Chronic diseases make up the bulk of the problems that modern health care must address. Each condition seems to have its own drivers–cholesterol for heart disease, airway hyperreactivity for asthma, neurotransmitter imbalance for depression and other psychiatric disorders, a buildup of amyloid beta in the brain for Alzheimer disease. What if all these conditions had similar origins? Today we’ll consider the evidence suggesting that hidden infections may be driving many chronic diseases.
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You could listen to this conversation through your local public radio station or get the live stream at 7 am EST on Saturday, March 21, 2026, through your computer or smart phone (wunc.org). Here is a link so you can find which stations carry our broadcast. If you can’t listen to the broadcast, you may wish to hear the podcast later. You can subscribe through your favorite podcast provider, download the mp3 using the link at the bottom of the page, or listen to the stream on this post starting on March 23, 2026.
How You Can Watch our Interview with Nikki Schultek:
Here is the YouTube video podcast of our interview with Nikki. We think you will find it compelling. Treating the causes of chronic diseases instead of the symptoms makes sense to us.
How Could Hidden Infections Be Driving Chronic Disease? Nikki’s Story
We begin this episode with the personal account of Nikki Schultek. She is a patient who has transformed herself into a research leader after a horrendous experience with unexplained chronic disease. She was a healthy active young mother whose lifelong well-controlled asthma suddenly took a dramatic turn for the worse. She then developed atypical pneumonia, heart arrhythmia and interstitial cystitis, along with a slew of autoimmune conditions. All the doctors could tell her was that these were idiopathic conditions driven by inflammation. As she notes, “idiopathic” basically is doctor-speak for we don’t understand what is going on here. When she developed neurodegenerative symptoms that made her physician suspect MS, she was terrified.
That low point became a turning point. Her background had equipped her to read scientific studies, so she began trying to figure out what was driving chronic disease in her own situation. A search linking atypical pneumonia and interstitial cystitis led her to the clinician who was able to help her regain her health, Dr. Charles Stratton. He had conducted a small study linking both conditions to a respiratory infection caused by Chlamydia pneumoniae.
What Is Chlamydia pneumoniae?
When people hear “Chlamydia,” they think immediately of the sexually transmitted infection caused by Chlamydia trachomatis. Although the organisms are related, they have completely different modes of transmission. People catch C. pneumoniae (Noo-mo-knee-eye) simply by breathing in air that contains infectious respiratory particles.
These bacteria are extremely common, but it is difficult to detect an infection. That’s because C. pneumoniae hides out inside human cells. It doesn’t show up in blood tests or urine cultures. The study that caught Nikki’s eye used PCR, polymerase chain reaction, which detects DNA. That analysis revealed that 80 percent of the women in the study with interstitial cystitis had C. pneumoniae. The researchers concluded that this sneaky pathogen can lead to chronic inflammation.
The Link Between C. pneumoniae and Asthma
Remember that Nikki’s troubles started with a severe asthma exacerbation. Research has shown a link between that infection and hard-to-treat asthma (PLoS One, April 19, 2021). When Dr. Stratton tested Nikki, they discovered that she indeed harbored a C. pneumoniae infection. The treatment required multiple antibiotics over a prolonged period of time. Luckily, it eventually cleared the interstitial cystitis, the neurodegenerative symptoms, the other autoimmune problems and brought her asthma back under control.
Other Pathogens Causing Trouble
C. pneumoniae was not the only germ lurking in Nikki’s body. She discovered that she also carried Borrelia burgdorferi, the organism that causes Lyme disease. In addition, an examination of her red blood cells revealed both Babesia and Bartonella, possibly transmitted by the same tick bite that gave her the Lyme disease.
These experiences inspired Nikki to start the Intracell Research Group, the Pathobiome Research Center and the Alzheimer’s Pathobiome Initiative. All are aimed at discovering if hidden infections such as C. pneumoniae or Babesia or Borrelia burgdorferi could be driving chronic disease such as dementia.
More Research on Covert Pathogens Driving Chronic Disease
One of Nikki’s colleagues at the Alzheimer’s Pathobiome Initiative as well as at the Philadelphia College of Osteopathic Medicine is Dr. Brian Balin. He has spent more than 25 years studying the connections between C. pneumoniae infections and brain inflammation. This, in turn, has been linked to neuroinflammation and dementia.
Dr. Balin points out that respiratory pathogens like C. pneumoniae are accustomed to entering the body through the nose. The nose offers access not only to the respiratory tract, but also to the brain. However, it can be difficult to detect microbes in the brain while the patient remains alive. This has limited research on infection and cognitive impairment in the past (Alzheimer’s & Dementia, Nov. 2023).
The COVID pandemic poses another huge risk. Like C. pneumoniae, the SARS-CoV-2 virus often enters the body through the nose. From there, it has ready access to the brain (Frontiers in Aging Neuroscience, June 13, 2025). Further, when the immune cells called macrophages respond to these infections, they engulf the pathogen and may carry it throughout the body. Might long COVID be the latest example of unacknowledged infection driving chronic disease?
What Are the Implications for Treatment?
If it can be firmly established that pathogens trigger the inflammation driving chronic disease, that offers several different approaches for treatment. First, we would need to use a high level of suspicion and appropriate technology (such as PCR) to detect infection. These bugs don’t show up through urine cultures or other typical diagnostic techniques.
Secondly, we would need to figure out treatment strategies. Antibiotics can be useful, but they may not be the only tools. Vaccines could help the body fight off these pathogens. Specific antibodies might also be developed to block them. In addition, phage therapies targeted to specific bacteria may also work when antibiotics cannot.
If you are unfamiliar with the idea of phage therapy, you might want to listen to our radio shows on this topic. Just think of these viruses the way you think of the enemy of my enemy. That entity becomes your friend!
Here are some interviews you may find intriguing:
Show 1155: Can Bacteriophages Save Your Life?
Show 1407: Battling Superbugs with Nature’s Viral Warriors
This Week’s Guests
Nikki Schultek is Founding Director of the Pathobiome Research Center, and Research Assistant Professor at Philadelphia College of Osteopathic Medicine , Executive Director and Co-Founder of the Alzheimer’s Pathobiome Initiative (AlzPI), and Principal and Founder of Intracell Research Group, LLC. A former life sciences professional with Pfizer and Genentech, she now works to unite global researchers studying infection-associated chronic illnesses, including Alzheimer’s disease and other brain diseases.
Following her own recovery from Lyme Disease, Chlamydia pneumoniae and co-infections, Nikki builds and leads patient-centered interdisciplinary research collaborations to examine microbial drivers of chronic diseases. She has catalyzed philanthropic funding to launch AlzPI research at multiple academic centers and co-lead authored a 2023 roadmap in Alzheimer’s & Dementia outlining a rigorous strategy to investigate infections in brain disease.
www.PCOM.edu/research/pbrc
www.AlzPI.org
www.IntracellResearchGroup.com
Nikki Schultek, founder and director of Intracell Research Group, LLC
Brian J. Balin, PhD, is a tenured Professor of Neuroscience and Neuropathology at the Philadelphia College of Osteopathic Medicine. He directs the Center for Chronic Disorders of Aging (an Osteopathic Heritage Foundation Endowed Center), and the Adolph and Rose Levis Foundation Laboratory for Alzheimer’s Disease Research.
An internationally recognized Alzheimer’s researcher, Dr. Balin has spent over 25 years investigating links between infection—particularly Chlamydia pneumoniae—and neuroinflammation, blood–brain barrier dysfunction, and neurodegeneration. His NIH- and foundation-funded work has significantly advanced the “pathogen hypothesis” of Alzheimer’s disease and Dr. Balin is regarded as a global expert and pioneer in this research field. Dr. Balin is a Co-Founder of The Alzheimer’s Pathobiome Initiative (AlzPI).
