't know; there are three animal studies that I'm aware of; two of them suggested it can be sexually transmitted.
One did not find any. This is still a gray area. I do know doctors who believe that spouses should be treated to prevent a Ping-Pong kind of back and forth transmission between married or sexually active couples; I have not done that. One thing that I've seen, and I know one other doctor who has mentioned this, is I've seen patients, spouses get tested who are asymptomatic, and they do have some Lyme antibodies.
I don't treat them; I don't. Actually, I don't treat asymptomatic people quite frankly, except in that prophylactic period that we were discussing before. And I certainly warn them, but it's unclear to me that they are actually going to come down with the clinical illness; I haven't seen it yet.
[00:31:26.08] Scott: My observation has been that oftentimes the asymptomatic partner is the one that has the more clearly positive test results, and my thought process is maybe that's an indication that their immune system is responding in a healthy way. So it's interesting that you also see the positives in the asymptomatic partners in many cases.
In Lyme disease complex, how much of the disease presentation is the bug versus the host response to the bug in terms of inflammation, mast cell activation, histamine, autoimmunity. Do we want to focus on eradicating, if that's even possible, or killing the bug? Or do we want to focus on creating immune tolerance and integration within our microbiome?
[00:32:13.00] Dr. Kinderlehrer: The answer to your either-or question is yes. So what I mean by that is it's all of the above. Just so to give your listeners an idea more precisely what we're talking about. I often use the example of Rheumatic fever. So what happens is a kid gets a strep throat, antibodies to the strep, then attack heart valves because there's some sort of structural cellular similarity between the strep and the heart valves.
So what is that? Well, it's an infection, you got strep, but it's also an autoimmune reaction. Our own immune system is now attacking our own cells in our heart. And that's Rheumatic fever. Well, this is what happens with Lyme and Babesia and Bartonella; these bugs do not attack hardware, they're not invading and destroying cells the way a strep throat or a wound infection is, and then you get all sorts of local inflammation. What they're doing is attacking software. And as you're suggesting, now we have dysregulation of the immune system, nervous system, and the endocrine system and then all sorts of other organ dysfunction that's downstream from there.
I think we do all of the above, but we do it carefully because systems become so over-sensitized that we try to knock the bugs down, and I don't know how often we actually eradicate these bugs from our bodies. I do have patients who've been off treatment for years and doing just fine. I still can't prove that the bugs aren't there.
And I do a whole lot of treatment to try to decrease these autoimmune responses, as well as the dysregulation associated with them. This discussion actually goes back to the late 1800s, when Louis Pasteur, he's considered the father of the germ theory. But the somewhat apocryphal story is when he went to this French academy of science he had, he had two birds, and one of them was quite healthy, and the other one was quite dead.
And he said he had; I think he had given both of them anthrax. But one of them was poorly fed and kept in a cold environment, and the other one was well fed and nourished, and you could see the difference, right? He said it's not the bug, it's the terrain. There's no question we've got to be working on the terrain, and that's got to be a huge focus.
And to the degree we're able to, I really try to knock the bugs down. And so what can I say, a pincer kind of movement to try to deal with all of that. But it's very clear that just trying to knock the bug down doesn't work in so many of our patients, particularly ones who've been sicker longer. If we get people within the first year, they often don't have all this disruption.
But really, by the end of the year going on to decades, which as you know we see people have been sick for decades undiagnosed, they tend to have all sorts of systemic inflammatory problems. I've been particularly interested in, as you know, I've just actually had a couple of articles published on PANS, Pediatric Autoimmune Neuropsychiatric Syndrome.
I've actually, in the second article, I actually made a case that I really think we should rename this as microbial induced autoimmune neuropsychiatric syndrome because it's not just pediatric, and it's not just acute onset. And it's really common. I think that if we were doing Cunningham panels looking at those anti-neuronal antibodies and our patients with psychiatric Lyme disease, we'd find a lot of positives. These are autoimmune reactions causing a brain on fire, causing severe psychiatric symptoms.
And we've got to do everything we can to decrease that inflammation. And part of that is knocking the bugs down to the extent that we're able to, without increasing inflammation by hurting people. And the other part is trying to stabilize what's going on in terms of the immune system.
[00:36:46.27] Scott: Yes. And I know I personally had a positive Cunningham panel when I had a significant mold exposure as well. So I think there's so many things that can trigger these immune dysregulations.
When we consider anxiety, depression, rage, OCD, I generally think of Bartonella. I know some people also think of Babesia. What are the common microbial issues that you find that lead to neuropsychiatric symptoms?
[00:37:15.20] Dr. Kinderlehrer: Well, I agree with you. The first bug that gets indicted is Bartonella, it's huge. Very interesting, I don't know if you saw it, but Ed Breitschwerdt and colleagues, as you know, he's maybe the foremost Bartonella expert in the country. He and his colleagues had a paper come out just this past December.
They described 29 people who developed positive Bartonella testing, either serology or PCR testing, 24 of them develop neuropsychiatric symptoms, at the same time, they develop skin rashes. But their skin rashes are with mainly the Bartonella striae, and you can Google this and, you'll see the pictures of the striae; I mean, it's really impressive pictures of like 24 patients.
So Bartonella huge, and it's associated, as you suggested, anxiety, panic attacks, depression, suicide, irritability, anger, rage attacks. But even psychosis and bipolar disorder and depersonalization and personality disorders. Yes, Bartonella is awful that way. And I would say Babesia, which is interesting. But there's no really solid documentation in the literature that Babesia causes neuropsych symptoms. I've looked hard, and it's included; when you look at articles say by Bob Bransfield and also by Brian Fallon, they'll include Babesia as causing neuropsychic symptoms.
But when you look for case histories and any hard data on it, it actually isn't there. The closest it comes, Amy Cross and Craig Shimasaki and our beloved Dr. Jones and an immunologist, they had a paper come out, it was last month, I think. In which they described the case of a girl who started with strep and then developed a PANS-like syndrome.
And when she was tested, it turned out she had Lyme, and she also had Babesia. And so she had three infections, she had strep, Lyme, and Babesia. And they made mention in that article, and of course, she also had a positive Cunningham panel. They said the single drug that seemed to make the most difference was Clindamycin, isn't that interesting? Because, as you know, Clindamycin is mainly hitting the Babesia.
And so it implies that Babesia may be able to trigger PANS as well, it's certainly not hard; there were multiple microbes involved. So Babesia, I can tell you from personal experience; I can tell you from my clinical experience. Even if I can't back it up in the medical literature, can cause an awful lot of anxiety and depression; it certainly did in me.
And then I think a not uncommon cause of PANS type syndromes is Mycoplasma. I see a lot of like elevated Mycoplasma titers, I mean really elevated, not past infections, not old infections with a mild elevation in IgG, but levels in the thousands of IgM and IgG. I see it more in the younger age; I see it occasionally in older people.
