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Welcome to the Oncology Brothers podcast! In this episode, we dived deep into the world of bispecific antibodies approved for multiple myeloma. Joined by myeloma specialists Dr. Hamza Hashmi from Memorial Sloan Kettering and Dr. Cesar Rodriguez from Mount Sinai, they discussed the latest updates, clinical pearls, and practical insights for community oncologists. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Apple Podcast: https://podcasts.apple.com/us/podcast/oncology-brothers-practice-changing-cancer-discussions/id1653340966 Follow us on social media: X/Twitter: https://twitter.com/oncbrothers Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ Key topics included: Overview of bispecific antibodies, focusing on GPRC5D and BCMA-targeted therapies. Detailed discussion on talquetamab, teclistamab, elranatamab, and linvoseltamab, including dosing, side effects, and management strategies. Insights on managing cytokine release syndrome (CRS), neurotoxicity, and other side effects like dysgeusia, skin toxicity, and infections. Prophylactic measures, including the use of IVIG and tocilizumab, to enhance patient care and quality of life. Whether you're a healthcare professional or simply interested in the latest advancements in cancer treatment, this episode is packed with valuable information. Don't forget to like, subscribe, and check out our other episodes for more insights into oncology! #MultipleMyeloma, #BispecificAntibody, #ICANS, #CRSmanagement, #OncologyBrothers
In this episode, hear Doris K. Hansen, MD, discuss the management of relapsed/refractory multiple myeloma with bispecific antibodies including: Practical differences among approved bispecific antibodies Toxicity profiles of approved bispecific antibodies When to refer patients for evaluation for immunotherapies Considerations for sequencing bispecific antibodies in the relapsed/refractory setting New findings with combination regimens with bispecific antibodies Program faculty: Doris K. Hansen, MD Assistant Member, Blood and Marrow Transplant and Cellular Immunotherapy H. Lee Moffitt Cancer Center & Research Institute Assistant Professor University of South Florida Morsani College of Medicine Tampa, Florida Link to program page:https://bit.ly/4nufxr2 Get access to all of our new podcasts by subscribing to the Decera Clinical Education Oncology Podcast on Apple Podcasts, YouTube Music, or Spotify. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.
Advances in immunotherapies for multiple sclerosis and related disorders have increased the risk of infections and raised important questions about vaccination efficacy. This episode reviews infection risks across treatment classes, emphasizes the importance of monitoring and patient education, and discusses optimal vaccine timing to preserve protective immune responses. In this episode, Aaron L. Berkowitz, MD, PhD, FAAN, speaks with Avindra Nath, MBBS, FAAN, coauthor of the article "Infection Risk and Vaccine Considerations in Multiple Sclerosis and Related Disorders" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Berkowitz is a Continuum® Audio interviewer and a professor of neurology in the Department of Neurology at the University of California, San Francisco, in San Francisco, California. Dr. Nath is the chief of the Section of Infections of the Nervous System at the National Institute of Neurological Disorders and Stroke, National Institutes of Health, in Bethesda, Maryland Additional Resources Read the article: Infection Risk and Vaccine Considerations in Multiple Sclerosis and Related Disorders Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Full episode transcript available here Dr Berkowitz: Over the last decades, there has been a revolution in the treatment of multiple sclerosis, neuromyelitis optica spectrum disorder, and other immune-mediated neurologic conditions with countless new, highly effective medications. However, with every new treatment comes new risks; and in the case of immunomodulatory therapy, many of those risks relate to infection. Today, I have the privilege of talking with an expert on this topic, Dr Avindra Nath, about the infectious risks of treatments for multiple sclerosis and other immune-mediated neurologic disorders. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Berkowitz: This is Dr Aaron Berkowitz, and today I'm interviewing Dr Avi Nath about his article on vaccine considerations and infection risk in multiple sclerosis and related disorders, which he coauthored with Dr Amit Bar-Or. This article appears in the April 2026 Continuum issue on multiple sclerosis. Welcome to the podcast, Dr Nath, and could you please introduce yourself to our audience? Dr Nath: Thanks very much for inviting me to this podcast. I'm absolutely delighted to have the opportunity to discuss our areas of interest and expertise related to infections and vaccinations for MS patients. My area has been studying the infections of the nervous system since the beginning of the AIDS pandemic, and over the years and decades, we've developed expertise related to various types of CNS infections. That includes ones that are developing in individuals who have immune compromise due to a variety of different reasons. Dr Berkowitz: Fantastic. Well, glad to have the opportunity to speak with you today. When I was in medical school---and you were my attending, actually, we were just reminiscing, which we probably think was not that long ago, but is now over twenty years ago---there were just two medications for MS, right? Beta interferon and glatiramer acetate. And now we have over a dozen, and it's amazing to think of all the progress in these last two decades, as well as for related diseases like NMO. I don't think we even had the aquaporin-four biomarker, right, when I was working with you as a med student in the early 2000s. Dr Nath: And that certainly dates me a lot. Dr Berkowitz: Both