Brian Balin, PhD, Philadelphia College of Osteopathic Medicine
Listen to the Podcast
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Transcript of Show 1466:
A transcript of this show was created using automated speech-to-text software (AI-powered transcription), then carefully reviewed and edited for clarity. While we’ve done our best to ensure both readability and accuracy, please keep in mind that some mistakes may remain. If you have any questions regarding the content of this show, we encourage you to review the original audio recording. This transcript is copyrighted material, all rights reserved. No part of this transcript may be reproduced, distributed, or transmitted in any form without prior written permission.
And I’m Terry Graedon. Welcome to this podcast of The People’s Pharmacy.
You can find previous podcasts and more information on a range of health topics at peoplespharmacy.com. Chronic diseases continue to plague humans. We’re good at treating symptoms, but the root causes often remain a mystery. This is The People’s Pharmacy with Terry and Joe Graedon.
Are pathogens responsible for many of our most troubling and persistent conditions? We don’t think of heart disease, arthritis, or Alzheimer’s disease as having an infectious origin, but might they?
Our guests today are studying the connection between infection and chronic disease.
Not every pathogen is obvious. Some like to lurk inside cells where we have a hard time detecting and eradicating them.
Coming up on The People’s Pharmacy, how hidden infections can lead to chronic disease.
In The People’s Pharmacy Health Headlines: The American Heart Association and the American College of Cardiology have just issued new guidelines for preventing heart disease.
For one thing, the experts suggest starting cholesterol testing much younger, possibly even in childhood. Younger adults, between 20 and 30, should aim for LDL cholesterol levels below 100. People at higher risk will be encouraged to get their LDL level below 70.
Cholesterol is not the only risk factor addressed by the new guidelines. They also recommend testing for lipoprotein A, also known as LP little a. This is an independent risk factor for atherosclerosis. The cardiologists who compose the guidelines want their colleagues to use a new risk calculator that evaluates a much longer risk period than the previous calculator did.
People with heart disease and those with diabetes need more intensive treatment than those at low risk. The guidelines also suggest measuring coronary artery calcium in cases where there’s any question about starting a statin medication to lower cholesterol.
Harvard researchers and their Mongolian colleagues have just published a study of vitamin D3 supplementation during COVID infection. Patients from both the U.S. and Mongolia were recruited.
Over 1,700 volunteers with newly diagnosed COVID-19 infections participated. They were randomized to receive either vitamin D3 or placebo. The dose of vitamin D was 9,600 international units for the first two days and 3,200 IUs daily for the next month.
There was no difference in symptom severity or chance of hospitalization while people were taking the vitamin or placebo. There was, however, an intriguing hint that people who were taking vitamin D3 were less likely to develop long COVID after their infection. This reduction was not statistically significant, but the signal was strong enough that it deserves further study.
For decades, doctors have prescribed metformin to help people with type 2 diabetes control their blood sugar. Some studies have suggested that this compound may also help reduce the risk of developing certain cancers. Now, researchers have analyzed data from five Nordic countries to compare 13,050 people newly diagnosed with esophageal squamous cell carcinoma to 130,500 healthy people of similar age and sex.
Esophageal cancer is quite dangerous with low survival rates. The scientists report that people taking metformin had a 36% lower likelihood of being diagnosed with esophageal squamous cell carcinoma than those who were not. Higher doses were associated with even lower risk, about 48%. The authors note the observed association between metformin use and a significantly decreased risk of this cancer suggests a possible role of this drug in cancer prevention and treatment.
Influenza cases are trending down at long last, though the CDC reports overall seasonal influenza activity remains elevated nationally. The agency notes that hospitalizations from influenza were the third highest since the 2010-2011 flu season.
The CDC estimates that there were 27 million illnesses, 350,000 hospitalizations, and 22,000 deaths from flu so far this year. How well did flu shots work? Well, not so good. The H3N2 subclade K variant surfaced after the vaccines were in production, so the shots were far less effective than usual.
Americans have made some important health changes over the last several decades. In particular, smoking is down dramatically. Life expectancy has improved over that time, except during the pandemic. Even before that, though, life expectancy in the U.S. had kind of flattened.
Now, analysis shows that younger generations, born since 1970, have higher mortality from cancer, cardiovascular disease, and other causes than previous generations. If these trends continue, the U.S. could experience a sustained decline in life expectancy.
And that’s the health news from The People’s Pharmacy this week. Welcome to The People’s Pharmacy. I’m Terry Graedon.
And I’m Joe Graedon. Many of our most challenging conditions remain hard to cure. That’s because modern medicine has become very good at treating symptoms. We can ease the pain of arthritis, open airways for people with asthma, and overcome urinary tract infections with antibiotics.
But we often don’t know what’s actually causing these chronic health problems in the first place. Is there a connection with hidden infections?
To help us answer that question, we turn to Nikki Shultek. She’s founding director of the Pathobiome Research Center and research assistant professor at the Philadelphia College of Osteopathic Medicine.
Nikki is also principal and founder of IntraCell Research Group and executive director and co-founder of the Alzheimer’s Pathobiome Initiative. She worked as a life science professional for Pfizer and Genentech at the start of her career. Then she had a devastating personal experience with chronic illness.
Welcome to The People’s Pharmacy, Nikki Shultek.
Thank you so much, Terry and Joe, for having me. I’m incredibly grateful to be here today with both of you.
Nikki, you have had quite a journey. Could you please share with our listeners your chronic illnesses associated with pathogens? Because I think this is still a field in evolution. What happened?
Absolutely. So I like to say my journey began 10 years ago, closing in on 11 years. And I went from being essentially a relatively healthy, athletic, I was a runner, mother of two children, enjoying my early 30s to being someone who was just one diagnosis after another, chronically ill. And if anyone has seen that show Mystery Diagnosis, it was sort of like that.
I had about a dozen specialists helping me. And I, you know, really was unable to get a clear picture of what was actually driving the different diagnoses I had. So what I will fast forward with today is essentially I have what is known as infection-associated chronic illness. That is what was happening to me at the time.
But at the time, I was just being diagnosed with one autoimmune condition after another. And I ended up having this terrible respiratory symptom. So I’d had asthma my entire life, and I developed something that was different than my typical asthma. Yes, my asthma had become incredibly severe suddenly, but also I had a symptom called air hunger, which was truly like a desire for oxygen.
And this symptom came along with another odd symptom, which was one swollen joint in my finger.
Mmm Hmm. At that time. And so I went to my asthma and allergy physician who had seen me for years. He said, oh, you must be having an asthma exacerbation. And I was totally, that’s a reasonable conclusion, right? Prescribed prednisone, which is not uncommon for people that have asthma.
And unfortunately, 20 milligrams turned to 40, 40 turned to 80.
And I continued to go the wrong direction with my breathing. And I got this rattle in my lung and I’m going, oh, my goodness gracious, what’s happening here? So I ended up, to make a long story short, with multiple pulmonologists just on the lung issue alone, a scan to look for pulmonary clots, pulmonary emboli. I was then subsequently having strange heart palpitations, found out I had developed an arrhythmia.
And how old were you at that time?
So that’s pretty unusual…
Well, 33, about to be 34, yeah.
…for a healthy, middle-aged woman who exercised?
Non-smoker, actually a runner. I had taken up running half marathons, so probably the best physical shape of my life. And my asthma had been previously very well controlled on GlaxoSmithKline’s purple disc, the Advair, for like years. Didn’t have an exacerbation or a serious turn in my illness.
What happened next was systematically the illness spread around my body, essentially. And I went from having just respiratory symptoms to developing what is known as one of the top 10 most painful conditions someone can have, a bladder pain disorder called interstitial cystitis.
Oh, yes. We have heard of this. It sounds awful.
Yeah, it’s essentially for the listeners that have had a urinary tract or bladder infection, it’s like walking around like that in perpetuity. And so when that happened to me, you know, I was quite frankly crushed. I had also started to become increasingly fatigued. I noticed cognitive symptoms. I noticed changes in my mood and my affect, which of course, now I’m walking around with difficulty breathing and bladder pain.