Mycoplasma is a common respiratory infection, but it can also be tick-borne, and it can cause serious systemic inflammation. Vasculitis, all sorts of neurological problems. So those are the three bugs I'm most associated with, but certainly, Lyme can cause some of these things by itself, it's very hard to separate. Most papers, most studies, and case series on Lyme disease, they don't dissect out the role of co-infections. And as you know, the testing for co-infections isn't very good, so it's hard to do.
[00:41:33.05] Scott: Plus, as you pointed out, who has just Borrelia, probably not very many people, right? There's always some co-infections that are part of that puzzle as well. One of the things that I liked in the book was how you talked about the cranial nerves. And I don't hear people talking a lot about the cranial nerves. You talk about the seventh cranial nerve, or the facial nerve being impacted in Bell's palsy.
The eighth or vestibulocochlear, playing a role in tinnitus and vertigo. Both very common in the Lyme community. The tenth being the vagus nerve that can lead to all kinds of issues with swallowing, heart palpitations, can be involved in SIBO. Are there interventions that are aimed at improving the health of the cranial nerves? While we're working to reduce microbial burden?
[00:42:23.17] Dr. Kinderlehrer: You know it's a good question, it's a very good question. I would say that my attitude around treating that is really not much different from treating peripheral neuropathies. Where people get all sorts of stabbing and sharp and burning and electric type pains, as well as numbness and tingling and even paresis or weakness. These are all neuropathies; just one is cranial neuropathy, the others are peripheral neuropathies. There are things that we can do that can help the health of our nerves. More recently, when I said recently, I mean in the past year or so, I've been using high doses of melatonin.
And sometimes that can make a profound difference. But also, alpha lipoic acid can be very helpful. Antioxidants and high doses of B12. We sometimes give really high doses of B12 injections, it's good to know that you can't overdose on B12. Jonathan Wright, who was a mentor to me about 50 years ago, he said the only way you can overdose on B12 is you if you fill up a bathtub with it, and then you drown in it.
So it's really hard; we give very high doses, particularly methylcobalamin that sometimes can really help with neuropathy. And we're going to treat the bugs as aggressively as we can. You mentioned some of the eighth auditory nerves; some people get hearing loss from Lyme disease.
[00:44:02.24] Scott: It's interesting that the methyl B12 is well-tolerated because my observation has been that consistent use of high doses of methyl B12 can overstimulate methylation and trigger the activation of viruses and detoxification that people are not ready for. So I mean do you see that in some people, that there's a time when they're not ready for the methyl donors?
[00:44:27.00] Dr. Kinderlehrer: Yes. When I see patients who have some significant mutations in the methylation pathway, we go very slowly in terms of adding the cofactor nutrients, as well as adding the 5-methyltetrahydrofolate, because of the MTHFR mutations.
There are some patients who, if I gave them something like Thorne Methyl Guard, which has activated B vitamins and some betaine and other nutrients to facilitate a few different enzymes in the methylation pathway.
They have what feels like a Herx, and I think it's for the reason you said that suddenly the metabolites, which are toxins in the cell, are being metabolized. And now put into the bloodstream, and it's faster than our bodies can excrete them. So I will go slowly with replacing these, depending on how fragile I see the patient.
[00:45:32.09] Scott: This next question I'm excited to get your thoughts on, and that is the connection between altitude and people with Lyme disease. And in polling people over the years, I've seen half the people they say they do better at high altitude or high elevation, half say they do worse.
I've seen some people that have actually suggested that their patients go too high altitude, and that can lead to reductions in C4A, for example. So what are your thoughts in these Lyme complex patients? Is altitude a good thing or a bad thing?
[00:46:05.11] Dr. Kinderlehrer: That's interesting because we should be talking about altitude and attitude both, right? It's interesting; I don't have the same experience you do with some exceptions. First of all, I'm living at five thousand two hundred and eighty feet in the mile-high city, right? Before this, I lived in Santa Fe, which was seventy-five hundred feet.
I have many patients who say when they go to sea level, they go to Arizona, or they go to the east or west coast, they feel much better. On the other hand, traveling there can be a problem. If they're spending more than a few hours in a plane, the oxygen saturation is kept equivalent of around 8,000 feet of altitude.
So I have patients here in the Denver area, Boulder area where about 5,000. If they go up to Vail or Aspen and get up to eight, nine thousand or go on in the mountains, which can be twelve to fourteen thousand. They tell me that they crash, and the reason for this is that the Lyme bacteria prefer low oxygen environments.
It's a facultative anaerobe, which is just a fancy way of saying they prefer not to get oxygen, which is one of the reasons why people get some benefits from hyperbaric oxygen, which forces really high levels of oxygen into the cells. So at these low oxygen environments, the Lyme bacteria come out and party. And I have a couple of patients that you've described, who say I feel better at altitude, and I don't have an explanation for it.
I'm wondering if that has something to do with how the co-infections feel about lower oxygen. I don't know; I don't know the answer to that. All I can say is in my clinical experience; I see many more people not dealing well by going to higher altitudes.
[00:48:07.01] Scott: We talked in great detail in episode 111 about the promise of Disulfiram in Lyme disease, particularly for Borrelia, possibly for Babesia. Some people have done incredibly well, others not so much; others maybe have some side effects, particularly when self-treating or being too aggressive. Just briefly, what are some updates that you can share with us since we had that in-depth conversation on the use of Disulfiram in your patients?
[00:48:36.12] Dr. Kinderlehrer: Yes, thanks for asking that, because things evolve, right? And that discussion was just a bit over a year ago. It was really into the first year of our using the Disulfiram in more patients. Dr. Liegner, I think in 2018 had started, but most of us in 2019, I started in early 2019 on the basis of just conversations with Dr. Liegner recommending the Disulfiram.
And it turns out to be a somewhat thorny issue, it's a combination of, this has been a breakthrough drug for some people, they've done really well. And there are a lot of people that don't tolerate it at all, that is the Herx on the lowest doses; they even can develop neuropathy on the lowest doses. And then there are people in the middle.
So Dr. Liegner, as you know, he actually had an article published; it was probably I don't know, maybe a month or two ago. He sent it to me and about his first 70 patients where he had these really good outcomes. And when I asked him about the outcomes and the side effects, it was clear to me that he actually has a different patient population than I do.
He was not seeing Herx's reactions at taking 31.25 an eighth of a pill every three days. He wasn't seeing that. I was seeing that on even lower doses. He was not seeing neuropathy at these low doses; I was seeing that. And I just appreciated that okay, we do attract different populations of patients, and I happen to attract a very sensitive population.
And these sensitive people are also going to have more detoxification issues. So it's interesting; one of the things I've found, though, is that I've had people start on the low dose and do very well. I mean, ridiculously well. I wrote an article; I think it was posted in November on the Lymedisease.org website. In which this patient of mine, who she'd had Lyme for 20 years and she'd been treating on and off. She generally responded to treatment, but never a hundred percent.