And at this point in time, you know, it was really scary. My kids were just three and five. And I remember vividly the day my bladder pain began was on a Halloween morning. And later that day, trying to focus on just enjoying taking the little guys trick-or-treating in their cute outfits. And just being, you know, deeply concerned over why I had this pain.
And the word idiopathic became my enemy. Idiopathic is a fancy way of saying we don’t know.
Why, right? And I’m going, inflammation, inflammation. You know, I start thinking about this. And one thing that I noted was antibiotics. I ended up getting prescribed antibiotics for the terrible lung situation.
People are very familiar with the Z-Pak. So that drug is azithromycin. I was placed on it first for 10 days. My air hunger went away. And then I relapsed. So they treated me again and again. And then I got a month-long prescription for that drug. And that kind of got my breathing in sort of like a serviceable but not great place. But at least I wasn’t gasping for air every night.
And then the worst thing that happened to me during this horrible year was it was closer to my 34th birthday. I developed neurodegenerative symptoms that my primary care doctor thought could be MS.
Super scary. I mean, that’s kind of a challenging diagnosis. As bad as you were, now all of a sudden somebody’s saying, well, maybe you’ve got MS as well.
Yeah, it’s one of the hardest things I’ve ever had to experience. I would truthfully go to church in sweatpants, sit out in the parking lot, and cry and pray in the parking lot because I felt like I was too much of an emotional wreck to go inside.
At this point, I was, you know, when I thought that MS could be, you know, waiting for a neurology appointment, of course, you can’t get those very quickly when you’re a new patient. I had had a brain MRI and I just, I’ve, I, it never felt more of a sense of terror in terms of fear. And it was mostly fear because I was a mom, not like fearing my own existence, you know, being, you know, very limited and painful, but more so how it would impact my children and my husband.
And so I started making plans someone in their early 30s shouldn’t have to make. I started, you know, writing things down that I, in case I lost more of my faculties, because I had previously worked for a pharmaceutical and biotechnology company. I knew a lot about medicine and health care, and I knew that I was an unwell person without a proper diagnosis.
So at this point in time, once the desperation part kind of faded, it turned into this like sense of resolve, right? Like I accepted that I might have MS. I actually came to terms with that. I don’t, by the way. You know, I had no lesions on my MRI and didn’t feel like a really beautiful answer. It felt like, why am I still so sick, right? I didn’t really have an answer. I had knowledge.
The neurologist said to me, well, it doesn’t mean you don’t have it. I see people like you all the time that may for 10 years have symptomatology, and then eventually they develop the lesions.
Oh, boy, how helpful is that?
It was hurtful. It felt cold. And at that time, I remember saying, do you know anything about Lyme disease? And we’re in Connecticut. I was living in Connecticut at the time. I was at the Hartford Hospital. And he said, I don’t know much about that. And, you know, he could have just been having a terrible day. You know, I mean, health care is not an easy environment.
And so I try to, my experience has taught me to approach everything with kindness and curiosity. You never know what someone is experiencing.
But in a nutshell, what happened next was very important. I decided to turn into the researcher part of me. I was always an intensely curious person that loved science. And I wanted to live. So I did a Google search.
And the first thing I looked up was actually atypical pneumonia and interstitial cystitis. One of my diagnoses with the respiratory issue was atypical pneumonia. Okay.
And what came up was a study that saved my life. A small study. Dr. Charles W. Stratton from Vanderbilt, the late Charles W. Stratton, and a urology colleague of his, he had been studying this unusual bacteria transmitted through coughing and inhaling infected respiratory particles called Chlamydia pneumoniae.
People hear Chlamydia, they think sexually transmitted infection. But that’s a different bacteria in the same family, in the same genus.
They’re relatives, and it’s the respiratory form. What people don’t realize is how common it is in the human population. It’s really ubiquitous, meaning we’re nearly all exposed to it in a lifetime.
And I had never heard of it. And I read the study and it was sort of startling. It was a small cohort, a small group of women with my bladder pain diagnosis tested using PCR, which we all became very familiar with during COVID, right? Looking for…
Polymerase chain reactions.
Indeed, Joe. And then they didn’t do typical urinalysis, which would never pick up on something like chlamydia because it has to live inside our building blocks, the human cells. So it wouldn’t be just floating around, free floating in the urine, and it wouldn’t be detectable this way.
And you can’t culture it out of urine.
No, you can’t. So they did this PCR of the urine, and 80% of the women had evidence of Chlamydia pneumoniae. And the conclusion was this. The study’s too small to have any really meaningful results come from it, but that this organism can lead to chronic inflammation.
And that got me deeply curious next. Oh, boy, I’ve had asthma my whole life. This is a chronic bacterial infection. So I did a search on PubMed for Chlamydia pneumoniae, the bacteria, and asthma. And I will say it changed the trajectory of the rest of my life.
You know, I decided to start reaching out to the people publishing in the space. There were hundreds of thousands of publications on Chlamydia pneumoniae and asthma, and quite a compelling association with severe asthma, which I had been diagnosed with.
And at this point in time, I ended up reaching out to some of the what would become today the founding members of a global team focused on interdisciplinary collaboration and the doctor, Dr. Charles W. Stratton, who saved my life, as well as the wonderful Dr. David Hahn, who spent his career studying infection and asthma.
You’re listening to Nikki Shultek, founding director of the Pathobiome Research Center and executive director and co-founder of the Alzheimer’s Pathobiome Initiative. She’s also research assistant professor at the Philadelphia College of Osteopathic Medicine and principal and founder of IntraCell Research Group.
As a former life sciences professional with Pfizer and Genentech, she’s now working to unite global researchers studying infection-associated chronic illnesses.
After the break, we’ll learn more about C. pneumoniae.
Some doctors are quite wary about sustained antibiotic treatment. Why did they object?
How long did she have to take the medicine?
We’ll also talk about silos in medicine. How could we break them down so doctors could treat the root causes of illness?
You’re listening to The People’s Pharmacy with Joe and Terry Graedon. Welcome back to The People’s Pharmacy. I’m Terry Graedon.
Many healthcare professionals have been taught that antibiotics can kill off most pathogens, such as Borrelia burgdorferi, within several days. That’s the bacterium that causes Lyme disease. For many patients, two or three weeks of doxycycline solves the problem.
But there’s growing evidence that 10 to 20% of people who catch this bacterial infection experience post-treatment Lyme disease syndrome. Could this kind of infection connection also be responsible for many other health problems?
The infection connection should not be a big surprise. People who catch chickenpox as children are susceptible to shingles many decades later. The virus hibernates in the body until conditions allow it to cause trouble again.
Our guest is Nikki Shultek. She’s founding director of the Pathobiome Research Center and research assistant professor at Philadelphia College of Osteopathic Medicine. Nikki is also principal and founder of the IntraCell Research Group and executive director and co-founder of the Alzheimer’s Pathobiome Initiative.
She has just described her personal experience with infection-related chronic illness.
Nikki, that sounds like a really amazing and frightening situation that you were in. And now, as you have found out that Chlamydia pneumoniae is very common, what else did you learn about it? And how did you recover? Because it looks to us as though you’re doing much better today.
I am. So to fast forward a bit, Dr. Stratton, Charles Stratton from Vanderbilt, ended up diagnosing me officially with Chlamydia pneumoniae infection. I did have it. I also had Lyme disease and various co-infections that I acquired living in Connecticut.
So I believe it was a multi-hit for me, quite honestly, Terry. It was a tipping point. I’d likely had the Chlamydia and Mycoplasma pneumoniae infections my whole life, having childhood asthma and a lot of illness, a lot of strep infections.
And then, you know, multiple antibiotic therapy placed me in remission. And at the time, I was a little uncomfortable with the idea of using multiple antibiotics for a prolonged period of time.
However, Dr. Stratton, being an unbelievable educator, provided me with evidence to suggest that in certain severe cases, particularly when neurodegeneration was at hand, and that was the symptomatology that I was really most worried about, that it could be warranted when the risk of the disease outweighs the risk of the treatment.
And so I’m very lucky to be here and be well and have found an answer to it. Although I will say I’m not as well as I was before all of this happened to me. I have to take quite good care of myself.
The idea of sustained antibiotic treatment is a little challenging for most physicians, including some of the infectious disease experts, because it’s like, well, 10 days, one and done, you know, you should be fine. And you weren’t fine.
Well, and of course, they worry about antibiotic stewardship and what will we do when, not if, but when all of the antibiotics we currently have available lose their effectiveness.
So how long did you have to take, for example, azithromycin, Z-Pak, and some of the other antibiotics to finally rid yourself of these pathogens?
You know, my answer will not be appealing to some. I’m not really of the belief based on the literature and our research that you can actually get rid of some of the infections once they have been on board. So people are very familiar with the use of long-term antibiotics and physicians are comfortable with it in certain settings. And it’s a bit nonsensical.
If you ask me as a patient, you can have prolonged doxycycline or minocycline for acne, many years of therapy. For chronic urinary tract infections that are recurrent, patients will be placed on antibiotics in perpetuity at times. They’re used for chronic obstructive pulmonary disease, which can be very serious. They are used for asthma. We have a 3,200 patient clinical trial enrolling. One of the study sites is Chapel Hill as we speak. That’s called I Treat PC.
But then for people suffering with neurodegenerative symptoms and crippling bladder pain and, you know, that it could be considered potentially controversial, and that comes to a bigger problem.
And Terry, you mentioned stewardship. So I had the privilege at Pfizer to work in the antibiotic space. I launched a drug for MRSA infections, which is that drug-resistant staph. And I used to attend ID grad rounds, which is the infectious disease specialists, you know, Uber meeting where they talk about tough cases and learning. And I loved it. I was very disturbed by the idea of taking prolonged antibiotics when it was suggested to me by Dr. Stratton. And he knew my background and he was an infectious disease specialist and a medical microbiologist.
But you have to actually, when you talk about stewardship, you have to stay in reality. 80% of antibiotics in the United States are used in agriculture. Okay. So the animals. Absolutely. So you should not prescribe antibiotics to people that have upper respiratory tract infections that are viral, right? That’s the low-hanging fruit for stewardship. And it’s not to say that it’s not important, but I do believe the emphasis on stewardship has led to under-treatment of certain very detrimental infections, including the bacteria that causes Lyme disease, Borrelia burgdorferi.
And it’s an economic problem. Antibiotics are not profitable. And so this has been a really, you know, where understanding the business side of things is critical for me in my current work, you know, building research collaborations to unravel how infections can drive chronic diseases with emphasis on the brain is understanding the economics that are at play and the politics.
And sometimes you have to take these antibiotics, not for weeks, but for months, and in some cases for years.
Yeah. So for me, just to answer your earlier question, for a number of years, I had multiple antibiotics. My case has been constantly evolving like many patients like me. Because of my enrollment in a IRB study at North Carolina State, I learned I have chronic babesiosis, which is a chronic parasitic infection that is transmitted by the same tick that I likely got Borrelia burgdorferi, Lyme disease bacteria from.
This little sneaky parasite likes to hang out inside your red blood cells. And it is the likely culprit of my air hunger 11 years ago. That was a symptom that never made sense indeed, because asthma doesn’t normally, my asthma, the etiology of it, it had never had air hunger. And I remember saying to my doctor, something is different here.
And that is the thing that I’ll, I like to impress upon people listening that could have illnesses. You as the patient have an intuition and a level of intimacy with what your body is experiencing. And you need to find a clinician that listens and hears you and sees you.
So you have the experience of what your body has done before, and you need to pay attention when it does something different.
Absolutely, you do. And for me, unfortunately, I have previously relapsed any time antimicrobial drugs have been removed. So I have a maintenance therapy plan with my doctor, and I’m very fortunate that I actually have because Dr. Charles Stratton passed away four years ago. I’m under the care of a ILADS physician, International Lyme and Associated Diseases, which is the only infection-associated chronic illness practitioner group in the world.
One of the problems that we’ve encountered over many decades of interviewing a variety of patients and physicians is the silo problem.
So there are specialists, super specialists. And the cardiologists may not be talking to the infectious disease experts. And the dentists may not be talking to the cardiologists.
And so you have all of these different specialties and the dentists are saying, well, yes, you do have gum disease, but they’re not talking to the cardiologist to say, well, if there’s a gum infection, that may be affecting the heart valves and that may be affecting the vessels in the heart.
And of course, we know, but cardiologists don’t always remember that Lyme disease can affect the heart as well.
Absolutely. Joe and Terry, such an astute observation. And literally what you just said encapsulates my observation as a patient, a human hockey puck, as I call it, going through the medical system, being passed from one specialist to the next to address these different bodily systems that were all not working properly, you know, including my food stopped digesting properly during this horrible year. So now I’m having a colonoscopy.
No one was talking to each other. And I remember thinking, who’s going to piece it all together? There’s an underlying driver. And so when I found the information about chronic infection and illness, it made so much sense.
And then, you know, talking with Dr. Stratton, Dr. Hahn, and beginning to informally, in a grassroots manner, start bringing people together, I had this thought. It wasn’t a new thought for me. I had always been a collaborative person. And in my time in pharma and biotech, I was working in this manner, too, trying to connect stakeholders so that we could advance outcomes for patients.
Well, what I decided I could do to help when I went into remission on the multiple antibiotics, I knew I needed to help, right? This is a huge problem. I wondered how many MS cases were indeed infections that were undiagnosed. So I knew we needed to advance research around it and raise awareness. And I thought the best thing I could start doing was introducing these folks to one another if they didn’t already meet. So the infection and asthma people with the infection, looking at bladder pain disorders, looking at neurological disorders, looking at musculoskeletal or, you know, joint disorders. Let’s start there.
And I like to joke that we arrived to the space on the chlamydia train, this bacterial infection. Most of the people in the initial group, which was started in 2017, IntraCell Research Group, by me. And, you know, it was really to begin introducing folks to one another. I didn’t know what it would turn into, quite honestly. I’d been a stay-at-home mom for eight years. And, you know, I’d been extremely ill. And the idea of research collaboration was born, multidisciplinary research collaboration.
Fast forwarding to today, in 2023, I had the privilege with a number of amazing colleagues from around the world, incredibly diverse in experience in all ways, the Alzheimer’s Pathobiome Initiative.
And I guess I’ll start by saying, what is a pathobiome? So people know microbiome. And I think the word microbiome gives off kind of like a fuzzy, warm vibe of like everyone collaborating with one another, kind of like my team, you know, commingling happily. The pathobiome is your unhappy state. It refers to potentially, you know, different infections or organisms that might be in your body that now for one reason or the other are having a bad reaction with your immune system. They’re making your immune system angry.
And so the pathobiome, I sometimes refer to these as the organized criminals. You know, they’re infections that become disproportionate and can cause inflammation and other consequences. So this idea of a pathobiome takes into account each unique response that a person’s immune system can have to an infection. And we saw this with COVID. Some people got little to no symptoms, tested positive. Other people died.
Some people remain ill today.
It’s the number one pediatric illness. It surpassed asthma as the number one chronic illness in kids is long COVID.
So this research consortium of ours is comprised of, we have Dr. Ed Breitschwerdt, who’s a doctor of veterinary medicine. We have microbiologists, people focused on fungi, like Dr. David Corey, who’s also an immunologist. We have folks like Dr. Brian Balin, focused on intracellular bacteria, virologists like Kevin Zwezdaryk, neuroscientists like Dr. William Eimer, respiratory infection experts like Dr. David Hahn.
And our team has more than 30 people globally collaborating actively with one another in order to essentially accelerate innovation and raise awareness, but also to bridge silos.