And when she came to me, we started her back on antibiotics, and she was having trouble with the antibiotics, and I said, well, let's try the Disulfiram. Well, on an eighth of a tablet every three days, she did better than when she was on the antibiotics. In fact, she's pretty much asymptomatic. And I said we're not going to increase this dose, we're just going to leave you on this dose, and at some point, we'll take you off of it, but this is great. I have a patient; oh, by the way, if we tried to increase it from an eighth of a tablet every three days to every two days, she would hurt.
We just kept her on every three days. I had a similar patient who is on a 16th of a tablet, that's like 15 plus milligrams every three days, the same story, she's doing very well. And if she tries to go to every two days, big problem. So I've had some patients as we're increasing the dose, they're doing well, they're doing well.
And then I have these people check in every two weeks, and I say okay, we're going to add one-eighth of a tablet every three days, and they crash. I mean, as a physician, the last thing you want to do is give something that's going to harm the patient. I've become somewhat gun shy because of that. So if I'm seeing a positive response like these two women I just mentioned, I'm going to stop increasing the dose right there. And say we're just going to leave you on this for quite a while.
It's interesting Dr. Jayakumar Rajadas, the Stanford investigator who pretty much put Disulfiram on the map. He initially said he thought that Disulfiram was anti-inflammatory. But when I spoke to him later on, he agreed that no, it probably can increase inflammation. And I've seen that in patients; I've seen it make mast cell issues much worse in some patients.
So when I put people on Disulfiram, I do it very cautiously. And I have people take a lot of support for the liver, for the nerves. And very strict diets and very strict warnings of symptoms that could happen. They have to check in every two weeks. And if we get to a dose where they say I'm feeling really good, I don't even increase it anymore; I don't try to get to that so-called target dose of four to five milligrams per kilogram and leave them on that for eight to ten weeks.
Which was the original schedule that Dr. Liegner has been using. I think we just have to do what we've always done, which is treat every patient as an individual and be careful.
[00:53:44.19] Scott: I want to jump into some more conversation around Borrelia, Bartonella, and Babesia. And I kind of want to do this as a little bit of a rapid-fire around, asking you about the top three or four may be symptoms of each one.
Your favorite lab test and the top few treatments that come to mind as being the most exciting or the most helpful for you. So let's start with talking about Borrelia, what are some of the top symptoms that come to your mind when you hear Borrelia?
[00:54:14.19] Dr. Kinderlehrer: You know that's actually the hardest for me, because as we were talking about before, when do I see Borrelia without co-infections. I only see it in acute Lyme patient. I saw maybe three people last year with acute Lyme, relatively acute Lyme disease. Of which two of them had significant co-infections.
So how often do I see this? I can tell you that I associate it with, Borrelia with fatigue, with muscle aches, with joint pains. And I associate all of them with those symptoms, as well as headaches and impaired cognition, and some mood issues. So that would be like where the Venn diagram overlaps, but then like if we went to Bartonella as we were describing earlier if you see a predominance of neuropsychiatric symptoms.
But Bartonella is also known to cause a lot of eye problems, to cause a lot of gastrointestinal problems, and to cause what can be these skin problems, which can really basically slam dunk the diagnosis. But again, Bartonella can cause all those other symptoms where the Venn diagrams overlap with the muscle aches and the joint pains and the headaches, and the impaired cognition.
With Babesia, we're particularly looking for sweats, particularly night sweats. I should mention that Bartonella tends to cause day sweats, Babesia night sweats. Babesia tends to cause this air hunger problem, which we're also seeing in COVID patients, right? And what else? Migraine headaches, a lot of headaches, and neck pain.
And anxiety, for sure, I'm also, again, have to add in the fatigue and all of that stuff that's in the center of the Venn diagram. So it can be hard just to separate out exactly what's causing what, but sometimes we do it on the basis of the Herx's reaction to a given intervention.
[00:56:28.06] Scott: Favorite test for Borrelia?
[00:56:30.20] Dr. Kinderlehrer: My favorite test would be the Lyme Immunoblot, which is done by a few labs. I have the closest relationship with IGeneX. It's interesting by mistake. I had a patient tested with both the standard Western blot and the Immunoblot, and the standard Western blot was negative, and the Immunoblot was positive.
In other words, it's worth paying the extra 200 bucks because what you're testing for is Borrelia burgdorferi sensu latu versus sensu stricto, which I hate to get that technical, but the one test for just the very one strain of Borrelia burgdorferi. And the other one tests for like eight of them, that can also cause a Lyme disease.
[00:57:16.14] Scott: Yes. And I think the other thing for people to know with the Immunoblot as well is not to forget the tick-borne relapsing fevers. And it is a separate Immunoblot from IGeneX. So if you're ordering just a Lyme Immunoblot, and you're dealing with tick-borne relapsing fever, which in California is as prevalent or more than Lyme Borrelia, you could still have a false Lyme Immunoblot and still be dealing with a Borrelia that may present similarly, may respond to treatment similarly. But you may not be getting the right test.
[00:57:47.28] Dr. Kinderlehrer: Very good point. So we're mainly talking about Borrelia miyamotoi, and it generally does not cause the rash. But otherwise can look exactly like Lyme disease in terms of how it clinically manifests, and you're not going to get a positive Lyme test; you have to actually test for tick-borne relapsing fever.
[00:58:11.16] Scott: Favorite tests for Bartonella?
[00:58:13.20] Dr. Kinderlehrer: That's a good one. I've been getting; I'm going to end up stepping on some toes here, I apologize. But I've been getting the best results from IGeneX, where they have a Western blot, and they look at four different species. Now I know that Galaxy Lab; while they do a whole cohort of different tests, their specialty is Bartonella. They will do serological, i.e., antibody testing to Bartonella henselae and Bartonella quintana.
This is what standard labs do anyway. But then they have this specialized medium where they grow the bugs and then do PCR testing on that. I have not been getting many positives that way. And I've talked to a colleague of mine I won't name who said he's not been impressed either, even though they consider it the gold standard. The truth is, with Bartonella, even with the improved testing at IGeneX, I still mostly depend on my clinical diagnosis.
[00:59:22.27] Scott: And favorite tests for Babesia?
[00:59:26.17] Dr. Kinderlehrer: Okay. Well, if it's acute Babesia, I'm going to look for probably not fine, but evidence of hemolysis. This is when blood cells break up. And you can find that in the blood; you can find that in the urine, in terms of really trying to nail it.
Mostly, I'm going to be looking for both Babesia microti and Babesia duncani, and some people have both. And I'm using standard antibody tests for those. Again, I tend to use IGeneX if people can afford it. And Medicare, it's important that people know that IGeneX accepts Medicare. So I use it a lot then.
[01:00:05.27] Scott: Let's talk about a few of the treatments that are exciting you the most; I know we could do a whole podcast on each one. But when we talk about Borrelia, what are you seeing right now that's the most clinically helpful for your patients?
[01:00:17.18] Dr. Kinderlehrer: It's interesting because Lyme has generally been the easiest to treat of these; that is, the co-infections are much more stubborn and often causing more serious illness. Whereas, the initial attitude that I had, and I know many of my colleagues had, was well, let's go after this one that's causing the most symptoms be it the Babesia or Bartonella or whatever.
I can tell you that my attitude is has changed to let's go after low-hanging fruit. That is, if we can knock down the Borrelia, it's going to be easier to treat the Babesia and the Bartonella. Because these bugs somehow really do help each other out in terms of inflammatory responses.
So I use combinations of antibiotics, pharmaceutical antibiotics, and botanical antimicrobials; depending on whether or not I think the person is fragile or not fragile, I will start with pharmaceutical antibiotics. And I always start everything one at a time; I always stagger the onset of any of these interventions to see are they tolerating it. If they're Herxing, I want to be careful with that. I certainly don't want people to be Herxing on two things at once, and I never start on a full dose. I always have people start on a half dose or even a quarter dose, depending on how fragile I see.
So for Borrelia, I might give them something like a macrolide and a cephalosporin, or if not a cephalosporin, I might give them penicillin or Augmentin or even Amoxicillin in kids. That's the combination I most often use for Borrelia. I might add hydroxychloroquine, which actually increases the effectiveness of the intracellular antibiotics, which are the macrolides and the doxycycline.
I already mentioned I don't use doxycycline that much, even though it is the best drug if people have Ehrlichia or Rickettsia infections. And then what I do is try to transition people onto herbals. So I might add Samento and Banderol, which, as you know, there have been studies that suggest it hits Lyme even in the cyst form, and it hits biofilms, and it's hitting the spirochetal form. Our pal Dr. Eva has shown this stuff at University of Hartford.
And meanwhile, the Banderol is also going to hit Bartonella. So this is what it might look like. I start people on, say Amoxicillin, and they start on half dose, and after another week, if that's fine, they go to full dose. If they're still fine, start on a half dose of Zithromax or Biaxin a half dose, another week full dose, okay now we've got a pretty good program for the Lyme. As you know, we're hitting the co-infections but not very well with those.
There is some activity against both Babesia. Well, not just both, the Babesia, Bartonella, and Mycoplasma, we're heading to some degree but frankly not very well. The next step is I'll start to go after the next co-infection that I think is causing the least problems. More often than not, Bartonella is the last thing I try to hit. Particularly because it's usually, usually when Bartonella is there, it's causing the most problems.
And I leave that to last because I really think if we lower the temperature by knocking these other bugs down, we'll have better luck and be able to deal or not have to deal with as much inflammation caused by trying to knock off the Bartonella. I think the Bartonella causes more immune dysregulation, more autoimmunity than any of these bugs.
There's at least a dozen different well-established autoimmune conditions associated with Bartonella, everything from colitis to Hashimoto's thyroiditis, and I published a paper a year ago on primary sclerosing cholangitis and Bartonella. And like I said, there's and different juvenile rheumatoid arthritis. I mean, Bartonella is associated with so many autoimmune conditions, and when we try to treat it, oh my god, the inflammation can be terrible.
Sometimes I'm looking for the weakest thing to treat them with. So that's the sequence I use. But then getting onto the other bugs, I use a lot of Malarone. Which as you know, is a combination of Atovaquone and Proguanil, so it's two anti-malarial, starting on low doses, working up to an average of two tablets twice a day in an adult.
But I'll also use Mepron, which is just straight Atovaquone, and often it has to do with which one's covered by the patient's insurance. But there are other anti-malarial, and certainly, if there's anything nice you can say about Babesia, is that we do have a lot of things to treat it with. So we have in terms of drugs, Krintafel is getting more attention.
And Lariam, which I don't use because there are some patients who have awful psychiatric reactions to that drug. And among the herbal antimicrobials, we have a whole bunch. Artemisinin was first and foremost, and then we have Mimosa pudica, which is an Asian herb anti-malarial. We have Cryptolepis, which is an African anti-malarial and Sida acuta and so on.
So it's great to have that many options and see what people tolerate, and usually, we can find some combination. And then going on to Bartonella, I use a lot of Bactrim, which is sulfamethoxazole-trimethoprim. This is a very common antibiotic used for urinary tract infections, also used to treat sinus infections and MRSA, methicillin-resistant staph.
One thing to be aware of is that it probably causes more allergic reactions than any of the other antibiotics we use. People allergic to sulfur drugs, you don't use Bactrim. I just had a patient develop Stevens-Johnson syndrome; this is a very serious condition. It could be the first time in my career I've seen Stevens-Johnson syndrome, after taking like two days of Bactrim.
So thank god he's okay after I tufted it out with the dermatologist on putting him on prednisone, but he is doing okay. So Bactrim is a very decent drug, Rifampin is a very good drug. The issue with Rifampin is that it stimulates the cytochrome system, which in turn metabolizes a lot of other drugs, including, for example, Atovaquone. So levels of those drugs are going to go down, levels of thyroid will go down. Levels of hydrocortisone will go down if you give people Rifampin.
So you have to adjust a lot of things. Other medications might have to be adjusted too, and so that's an issue with Rifampin. There are things that have the opposite effect on the cytochrome system, so that includes grapefruit, grapefruit seed extract. It's interesting Biaxin has the opposite effect, also silymarin or milk thistle. So there's a handful of things we can give that try to balance it out, but we don't really have a way of measuring it, and Rifampin's very strong that way.
Probably the best drug in terms of treating Bartonella and mycoplasma are the fluoroquinolones. So this is Cipro, Levaquin, Avelox. Well, and they also have the worst side effects, and what's more problematic than just having side effects is there are some side effects that don't necessarily go away when you stop the drug. So it's one thing to get a side effect; you say okay, stop the drug, and you're okay.
But the one that's best-documented is patients can develop chronic tendonitis, and some have even gone on to tendon rupture, which is not fun. You know that's a big surgical problem and debilitating. So if I'm going to use a fluoroquinolone, I might use it in someone who has a history of taking it for who knows what, for prostatitis or whatever.
And they say oh, I was fine on it and I said, oh good, we can go there. But if they don't have a history and they've sort of failed on everything else, or just haven't done that well on everything else. Then I will say, okay, the first thing we're going to do is load you up with magnesium, which can help protect the tendons. So I have them take as much magnesium as I can without getting diarrhea. And then, they start the fluoroquinolone.
And I tell them here are the symptoms you got to watch out for, inflammation in your achilles or around your knee or your elbow or even your neck, anything like that, stop the drug immediately. I think our patients with Lyme are more likely to develop those problems.
These drugs are prescribed all the time out there in the community. It's the most commonly used drugs for community-acquired pneumonia, but also urinary tract infections and sinusitis, and so on. These drugs are used all the time, and people don't seem to be getting into nearly as much problems as the patients with Lyme disease.
[01:10:22.18] Scott: So what you're referring to here is what people commonly hear of as “floxing” from fluoroquinolones. That is also a topic that I'd love to do a deep dive in a future podcast. I've reached out to some doctors that specialize in it, but if anyone has any suggestions, I'd love to hear that.