Nikki, you have mentioned that you have this international collaboration. You’re looking at conditions that may be caused by the pathobiome. And I’m wondering if you could outline for us a few of those potential conditions.
And in particular, perhaps Alzheimer’s disease.
Absolutely. So our Alzheimer’s Pathobiome Initiative team is actually working quite broadly in brain disease and infection. So over the holidays, we received a grant to study actually five brain diseases in relation to infection. ALS, Alzheimer’s, Parkinson’s, epilepsy, and conditions that affect children called PANS and PANDAS. These are pediatric neuroimmune infectious syndromes that can lead to perfectly healthy children having literally crippling anxiety, OCD, and some of these children die.
So we take this incredibly seriously. Some of the infections that have been associated with Alzheimer’s disease and other diseases, and this is an important distinction. We believe it’s so important to look at the whole human lifespan, at the diseases that are occurring that are associated with infections. That’s everything from MS to schizophrenia, you know, two diseases typically associated with advanced age.
And it’s literally pathogens from every category. Parasitic infections like Toxoplasma gondii have been linked with schizophrenia, have also been linked with Alzheimer’s disease. It’s organisms like herpes viruses, HSV-1 and HSV-2, the cold sore virus, that has been linked very strongly with Alzheimer’s disease and other chronic neurological and chronic illnesses. Chlamydia pneumoniae, of course, is strongly associated with Alzheimer’s disease, but also asthma, atherosclerosis, multiple sclerosis, reactive arthritis.
There are also fungi that have been associated. Indeed, when we published our research roadmap for the AlzPi team, the Alzheimer’s Pathobiome Initiative in 2023, we identified 86 cases of infectious dementias of all different types in which some of these were reversible with antimicrobial therapy. One of them was a stunning case of a person with a healthy immune system. They did not have HIV that got a rare fungal infection called Cryptococcus neoformans, and this person ended up getting antifungals and getting better. Their neurodegenerative symptoms went away.
Nikki, I’m so excited that you have taken your vast and deeply unpleasant and frightening experience, and turned into a researcher.
So you are a patient. You are leading a research collaboration. Tell us more about patient-led research because I think it’s not widely appreciated that patients can do this.
Absolutely. I have had such a privilege to learn over the last decade and to try to turn, you know, pain into purpose, truly. And I’m not alone by any stretch of the imagination. There are quite a few people out there like me that have not only had these journeys, but then become subject matter experts in a domain, can even be rare disease. You see this quite a lot. You see parents like me, you know, looking for a better future for their children.
And thus, what is the greatest motivator? I think it’s love. And so out of love, I think patients can become an unbelievable tool to researchers and become researchers themselves, which is the case for me.
I was very privileged that our president, Dr. Jay Feldstein at PCOM and Dr. Brian Balin, with whom I’ve collaborated for nearly a decade, saw the value in, you know, me becoming a, you know, bona fide member of the research team. I’m publishing in the space with the researchers. I’m creating, you know, and generating hypotheses, serving as a principal investigator on NIH submissions. It is the gift and blessing of a lifetime.
And I think that, you know, more purposeful integration and patients having a seat at the table, knowledgeable patients. There’s a book that I read called Range by David Epstein that I’m absolutely obsessed with, and it talks about remaining a generalist and how patients, actually, there are chapters of the book, whole chapters, about how patients and their experiences led to transformative change in particular disease domains.
Nikki, there’s a term that is used throughout medicine that ends in “-itis.” And “itis” means inflammation. And so we’ve got arthritis, bronchitis, colitis, sinusitis, dermatitis, gastritis, myocarditis, which is the heart, and cystitis.
And lots of other “itises” as well.
You know, the pharmaceutical industry, of which you once were a part, has become extraordinarily successful at dealing with “itis” conditions. Not the root cause, mind you, but the inflammatory reactions. So there are IL-2s and IL-4s and IL…
Interleukins. These are anti-inflammatory drugs and they’re impacting the immune system, which is why when you look at the commercials on TV for the rheumatoid arthritis drugs and the inflammatory bowel drugs and, you know, name it. The psoriatic arthritis drugs, they all say, well, yes, you could catch a bad infection, and that infection could be very dangerous, oh, and possibly cancer.
And you’re talking about attacking the problem downstream, at its earliest phase rather than at its ultimate phase when people are already in terrible shape and in pain and inflamed.
Can you help us better understand what you’re trying to accomplish by ‘the root cause’ and dealing with that, rather than the end result?
So what you said is so astute about the commercials on television, you know, with the various drugs. My children who, of course, you know, get to talk with me about various topics all the time in science. They both enjoy science and they drive me. You know, it’s my boys that really push me forward to help, you know, motivate me on a daily basis to make the world better. They’re 14 and 16.
They’ll go, “Mom, didn’t you say that some of these conditions can be triggered by infections? And the commercial says if you have an ongoing infection, not to take the drug. Isn’t that….?” So it’s so funny.
Another favorite question of my son, “Mom, if there’s a vaccine for human papillomavirus that can prevent cancer, wouldn’t we look at other viruses and other bacteria and cancer?” This was when he was 12. I was like, yes, and please do that for the rest of your life. Ask those questions.
So, you know, what’s really interesting is what we talk about isn’t just limited to infection, right? There are other potential root cause drivers. We talk a lot about the exposome, which is your exposures across the human lifespan, not just germs, but pollutants, toxins, your diet, etc. We think these things are all important root causes to look at, inclusive of infection. But infection is, just so you know, the number one driver of any “itis” in the human body.
And that is not me saying that. That’s in medical text sort of 101. If you look up inflammation in the National Library of Medicine on NCBI, you will see that the number one thing should be ruled out as an infection with any “itis.”
We believe, though, here’s an interesting caveat. So with diseases which have been accumulated over a lifetime, right, like Alzheimer’s disease, multiple hits potentially with different pathogens, different infections that come and go, relapses, we may indeed need some of those other drugs that were developed targeting various pathways as a multifaceted approach, because it’s not to say that the immune reaction isn’t harmful. It can be.
And that’s the caveat and the reason we believe it’s so important to have the immunology perspective and the diversity of these silos bridged while understanding infections because it may need to be a multifaceted approach like the way that we approach sepsis.
And as you’re talking, I’m thinking about the early part of your story in which you’re describing that you are having such difficulty breathing and they kept increasing the dose of prednisone that you were on. And I’m thinking prednisone. Prednisone interferes with the body’s ability to respond to pathogens. So counterproductive, no?
Absolutely. In my case, it absolutely was that time. And again, I don’t fault the clinicians. Actually, you have to fault the whole system, right? So in Connecticut, the state where Lyme, the town of Lyme is literally situated, you know, if you ask the majority of clinicians, what would you think if you saw someone with air hunger that had prior asthma, but they’re telling you it’s different and one swollen joint? They should be thinking tick-borne illness. They should know that babesiosis has a hallmark symptom of air hunger.
And Borrelia, perhaps, or just babesiosis.
Really it’s clinically significant for Babesia. And the most common one is Babesia microti. And that is what I have confirmed by North Carolina State, direct detection, so not antibody-based testing. So, you know, this is what’s key really is the education, but it’s across the whole spectrum. It’s patient awareness, it’s clinicians being educated in medical school. So there needs to really be a sea change.
So I do have a pet peeve, and that is the infectious disease experts should be embracing your research, should be really excited about the idea that infectious agents could be responsible for a great many chronic conditions.
And yet, a lot of the infectious disease experts seem to be obstructionists. Like, oh, no, there’s no such thing as long Lyme. And no, this thing about chronic fatigue syndrome, it’s all in your head.
And ILADS physicians, you’ve got to be very careful about them, right? That’s what some of the infectious disease experts have been telling us. They may be changing their tune now.
But how do you convert the ID, the infectious disease experts, from skeptics to allies?
It’s such a great question. So if you look at medical history, it just sort of repeats itself. This is human nature 101. When doctors Warren and Marshall, you know, they eventually win the Nobel Prize for linking a bacteria in the gut called Helicobacter pylori or H. pylori to the development of ulcers; for like a decade prior, they were called madmen. And these are by the thought leaders in the GI space.
So thought leaders, human nature is, you know, to attach ourselves to something. If we have a hammer, we want to see nails. And we have to become super aware of this. We try to be aware of this all the time as a research team, not to drink so much of our own Kool-Aid that we don’t see other ideas as being important.
The infectious disease, you know, sort of gaslighting of the chronic Lyme issue, I believe is about to change. You know, we have the current administration, HHS, Secretary Kennedy, Dr. Jay Bhattacharya, Marty Makary, and Dr. Oz all saying, you know, they’re emphasizing Lyme. So there are some very exciting developments happening.
That was beginning December 15th, 2025. And I do believe that there has to be adequate patient pressure and advocacy, very much like how HIV is now something that one can even prevent getting, right? There’s a preventative. You can have HIV. There has been such a huge federal investment due to a patient-led movement, right? Now, HIV hurts people fast and really it’s very virulent and very quick if unopposed. And so it was so blatant, right?
But even if you read back on the history of that, that required quite a movement from patients. Lyme and these infection-associated chronic illnesses are more like the simmering pot not boiling over. You know, it’s a chronic inflammatory process. It makes the person miserable, may rob them of quality of life, but they may not imminently die from it. And thus, it sort of has been underemphasized. But I do believe it’s changing.
I do have a particular question about cardiology, because if you were to poll 100 cardiologists, 99 out of 100, maybe 100 out of 100 will tell you heart disease is caused by cholesterol, in particular, LDL cholesterol. And if you ask them, well, what about LP little a?
They’ll go, oh, yeah, yeah, that’s coming along, and we’re getting a drug for that. And so, yes, we’re paying more attention because one out of five patients, they do have elevated LP little a, lipoprotein A. And then if you ask the question, what about gum disease? What about those bacteria that cause…
Yes. What about those bacteria that cause…
Porphyromonas gingivalis?
They look at you like you’re from Mars. Like, well, yeah, well, that’s not that important.
But actually, the research establishes a pretty strong connection.
…that infection could be connected to cardiovascular disease, it seems alien to the cardiology community and to the infectious disease community. How do we begin to change that?
We’re, I believe, and I am an eternal optimist, so take this with a grain of salt, we’re at a tipping point right now in history. There are so many favorable things happening in this space all at once, not just our work, but others. For example, a $49 million National Institute of Aging grant just went to a company developing a therapy targeting Porphyromonas gingivalis and targeting gingipains, which is the virulence factor that is believed to assault the brain.
Now, you mentioned gum disease. That bacteria, Porphyromonas, actually can affect how your blood-brain barrier that’s supposed to provide protection, it impacts it negatively. It also has been linked with, as you pointed out, other conditions. And so the federal investment for this, I think, is a big signal that this particular company, Lighthouse Therapeutics, has that support is evidence of a shift.
So the blood-brain barrier is supposed to keep stuff that doesn’t belong in the brain out of the brain. And you’re saying the impact of Porphyromonas gingivalis is to essentially make it more permeable, sort of like some infections make the intestines more permeable, and you get intestinal permeability, also known as leaky gut.
Indeed, yeah. Permeability of barriers is a big issue. One of the things that we’re studying within AlzPi and we have grants to look at is why are women two-thirds of Alzheimer’s cases?
And we know that estrogen actually helps the immune system and that as women age, we lose estrogen and barriers of different types become less sufficient. We have not enough information on what happens to the blood-brain barrier.
But I want to add the caveat is this. I heard at the National Academies when I presented, one of the other speakers referred to it as a portal. Indeed it is. It’s not really a barrier as much as it is a passageway that should be selective.
Now our immune cells can traffic in and out through the blood-brain barrier. And if you have an infection like a virus or a Chlamydia pneumoniae or a Borrelia burgdorferi or Bartonella henselae inside your immune cell, it’s like a Trojan horse.
Right. It would be exactly.
So Nikki, as we wrap up our conversation, what would you like our listeners to take home as the message when we start speaking about the infection connection with all of these conditions and all of these nasty pathogens?
You know, just to read and educate yourself as much as you can. I realize that having certain educational level is a great privilege. Our team tries to write op-ed pieces, not just medical literature. You know, it’s a passion of mine so that it increases the accessibility of information.
Always trust your gut. If you don’t feel heard by a physician, find another physician. You are, indeed, your instincts are, they can be very correct. And that if you need help with something that you think could be an infection-associated chronic illness, there are ILADS physicians, www.ilads.org. There’s a provider search with the caveat, many of these physicians do not accept insurance. That is a challenge.
That’s one thing that I really hope that Health and Human Services and RFK Jr. can help impact changes is how the payers, you know, reimburse for complex chronic illness triggered by infection so that other physicians can do what the ILADS doctors do and get training like the ILADS doctors have provided. And so really look for and consider root causes.
And if we put you in charge of medical education today, what would you like to tell all of the physicians and nurse practitioners and physician associates who may be listening, what should they be learning?
I think they should have infection-associated chronic illness in the differential. When they are presented with a patient that has multiple idiopathic disorders particularly, and if they’re waxing and waning, not to immediately go to a purely psychiatric diagnosis.
Although I would argue that the field of psychiatry is riddled with evidence that infections can indeed impact our behaviors, such as the development of OCD from Streptococcus infection in kids with PANDAS. Overnight, suddenly, you have a kid that’s counting. So I think looking for infections, but then that gets to another caveat, which is what tests you order.
So we do need better testing for some of these infections, but serology or, you know, looking simply for antibodies, antibody-based testing for herpes viruses, for Mycoplasma pneumoniae, Chlamydia pneumoniae, a tick-borne panel, which is offered by Quest or LabCorp, it’s a place to start.
There are better labs, one right here in North Carolina, Galaxy Diagnostics, offering, you know, world-leading tick-borne infection testing. However, you know, it’s outside the bounds of insurance is a challenge. IGeneX, too, out in California. But, you know, again, these are barriers for patients where they won’t be able to access it, and that’s not okay.
As you begin to look to the future, because you’ve described a whole bunch of conditions where there are specialists in each area in their silos, not talking to one another very effectively. What would you like to see for the future?
What is your hope for your initiative, in particular around Alzheimer’s disease, but some of these other conditions as well? What does the crystal ball tell you?
We really need a large federal investment from the National Institutes of Health. I don’t know that all Americans realize, but the most powerful engine for medical innovation in the entire world is our National Institutes of Health, our government. You know, the emphasis has to be on funding this type of work.
And we call that team science, and so does the NIH. There are certain mechanisms, you know, that allow research teams like ours that are incredibly diverse. And just to let everyone know, I did found a center at the Philadelphia College of Osteopathic Medicine a year ago. It’s called the Pathobiome Research Center.
We essentially need more philanthropists and the government to step up to fund work that allows teams like ours to unlock root causes of these diseases.
Why is the root cause so important in the 15 seconds we have left?
It is that we stop focusing on the downstream effects. You know, a lot of drugs that you see today predominantly are targeting various pathways to intercept downstream effects that are largely inflammatory or pathology. You know, like let’s target the plaque in Alzheimer’s.
Targeting the root cause allows us to understand why the human immune system developed that response in the first place and allows us to intercept.
Nikki Shultek, thank you so much for talking with us on The People’s Pharmacy today.
It has been an absolute pleasure. Thank you for helping us shed light on these issues.
You’ve been listening to Nikki Shultek, founding director of the Pathobiome Research Center and executive director and co-founder of the Alzheimer’s Pathobiome Initiative. She’s also a research assistant professor at the Philadelphia College of Osteopathic Medicine and principal and founder of Intracell Research Group, LLC.
She was previously a life sciences professional with Pfizer and with Genentech. Now she’s working to unite global researchers studying infection-associated chronic illnesses, including Alzheimer’s disease.