One of the tools that you talked about for Babesia was Mimosa pudica, which was interesting because I historically have heard of that more as a gastrointestinal parasite focus tool. I did not understand that it had any real systemic effect. And so I'm wondering, is that the traditional Mimosa pudica in a capsule? Is that a liposomal? What type of Mimosa are you using that's helpful for systemic Babesia?
[01:11:04.19] Dr. Kinderlehrer: Okay. So Mimosa pudica is an Asian herb, and it is a traditional anti-malarial that has been used systemically. And as you know, virtually everything we use for Babesia is an anti-malarial drug. Okay, it's interesting; I'll come back to that in a second. I had this patient tell me a story; this goes back at least three years.
She had Lyme and Babesia; she was doing fairly well, she's probably like 80 percent, then she comes in tells me this story. She'd had GI problems, and when we took gluten out of her diet, she was much better, and so I wasn't thinking too much about what was going on in her gut. But he had been online and seen who knows what online, and she decided to put herself on Mimosa pudica seed.
And this was a nurse, by the way, she said I passed tapeworms, an unbelievable amount of stuff, and then I can't tell you how much better I feel. I mean, my energy is like great now, and so on; she was now 120%. And I was like amazed. And I called up the people who make mimosa pudica seed, and I said explain to me what's the difference between this and Mimosa pudica, which I've been using to treat Babesia.
And they said okay, the Mimosa pudica to treat obesity is from the leaves and the stems, and this is from the seeds. Well, since then, so I use Mimosa pudica seed for Babesia a lot, it's often better tolerated than a lot of the other herbs that we use. As you know, everybody's different; we go with whatever works. But when I have people with ongoing systemic issues, and we feel like we've covered all our bases.
Sometimes I'll say take this Mimosa pudica seed for a month and watch your stools. Over 50% of them come back and say I can't believe what came out of me. And they have these worms, rope worms, and tapeworms and all sorts of whatever coming out of them.
I'm gradually agreeing with your pal Dietrich Klinghardt that maybe most of us harbor parasites and worms, but they're not a problem until our immune system goes awry because of these bugs and mold and so on. And now they're causing a lot of inflammation.
[01:13:31.29] Scott: So, which of the Mimosa pudica seed products are you finding clinically helpful? Is that the Cellcore Biosciences / Microbe Formulas? Or are you using something else?
[01:13:41.14] Dr. Kinderlehrer: I've been using the Cellcore formula.
[01:13:43.22] Scott: Yes, beautiful, great products. Bartonella can cause a number of GI issues, I've often wondered if the reason that Rifaximin works so well in people with SIBO is that it's going after Bartonella. And I'm wondering if you have any thoughts on the connection potentially between Bartonella and SIBO?
[01:14:02.16] Dr. Kinderlehrer: Well, it's a good question. The answer, I don't know if Rifaximin hits Bartonella. As you suggested, Bartonella can cause tremendous number of gastrointestinal problems, and interesting can cause everything from gastroparesis in which people are so severely constipated that they're not able to move their bowels without some sort of heroic intervention to diarrhea, and then everything in between. It can cause colitis, and it can trigger Crohn's disease.
We most often associate it with so-called irritable bowel syndrome as if that was an entity, but it's just non-specific symptoms of diarrhea and or constipation, and abdominal cramps, and often nausea and bloating and gas, the things we associate with SIBO. I find that treating the SIBO doesn't work that well unless we treat the Bartonella first.
So I've had patients go on Rifaximin, which I agree has been a very good drug for SIBO. But not see much difference. And these are people who've had very positive tests, right? And go on Rifaximin for a month even and nothing. And I think as you know, there's so many other conditions that often are going on the same time as the SIBO, so these people often have fungal overgrowth besides the parasites and the helminths, which are worms.
And then the tick-borne infections, including Babesia and Lyme which can cause all these gut problems. These people often have hypochlorhydria; I see so many patients with low stomach acid. And sadly, if they see the gastroenterologist, they get put on a proton pump inhibitor, which couldn't be the worst thing to do because it's further decreasing their stomach acid.
And low stomach acid is a big risk factor for developing SIBO because one of the functions of the acid is to kill bugs before they get into the intestines, including killing parasites and other microbes. I just want to mention to the audience that the most common symptoms associated with low stomach acid are bloating, gas, constipation, belching, and early satiety, which is a fancy way of saying when they eat, the food tends to sit in the stomach and take a while to go down.
This is a slow gastric emptying, and it's typically worse if you have a big steak or some big chunk of protein because the hydrochloric acid is necessary to break that down into amino acids, so it can be assimilated. So I just want to mention that hydrochloric acid is something that really can be a big; low hydrochloric acid can be a big problem in the gastrointestinal complaints.
[01:17:03.22] Scott: Dysautonomia or dysregulation of the autonomic nervous system is common in Lyme, can be related to co-infections, resulting in symptoms like dizziness, POTS, neural mediated hypotension, lots of symptoms that can happen with this nervous system dysregulation.
What are some of the top tools that you found for addressing the autonomic nervous system dysautonomia? And is there a connection between dysautonomia and Mast Cell Activation Syndrome?
[01:17:35.12] Dr. Kinderlehrer: Okay. So just to explain to your audience, we're talking about dysautonomia is dysregulation of the autonomic nervous system, which we can think of as the automatic nervous system. Because we're not consciously saying well, here's where I want to send blood, and here's what I want to get activated, here's what I want to put to rest.
So we have this nervous system that's telling our heart how fast to beat, it's telling our lungs how fast to breathe, and so on. And there's two arms, there's the sympathetic arm, which is mainly the accelerator, mainly stimulation, and this parasympathetic, which is mainly calming, it's the opposite as far as the GI tract goes. But mainly, the parasympathetic is calming; mainly, it's good to be in parasympathetic mode.
So we have an accelerator and a break; the whole point is to keep us in homeostasis. Dysautonomia is when we're no longer in homeostasis, it's doing this. And that's when you see the changes that you've mentioned. We see fluctuations in blood pressure fluctuations and pulse. POTS which is postural orthostatic tachycardia syndrome, is when you stand up, and suddenly your pulse goes from 80 to 120 or worse.
Neural mediated hypotension as you stand up and your blood pressure drops from 120 to 80 or 60, and you feel like you want to pass out or you do pass out. I have patients who really had to do that, really have passed out from standing up. And of course, those can occur simultaneously; the high pulse and the low blood pressure can be occurring in the same patient.
But there are a lot of other symptoms besides getting light-headed and dizzy; people can get anxiety and short of breath and even gastrointestinal symptoms and so on. There's a long list of symptoms associated with dysautonomia. But the ones that are most evident are the ones you've mentioned, particularly palpitations and lightheadedness.
And people often think, oh my god, there's something wrong with my heart, and actually there isn't, the heart's just responding to an abnormal stimulation. As far as POTS goes, and again these are people whose pulse rises; when they stand up, Midodrine is really the drug of choice.