After the break, we’ll turn to Dr. Brian Balin, an internationally recognized researcher on Alzheimer’s disease.
We’ll find out how he took a different path from most Alzheimer’s disease scientists to focus on the infection connection rather than considering amyloid accumulation as the prime mover.
C. pneumoniae is bad for the brain, but it might not be the only pathogen with long-term impacts. What else has Dr. Balin studied?
Might there be bacterial origins for many chronic diseases? Could this change our treatments for heart disease and stroke?
Find out more about the pathobiome and the infection connection.
You’re listening to The People’s Pharmacy with Joe and Terry Graedon. Welcome back to The People’s Pharmacy. I’m Terry Graedon.
Can hidden infections lead to chronic disease? A few examples are quite well known. For example, the bacterium Helicobacter pylori causes stomach ulcers that in turn can lead to gastric cancer. And gum disease caused by Porphyromonas gingivalis has been linked to heart disease and even Alzheimer disease.
We just spoke with Nikki Shultek about her experience and her work on hidden infection and chronic disease.
We turn now to her colleague, Dr. Brian Balin, professor of neuroscience and neuropathology at the Philadelphia College of Osteopathic Medicine. He directs the Adolf and Rose Levis Foundation Laboratory for Alzheimer’s Disease Research and the Center for Chronic Disorders of Aging.
Welcome to The People’s Pharmacy, Dr. Brian Balin.
Thank you very much for having me talk today.
We look forward to speaking with you. We have just spoken with Nikki Shultek about her experience. It was quite enlightening. But I’m wondering if you can put everything into perspective because for decades now, neuroscientists such as yourself and researchers within the pharmaceutical industry have focused on what I call the amyloid garbage disposal approach when it comes to Alzheimer’s disease. And you’re moving towards the infection connection approach.
Can you put us in perspective of what has changed?
Yes. So years ago, we, through a lot of serendipity, came across an issue about [an] infectious agent. The one in particular that I’ve been studying is a respiratory Chlamydia organism called Chlamydia pneumoniae.
And we found that this organism was in brain tissues that were examined postmortemly from Alzheimer’s individuals, or people that died from Alzheimer’s disease. And we felt that there was some issue here with this particular infectious agent being in the brain tissues of these individuals. And over time, what we’ve realized is that this type of infectious agent can actually enter into brain tissues through our sense of smell, but also through the blood-brain barrier.
And we think that it actually acts as a trigger for the early pathology that occurs in Alzheimer’s disease. And the early pathology that shows up is in the area of the brain called the entorhinal cortex, where you have direct input from the olfactory system, which basically is coming from our… originating in our noses through our olfactory nasal epithelium, olfactory neuroepithelium.
And because of that issue, we think that infectious agents actually can be the triggering type of process or lead to a triggering type of process that can actually lead to early change in the brain. And in this case, leading to the pathology, the early pathology of Alzheimer’s disease.
Now, this is in contrast to others that have studied the amyloid hypothesis for years, the amyloid cascade hypothesis. And that all originated from evaluation of genetic Alzheimer’s disease or familial Alzheimer’s disease, which is about one to three percent of all the people that get Alzheimer’s disease having that form. And that originated from looking at those individuals and determining that there were genetic mutations that led to the deposition overall of the amyloid peptides that accumulate in Alzheimer’s disease very early on.
Well, in our work, we also see those same amyloid peptides accumulating early on in brain tissues. And we’ve also seen that infection can actually turn on cells to process the larger amyloid precursor protein into these peptide forms.
So now we have a contrast. One is a genetic process that leads to this pathology, and the other is an infectious process leading to pathology. And this is why we think this is an underrepresented arena of understanding how infectious agents, and there may be many, that actually can lead to the same type of disease entity.
So you’re suggesting that this bacteria, Chlamydia pneumoniae, is not the only pathogen that might be affecting the brain?
That’s correct. So we think that of the work that’s been done over many, many years, there’s been evidence for the herpes simplex virus 1. There’s been evidence for Borrelia burgdorferi, the agent of Lyme disease. There’s evidence for SARS-CoV-2 to actually be involved as well. And then there are oral organisms. There could be systemic organisms. There could be gut organisms that could also be involved.
But what’s interesting about what we found was that this type of organism, this Chlamydia pneumoniae, is an intracellular bacterium. So it’s going to act very similar to a virus, actually, where it infects inside of our cells. Once it’s infected inside of our cells, it’s hidden from the immune response, just like the herpes virus would be or other types of viruses.
If these migrate into our brains, and also this would include also the SARS-CoV-2 virus, if these migrate in, they can then stimulate change in the cells within the brain proper. And this could be anywhere from changing the infected cell itself or getting response from the glial cells like the microglial cells that would lead then to an inflammatory response that would also then lead to more damage within the brain.
Dr. Balin, you just said something that sends shivers up and down my spine, and that is SARS-CoV-2, i.e. COVID. I mean, tens of millions of people in this country and hundreds of millions of people all around the world have caught COVID. And the question that you’re sort of raising is, well, will some of them develop Alzheimer’s disease as a result of this, what we’ll call viral infection that has really affected the whole wide world?
Yes, this is one of our greatest fears is that this is opening the scenario that there could be millions on the globe that may be destined for this type of change. And it may be that it’s not just from the SARS-CoV-2 virus, but also from other agents like what we’ve also found that are acting in concert with one another. And then you have the inflammatory response itself. If it’s generated and it’s maintained in a chronic fashion, now we have a chronic, potentially smoldering type of process that is occurring quite readily, I think, could be occurring in our brains without us knowing it because we are not having obvious symptomatology. Now, with the SARS issue and COVID issue, brain fog, memory issues, long COVID, these are things that may be giving us a clue that something is more chronically developing, along with then these other insults that are potential in our environment. For instance, pollution, air pollution, particulate matter, the diets that we have, the genetic risks that we have. These may be acting in concert to now drive the process, unfortunately, into a neurodegenerative arena leading to a dementia.
Dr. Balin, I wonder if you would tell us about your recent research collaboration with Cedars-Sinai, please.
Yes. So with the Cedars-Sinai’s work that was led by, or coming out of Tim Crother’s lab, we actually aren’t collaborating directly with them. However, our work really is compatible with what they’re finding with the Chlamydia pneumoniae organism in the retina.
So this organism, this goes to the organism’s ability, we believe, to actually become systemic as well. Once it’s inhaled into the lungs, this organism can be picked up by white blood cells that are surveilling all the vasculature in the lung tissues. And if it’s picked up this way, now you can traffic the organism within the white blood cell because the white blood cells will phagocytize the organism inside and traffic it around the bloodstream. So we think that that’s one of the ways that it’ll get into the vessels throughout the body and can also show up in the retina.
The other aspect of this is that in atherosclerosis, in cardiovascular disease, the Chlamydia pneumoniae organism has been recognized and involved and sought to be involved with aspects of that disease leading to the atherosclerotic process. So we know that this organism is one of those insidious types of organisms that can traffic around the body and use multiple mechanisms for actually getting into tissue sites.
So the Crother work is very significant and really follows from a lot of the early work we did where we found that the organism in human tissues, now we didn’t identify it in retina per se, but we found it in the olfactory regions of the brain, of human brains, and deeper in the brains themselves in Alzheimer’s disease.
But we also did animal modeling. And with animal modeling, we showed that the infection with this organism intra-nasally can get into the brain very quickly, but also they can get into the bloodstream fairly quickly.
Well, Dr. Balin, I’d like to just ask you the implications of this research, because it sounds like, well, if this nasty pathogen, C. pneumoniae, is getting into the brain, but also circulating through the body and maybe getting into the heart, there may be a bacterial origin for a lot of our chronic diseases.
I think most cardiologists blame you know, LDL cholesterol, but maybe there’s a bacterium that is also contributing to atherosclerosis and maybe to strokes.
How do we begin to change our mindset to recognize that chronic infection may be contributing to a lot of our ailments?
Well, it’s an excellent question. And I think what we need to do is to start having a better diagnostic approach to this question. And this would be something that we need to actually start instituting into the population at a much earlier age before any symptomatology actually starts to accumulate or starts to manifest.
And this goes to the sampling issue. So how do we sample for these types of agents? The typical sampling approach would be to look for a presence of antibody responses in the bloodstream to these different types of agents to see if we’ve been exposed that way, to see if antibodies have been developed to the organism. But we should be also sampling saliva and urine along with blood and maybe even doing nasal swabbing as well for some of these organisms too, as these are routes of entry into our bodies.
The other could be even stool sampling, for instance, and for instance, with the COVID issue, we found that the SARS virus, SARS-CoV-2, was showing up in wastewater. And these are ways then that we could actually evaluate different types of fluids from an individual to actually evaluate what is on board in a particular individual and whether those ingredients that are on board have been identified with other chronic issues that have shown up in the population.
So really quickly focusing on the outcome, it sounds like if we can identify these pathogens, we might be able to come up with treatments such as antibiotics.
Yes. And the antibiotic approach would be probably the original approach to be taken. I actually think, though, that we may be able to also manipulate our immune responses. Now, could that be through vaccines? It could be that as well.
It could also be through phage therapy, for instance, for some of the bacteria, where phage therapy, different types of bacterial phages or viruses that infect bacteria actually can be and are being designed, by the way, to actually change how an infectious agent could actually propagate in us so that it could be a phage that’s developed to kill off a particular type of bacterial strain.
There are many different ways of approaching this problem. Also, there’s novel ways of looking at the components of how bacterium and virus and fungi and parasites, how they infect our cells or our bodies, cavities or tissue sites, and blocking those capabilities through either potentially using antibody blocking to using protein-protein interaction types of blocking.
So these methodologies are being developed now beyond even the antibiotic approach.
Dr. Balin, I wonder if you could give us the historical perspective on Schopenhauer’s three stages of truth and why that might be relevant to Alzheimer’s research.
Oh, OK. Wonderful. Well, the three stages of truth: First, the work being ridiculed, and then violently opposed, and then being self-evident.
Well, historically, we’ve actually seen this in the medical arena. And if we take the example of Warren and Marshall actually proposing that Helicobacter pylori, a bacterium, could live in the stomachs of individuals and cause severe disease such as ulcers, MALT lymphoma, gastric carcinoma, and actually being criticized when they came out with those types of findings, criticized to the point that they were vilified.
The gastroenterology world thought these people were absolutely crazy. Well, they’re not crazy, okay? It’s been shown that you have an organism that can live in the mucosal layer of the stomach and in the lining and can lead to all these severe diseases. And yet it took about 100 years for that to be accepted.
Now, if we look historically here with Alzheimer’s disease, even in the day of Alzheimer and Oscar Fisher, they were considering that infectious agents could be involved with what they were seeing in human brain tissues at autopsy. And yet we’ve gone now over 100 years later, and many of us have been studying this for decades in the more modern age. And yet we still don’t have great acceptance that this is even a possibility.
So originally, there’s been ridicule. And then, you know, there’s been opposition because of ignoring what we’ve been doing over time and what others have been doing. And there are a lot of people doing this work, by the way, not just coming from my laboratory or in collaboration with Nikki with the Pathobiome Research Center or the Alzheimer’s Pathobiome Initiative, etc. There are a lot of people that are working on this issue.
And now we’re forcing the issue here that we have to accept that there is involvement. Now, understanding the involvement as far as causation goes is the key. And now we’re trying to come up with consensus approaches of how you detect, of how you actually even approach the experimental designs to actually prove causation.
The problem we’re faced with is you have chronic diseases and you have chronic infections and you have a combination effect here happening with genetics and the exposome or what we’re exposed to with the environment. So it’s not an easy process. But not to accept that we have infectious components is just keeping one’s head in the sand, I believe. So with Schopenhauer, I think we’re getting close to this, what’s becoming more self-evident.
Dr. Balin, one would think that the infectious disease community would be so excited about your research. And in fact, the idea that infectious agents might be at the causative stage of a lot of our chronic conditions, you know, anything with an itis at the end of it suggests inflammation, whether it’s arthritis or cystitis or bronchitis, fill in the blank “itis.”
And so I keep wondering, why has the infectious disease community seemingly been pushing back rather than embracing this approach?
I believe that one part of this is that with the infectious disease community, the traditional way of thinking about, for instance, a brain infection is that you would have a meningitis, an encephalitis, a meningoencephalitis, or an abscess that would be now forming from some type of infection in the brain.
What is not well accepted, I think, but should be, is that we have chronic infectious agents that can act in a very subliminal and very insidious manner to infect anywhere in our bodies, first of all. In the brain, we already know that there are a lot of organisms that can be harbored there, and you can get disease, and at times you don’t have disease.
A perfect example is progressive multifocal leukoencephalopathy, PML, which can arise after treatment, for instance, for multiple sclerosis. Well, this is a very severe disease. It is caused by a virus, ’cause the John Cunningham virus, which many of us actually harbor and probably the majority of the population harbors in their brains, but does not actually suffer from disease from that organism.
There are other organisms. The poliovirus, it’s an enterovirus, can be harbored in the brain and can lead to a post-polio syndrome, but it can also be harbored in the brain and you don’t have obvious deficit. The herpes simplex virus can be the same way. So we know that there are a number of different agents that can be harbored in brain tissues without obvious disease.
However, we also think that they can be activated to be involved with disease. The degree to which this is happening in our nervous system is something still in the discovery process. And that’s why the consideration of a pathobiome and even at times a microbiome, which I really still am questioning whether that could even exist in the brain. But a pathobiome for sure would be present there. But this falls outside of the typical designation an infectious disease person would actually be considering in this case.
We have one minute left. What would you like to see unfold over the course of the next decade with regard to this infection connection and this pathobiome? What’s your hope for the future?
We have tremendous chronic disease throughout our population. We need to start considering how infections and infectious organisms and these microbes are actually interfering with us or competing with us or working with us, how that actually is happening to understand how we are staying healthy or becoming diseased.
So these chronic issues are key, I think, for us as a future to really understand our health. So we need to monitor much better than what we’ve ever done before, and we need to start accepting that this is a reality and not continually questioning cause and effect. We have these on board. We still have to understand causation. How are things caused in time?
But we are uncovering that to a point where we now have to start monitoring and diagnosing and start affecting change prior to disease onset.
Dr. Brian Balin, thank you so much for talking with us on The People’s Pharmacy today.
And thank you so much for inviting me to talk as well. It’s been my pleasure.
You’ve been listening to Dr. Brian Balin, professor of neuroscience and neuropathology at the Philadelphia College of Osteopathic Medicine. He directs the Adolf and Rose Levis Foundation Laboratory for Alzheimer’s Disease Research and the Center for Chronic Disorders of Aging.
Earlier, we spoke with Nikki Shultek, founding director of the Pathobiome Research Center.
Lyn Siegel produced today’s show. Al Wodarski engineered. Dave Graedon edits our interviews. B.J. Leiderman composed our theme music.
This show is a co-production of North Carolina Public Radio, WUNC, with The People’s Pharmacy.
Today’s show is number 1,466. You can find it online at peoplespharmacy.com. That’s where you can share your comments about this episode. You can also reach us through email, radio at peoplespharmacy.com.
Our interviews are available through your favorite podcast provider. You’ll find the podcast on our website on Monday morning.
In this week’s podcast, Nikki Shultek will talk more about patient-led research and help us better understand the root causes of some chronic conditions. Should cardiologists be considering gum disease as a factor in heart disease, as well as the levels of cholesterol and LP little a?
What should health professionals be learning about the infection connection during their years of education? Dr. Balin also uses Schopenhauer’s three stages of truth to shed light on Alzheimer’s research. You could watch the interview with Nikki Shultek on YouTube. Look for The People’s Pharmacy.
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