And it works fairly well; it can raise blood pressure which often is a good thing, but there are some people where you don't want to raise their blood pressure, so you have to be careful about that. In some people, we give them beta-blockers. But we can only give them beta-blockers which slows the pulse if they don't have any problems with low blood pressure.
We have to be careful with that side effects of the beta-blockers. Meanwhile, we have to teach these people also don't get up suddenly, particularly at night, people wake up. Oh, I got to pee; they stand up and crash; it can be dangerous. So the low blood pressure, there are things we can do to help with that. One of them is have people take electrolytes with their fluids so that there you go; it's going to help maintain more volume in the blood to keep their blood pressure up.
Compression stockings, so the blood isn't pooling in the lower limbs, can help maintain blood pressure. Licorice root capsules, which decreases the breakdown of angiotensin. So now we have higher sodium-potassium levels, which will also increase intravascular volume, maintain blood pressure. And then there are drugs; the main drug we use is Fludrocortisone or Florinef, just 0.1 to 0.2 milligrams a day is often very helpful for those patients.
But I'll mention that something that can make those problems worse is if people have diabetes insipidus. So that's a condition where their pituitary gland is not releasing adequate amounts of antidiuretic hormone, which manifests as if they're taking a diuretic, right? It's a double negative; no antidiuretic hormone is like taking a diuretic.
So they're peeing all the time, and then they're drinking to make up for it. But they can't really keep up, so they're always dehydrated. That's going to make these problems much worse. I should also point out that they're going to become electrolyte depleted too, because usually they're replacing water, they're replacing the urine with water. But remember, the urine has electrolytes in it, but they're only replacing the water.
So these people need to also be taking lots of electrolytes. And then there are things we can do like pituitary glandular and desmopressin, which is a hormone drug to replace that. Oh, and then you asked something I learned fairly early from a patient of mine who had fairly significant dysautonomia was that there can be this histaminic reaction associated with it.
So that comes back to the Mast Cell Activation Syndrome. And I think mast cells are a great example of how everything is connected. I mean, you have nerves right up against the mast cells, and then you have the mast cells affecting nerves, affecting the hormones.
It's like everything is working together there, and of course, we don't really have separate systems; it's not like we have a separate immune system and separate endocrine systems; separate nerve systems and the mast cells are a great indicator of just that. These things are all impacting each other. And yes, we do see mast cell deregulation in association with dysautonomia, and then that adds to the symptoms that we see with dysautonomia.
[01:23:27.12] Scott: Let's dig a little deeper then into the. We know it's a significant contributor to the inflammation that many people experience to that immune dysregulation that we talked about. And what are some of the top tools that are helping your patients in dealing with Mast Cell Activation Syndrome?
[01:23:44.21] Dr. Kinderlehrer: This has become a really big issue. And again, one has to wonder did this exist before the past decade or two. Were doctors missing it that whole time? Or have we just become more inflamed, and now it's manifesting in yet another way? I'm suspecting that it's more the latter because we are seeing so much more inflammation and autoimmune issues in our general population. It's not just Lyme disease.
So mast cells are these very primitive white cells, and they contain almost 200 mediators, inflammatory mediators. Some of them are anti-inflammatory, but a lot of inflammatory mediators. And when they get triggered, and they can get triggered by any number of issues, we just mentioned dysautonomia, but guess what? Borrelia can trigger these things. Insect bites, colds, anything that can cause an allergy can trigger these things.
And then they release their contents; the process is called degranulation. And the substance that that's most well-known, of course, is histamine, and then we can see histamine reactions. But we can see other reactions associated with these inflammatory mediators; things like leukotrienes are much more, I mean decibels more inflammatory than histamine is.
But this is also how people get severe hives and even anaphylactic reactions, mast cell degranulation. So we try to work on it a number of ways. One is trying to stabilize the mast cell so it has a higher threshold before it's going to release its contents. And the ways we do that is with certain citrus bioflavonoids like quercetin and drugs like Cromolyn; it's also known as Gastrocrom, is its brand name.
Ketotifen is another drug that's available at compounding forms that can help stabilize the mast cells. And then we also give people antihistamines, and that's important as further down the line, and we give people diamine oxidase, which improves the metabolism of the histamine. But we also want to go to well, what's triggering this mast cell degranulation? That includes the bugs.
It includes all sorts of potential sensitizers. So some people with these mast cell degranulation issues, they have to be on very restrictive diets because some foods are much more likely to trigger mast cell degranulation than others. And the truth is I don't see many people who have the full-blown syndrome; these are people who are having hives and flushing and diarrhea and shortness of breath almost 24/7.
I've only seen that in really a couple of patients; most people more have some of those symptoms. And to the extent that we can decrease that reactivity, it really helps them symptomatically. I should mention we talked earlier about autoimmune encephalitis and particularly kids with PANS. Some of those kids do much better with medications like Gastrocrom. I've really seen huge, a huge response in some of those kids.
[01:27:29.01] Scott: You talk about mold in the book, and I'm wondering how commonly do you see mold as a primary issue in your patients? How commonly do you see it in your patients? Is it at times more significant than Lyme and co-infections? And then, beyond the implementation of binders, do you sometimes find the need to treat colonization of fungal organisms in your patients?
[01:27:52.24] Dr. Kinderlehrer: Yes, so all of the above. So we'll start with someone who I know you know, Joe Brewer he's an infectious disease doctor, and bless him; he recognizes and treats chronic Lyme. So his story is that he also has a population of patients who are diagnosed with Chronic Fatigue Syndrome.
And I asked him; I said, well, how do you distinguish Chronic Fatigue Syndrome from chronic Lyme because their symptoms are exactly the same? And by the way also look like post-COVID syndromes, right? And he said, well, if they didn't respond to Lyme treatment, then I simply call it Chronic Fatigue Syndrome.
Okay, so one of his patients with Chronic Fatigue Syndrome comes back with a mold toxin test done at RealTime Labs and shows it to him says, what do you think? He says I have no idea; I've never seen anything like this. I can tell you. Frankly, I've been an internist for more than 40 years up until a decade ago; I never heard about testing for mold toxins.
And most docs have never seen or heard of it. Okay, but Joe being the inquisitive mind he has, does a study. And he tests like a hundred people with Chronic Fatigue Syndrome, and he has like something like 50 controls. People with Chronic Fatigue Syndrome have a much higher levels of mold toxins than the controls.
So he starts talking to these people, and they give stories like, well, when I lived in Virginia, it was moldy there, and we really had a problem. But now I live in Kansas City, Missouri, and we have a really clean house; I really don't think I'm exposed to mold anymore. Well, Joe started thinking about this, and he came up with this idea that if they were exposed to mold, they could inhale it and even ingest it.
And now they have endogenous mold growth, and it's continuing to generate mold toxins because if they're getting rid of it in the urine, that's the test we did, it should have been gone by now if the exposure was ten years ago, unless they continue to be exposed, and if it's not an external exposure, it's an internal exposure. There's no question this is true; this flies in the face of what Ritchie Shoemaker claims. I understand that. But it's absolutely true, quick story about myself.
Which is that when I got Medicare, I decided to get myself tested. Hey, it's for free, why not? I had a really high level of mold toxins. I have no idea when I was exposed, but I did grow up in a 60-year-old house; probably that's where I was exposed. And so I started myself on binders, I was also doing saunas, and I was even doing an antifungal nasal spray.
Four months later, I tested myself; there was no change. I still had the same high level of mycotoxins. Then I put myself on Itraconazole, which is a systemic antifungal. After four months, it had gone down 50%. Another four months, another 50%. I mean to me, it was like we made the case here, that if you're going to treat mold toxins, certainly you have to make sure that the present environment is as clean. So this gets back to your original question, how often do I see problems? I see them a lot. I used to think of mold as well here's something we should look at if people aren't getting better; now I think about it the very first time I see a patient because it's just so commonly an issue.
And understand it's I think because they have Lyme, that they're more sensitive and toxic from the mold. That is, I see patients living in a moldy house, and they are sick from the mold. But they have all these family members who are living in the same old house, and they're not sick. So I think that the mold itself was not an initial problem, not the primary problem as you're suggesting. Now is that true 100% of the time? Probably not.
But I think more often there's been another insult, and then they've become really sensitive to mold. Unless they were, say, born with a very allergic tendency and started off from scratch. Or I should mention if they've had candida for a long time, which then makes them more sensitive to the ambient mold, and then they're going to have more problems both with mold sensitivity and potentially with the mold toxins.
I'll just mention for your audience that Fluconazole which is a great drug for Candida, does not work with this endogenous mold. Fluconazole is very good against yeast, which is a subset of mold or fungus. But it does not hit the larger spectrum of mold and fungi that we associate with indoor water damage molds, and those are the ones that generate the toxins that we're generally dealing with here.
I live in what's considered a dry state; I can't believe how many houses have mold problems here. It's really somewhat stunning; I think it has something to do with construction. Even when I lived in New Mexico, which is really dry, there were places all it takes is for the water to get trapped somewhere, like between walls or in the eaves or maybe under a kitchen cabinet, under a sink, and so on. Once it's trapped, you're going to get mold.
[01:33:26.19] Scott: You explore oxidative therapies like ozone, hyperbaric oxygen therapy, ultraviolet blood irradiation, hydrogen peroxide. I'm actually in the process of getting an EWOT or exercise with oxygen therapy system set up for myself. Which of these have you found helpful for your patients?
[01:33:47.24] Dr. Kinderlehrer: Okay. So basically, as you said, we're talking about oxidative therapies, which is not just oxygen; by the way, it has to do with electron transport. And they include just what you said hyperbaric oxygen, hydrogen peroxide intravenously, ultraviolet blood irradiation, and ozone which can be administered a whole bunch of different ways to cut to the chase.
I've seen the best results with combination of intravenous ozone and ultraviolet radiation. So what we're talking about is putting a relatively large bore needle into a vein, and then it looks like you're donating blood, okay. The blood's coming out; it goes through this UV chamber where it's getting the ultraviolet treatment, and then it's drawn up into a syringe.
The ozone gas is added to that. It immediately dissolves, so you're not like injecting a bubble of gas into someone goes back through the chamber and back into the arm. I mean the whole process; once the line is in, it takes well less than half an hour. And I've seen pretty good results with that; in fact, my youngest daughter it cured her.
Now when I say cured, I mean it's been at least 15 years since she was sick, and she did this for a year or so once or twice a week. She's great; I mean truly, if she has Lyme, you'd never know it, she's quite healthy.
So yes, and I've seen people get these other interventions, including hyperbaric oxygen and hydrogen peroxide, I have not seen as good results with those as I have with the combination of intravenous ozone and ultraviolet blood radiation.
[01:35:27.05] Scott: How important is the limbic system in recovering health? And do you use tools like Annie Hopper's DNRS or Ashok Gupta's the Gupta program to recalibrate or reboot the brain's alarm center? Kind of tying that back into your earlier comments about perception of safety in the world.
[01:35:46.26] Dr. Kinderlehrer: Really good question. So as you are pointing out, that limbic system is an alarm center; when a trigger happens way before our gray matter can interpret what's going on, our limbic system gets activated, and then we're in a flight or fight anxiety hyper-vigilant situation. And this causes a lot of distress in the body, we're in sympathetic mode instead of parasympathetic mode at that point.
And as you said, people who've experienced trauma have sensitive limbic systems; they get triggered very easily. And anything we can do to neutralize that really can have a profound impact on people's well-being. I do recommend Annie Hopper's program, and I do recommend Gupta's program to deal with that. There are now amazing things coming out with things like MDMA to treat post-traumatic stress disorder. They're also using psilocybin in both microdoses and in full-dose journeys and getting significant benefits.
So there's a whole world of things that I think may really help our patients with Lyme, because ultimately I want to know how can we retrain our immune systems to feel safety. So we're not so reactive whether it's reactive to people and events, or it's reactive to microbes or mold spores. A quick story, I don't know if you've ever heard of; I hope I remember the name correctly, Roswell Pennsylvania.
So the story is this, in 1960, investigators were very interested in this town in Eastern Pennsylvania, it's on the Delaware River. And they had a heart disease rate that was half the national average. So then, as in now, heart disease was the most common killer, at least pre-COVID. And here, they had half the national average.
And so they went in there, these investigators there was an epidemiologist and a sociologist, and I think they were expecting to see these vegetarian marathon runners. And instead, what they found was sedentary Italians eating lots of pizza and beer sitting on their porches. The story is that these families came across from the same town, Roswell, Italy when their quarries closed up, and they had to leave because there were no jobs.
And they came one at a time bringing their friends and even bringing their priest over. And they had a community that was almost like a wall around us, not that they kept people out but back then, people didn't move around like they do now, right? So they went from roughly 1900 to 1960 with a contained community where the emphasis was on the whole community and on the church, and doing things together.
And the investigators said these people they're not only not dying heart disease, they don't have ulcers, they don't have gallbladder problems, they don't have dementia, they're sort of just dying of old age, and they're happy. And the owner of the factory there lived next door to the people who worked for him, and there was none of this socioeconomic striations. And so my sense, because I've read about this a lot, I really thought about it.
My sense is that there was really incredible safety there. I had a personal experience, imagining what it was like to be there. And it was like I felt like I'm just this average guy, nothing great, nothing terrible. But I'm held and connected by this community. And I could feel inside me this tension leaving and this feeling of safety; it was palpable. And I don't think many of us get to experience that unless we've grown up in a real sense of community extended family, even just nuclear family, I don't think does it.
And so the question in my mind is how can we train our systems to experience that safety. And I think it takes place on all levels, so it's going to take place on the physical level where we do all these different interventions that you know well. But it's also going to mean dealing well on the emotional and energetic level, and processing trauma, and allowing whatever emotions there are, are there to flow to bring into consciousness our belief systems.
That if we grew up in a traumatic place, we might feel like the world is unsafe, or we might feel undeserving, or we might feel like we are weak and helpless. Another quick story, it was a bit over a year ago, there was a story that you may have heard about. It was in Fort Collins, Colorado, this guy's jogging outside of town, he gets attacked by a mountain lion, and he kills the mountain lion.
And I'm like, really? He did that. And he's interviewed, and he says, well, I got attacked by this mountain lion. And I remembered that I had cats when I was a kid, and if you put them on their back, they were sort of helpless. So I was able to get his claws off me and get him on his back, and I strangled him to death.
And I'm thinking like that belief system like okay, what do I need to do to deal with this, rather than I'm dead, I'm cooked, this mountain lion's going to maul me, and that's it. I was thinking like, wow, what did this dude grow up with that allowed him to experience that sense of empowerment, and then and then apply it. So it's going full circle here.
Whether it takes energetic interventions, emotional interventions, MDMA kind of interventions. Down to all the things we do to try to balance our physiology and knock bugs down that are triggering immune reactions or taking away foods or chemicals that are triggering reactions. And trying to facilitate all the detoxification channels we work on, I think it's all of the above.
[01:42:56.16] Scott: As we start to close our conversation, a couple of questions that maybe will help to summarize and bring it all together for people. When someone is recovered or asymptomatic, do you keep them on some type of maintenance antimicrobial protocol? If we can't fully eradicate these organisms, and that's my personal opinion, love to hear your thoughts.
But when we come to Borrelia and Bartonella and babesia, I personally don't feel like we eradicate them. How do we manage them long-term and reduce the potential for a return of symptoms?
[01:43:30.11] Dr. Kinderlehrer: I agree with you. I think it's not likely that we eradicate them, especially when we go to two or more co-infections. I would say that most of my patients, I keep on what one would consider long-term antimicrobial herbs.
So once they reach remission, I suggest let's just keep you on these herbs for at least a year, maybe longer, and we can check-in. And sometimes, the patients make decisions on their own. Some say I just really want to stay on these, it's insurance, and I'm doing so great; why rock the boat?
And other people say I'm tired of doing this, and I'm going to stop it. Thankfully, most of the patients have continued to do well. But I do see some patients who know some stuff starts to come back, and we got to intervene again.
[01:44:28.23] Scott: Our mutual friend Dr. Dietrich Klinghardt says the only way out is through. In the book, you use the quote, when you're going through hell, keep going. What can you say to give those that feel like they're in hell some hope to keep going?
[01:44:47.20] Dr. Kinderlehrer: Well, I think the biggest piece of data I can give them is 90% of my patients get anywhere from 80 to 100% better. And these are people who are really ill. I see patients who've been to other Lyme doctors, people who've been sick for years or decades. I've had patients who've been sick for 50 years without the diagnosis; I mean, it's really quite awful.
Most of them get better. And I think I embody that because I can tell I was in hell, and I was totally hopeless. And the only thing that stopped me from committing suicide was I have three daughters, who assured me that they would be upset if I did that even though it's hard for me to understand given how awful I felt.
And the other was I thought if I kill myself, it's really bad karma, and I'm going to have to come back and do this again, so let's get through it now. But I really was hopeless; I didn't know what to do, except to keep on telling myself that my perception of the world is if I'm looking through these glasses that are all muddled and dirty.
And I just have to hang in there to the point where my glasses can get clean, and now and well remind myself I used to be happy, I used to enjoy life. I use to feel gratitude and rewards and really enjoy things. And it was; I'd have to keep on reminding myself that there was life before I got sick that was really good. And that, therefore, it was possible to get back there.
And as you're suggesting, I think one of the biggest things I do for patients is give them hope, and part of that hope is based on my personal experience. And I think they get two things emotionally from when they come to see me the first time.
One is that I really care; I mean, it's important. I mean it's important to communicate that, and it's important that if you're not feeling it, you're in the wrong business. I mean, really, you need to care for what's going to happen to each patient. And the second is to give them hope like I really believe you're going to get better here and you're going to have to hang in there.
But be patient. And I think if they wouldn't bother to find me, as you know, I don't even have a website; people have to work to get to me. And the fact that they've ignored what their doctors have told them, the dozens of doctors they've already seen and then sought me out, they have some flicker of hope, to begin with.
[01:47:39.19] Scott: Well, we are grateful that you have hung out, grateful that you're so passionate about helping people. But also grateful that you have this new book “Recovery from Lyme, The Integrative Medicine Guide to the Diagnosis and Treatment of Tick-Borne Illness”. I'd love for you to show us the book, and tell us where people can find it.
[01:47:58.18] Dr. Kinderlehrer: The book is right here. This took about four years to write, but it was really a labor of love. And I'm hoping just to take all my experience from all my different trainings, and pass it on basically. And it's both for practitioners and for patients.
That is there's enough details, evidence-based stuff and like here's how you work this up and here's how you can address this issue. And it's written in leg language, so people can do a lot of this themselves or and or bring it to the attention of their physicians.
It is for sale really at every bookstore now. And if you can Google it on Amazon, there's lots of reviews from people like Dr. Burrascano and Dale Bredesen, people that you know for certain. I'm just really grateful that that's finally come to fruition.
[01:48:56.20] Scott: Yes, that's fantastic. My last question is the same for every guest, and that is what are some of the key things you do on a daily basis in support of your own health?
[01:49:05.10] Dr. Kinderlehrer: I try to get good sleep. I try to get outside as much as possible. I've always eaten well, that's never been an issue, I grew up eating well, and I never didn't. And I really try to follow my inner longing, inner drive, what feels right in the moment.
Like when I was writing the book, often I would finish work and see patients all day, and it's like I just want to get back to the computer and keep on writing that chapter. I'm really into it.
And more recently, I've been writing articles; I think you've seen a couple of them; actually just came out this week in the peer-reviewed literature, and I'm still working on others I'm working on. I sort of wait to see what I'm called to do in that moment.
The other big, huge thing in my life is I have three daughters and six grandkids, and I connect with them as much as possible. They're such a joy to me.
[01:50:10.00] Scott: This has been such a fantastic information-rich conversation. It is just the tip of the iceberg of the information that is in the book. So I urge people to get the book. It really just covers so many areas that we couldn't even begin to touch on today.
I appreciate that you took the four years to share your decades of wisdom and experience, and knowledge with all of us. And that you were so generous in your time today; I just want to thank you and honor you, Dr. Kinderlehrer.
[01:50:40.25] Dr. Kinderlehrer: It was really my pleasure. I really appreciate your offering this time and space to me and doing such a great job.
[01:50:48.12] Scott: Thank you so much.
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Disclaimer
The content of this show is for informational purposes only and is not intended to diagnose, treat, or cure any illness or medical condition. Nothing in today's discussion is meant to serve as medical advice or as information to facilitate self-treatment. As always, please discuss any potential health-related decisions with your own personal medical authority.