of us. Dr Nath: Yeah. Dr Berkowitz: Of course, with all these new treatments, these have been amazing advances for our patients, right? But these come with new treatment-related risks to monitor for with the immunomodulatory medications for MS and related disorders. And one of those most important risks is that of infection. So, your article reviews the potential infectious complications of medications used to treat MS, NMO, etc, and also covers considerations related to thinking about vaccines in this patient population. So, as the MS treatment landscape grows, I can say as a general neurologist, keeping up with all these medications and what to screen for and what to worry about and when to vaccinate just becomes more challenging every year. And your article has so many helpful tables, some organized by medicine, some organized by- sorry, medication, some organized by infection, some by vaccines. So, this is gonna be a great resource for our providers to print out and tape up in their clinic rooms. We won't be able to get into all the depth and detail that you have in this article today, but I do want to focus on some of the key points here related to the common medications we use for MS and which infections to think about and which vaccine considerations we might need to keep in mind for these medications. But before we delve into the drugs, I just wanna ask you more broadly, you talk in the article about the challenge of patients with immune-mediated diseases who are on immunomodulatory therapy being at risk for both flares of their disease and for infections; and these infections can present somewhat atypically, right, in immunomodulated hosts, to maybe coin a term you can correct me on, because they can't mount the full inflammatory response. So how do you approach new symptoms in patients on these immunomodulatory medicines as far as distinguishing disease flare from a treatment-related infection? Dr Nath: So, I have to say that although a lot of new treatments have come along for MS, and they've really, you know, improved the outcome tremendously and there are so many different options, it has also kept people like me relevant because they cause a lot of various types of infections, and so keeps me in business all the same. But just as you mentioned, there's so many of them, even I have difficulty keeping track of what does what. So, you do need to be able to refer back to published literature, and the tables, I hope, will be quite useful in that regard. You're absolutely right, and you can get new infections, you can get reactivation of existing infections, and you can get atypical presentations of various types of infections that you may not normally think of. So that presents multiple challenges to the treating physician. The other interesting thing about MS is, just as you mentioned, that you already have CNS lesions to begin with. Now, on top of it, you have an infection, so now how to sort out what is the existing disease and what is the infection, it can again become challenging. But one thing is for sure: all these infections are caused by an organism. So, what you really need to do is, the underlying diagnostic is to demonstrate the presence of the organism. Whether you demonstrate it depending on the infection in the spinal fluid or in the brain or, you know, some peripheral organ system, that is going to be key to making the diagnosis. So, all your clinical acumen is good, but that alone may not be sufficient. Dr Berkowitz: Very good. So, when you see a, a patient now who has a new neurologic symptom in the context of an immune-mediated disease who's on immunomodulatory therapy, what goes through your mind? Are you thinking this disease and this drug, and sort of what are the infections, and does the syndrome match? Or are you thinking, you know, you can't always rely on the imaging to distinguish between, say, a flare of an MS and PML because white matter lesions could look similar? How do you sort of approach this scenario when it comes up? Dr Nath: So, you're right. You have to keep an open mind so that even though you know some infections are more likely to occur with certain types of medications, that doesn't mean that others cannot occur. So, I think when you first see the patient, you should not jump to conclusions, but rather have an open mind. But yes, for example, your patient is on natalizumab, the chances of PML are going to be high. It's a very interesting drug. It does not cause immune compromise in the periphery, but what it's doing is preventing these cells from getting into the brain. So, because then it's acting at the blood-brain barrier. So that means that organisms that are already present in the brain have an opportunity to get reactivated. Turns out you don't have a lot of organisms in the brain, except JC virus seems to be one of them that does somehow, in some individuals, manage to reside out there. And so that can get reactivated. It can get reactivated in the periphery and then enter the brain, too. So, where the very specific mutations have to occur in that virus in order to take residence in the brain. That would be a suspicion that you might have, and MRI can be useful in, again, helping you think about that possibility. If you have typical lesions involving the U fibers, they're demyelinating, usually you do not have much edema around them because patient is immune compromised, but certainly within the brain in these individuals. And so, then you need to demonstrate the organism. The demonstration of the organism should be in the spinal fluid and not in the blood because in the virus, it can-- is reservoir in the kidneys and in the lymph nodes, and periodically it'll shed into the blood. Detection of the organism in the blood can be a false positive, but in the spinal fluid, it shouldn't be there unless you have an infection. Or if you cause a traumatic tap, I guess, if a patient is viremic, that's a possibility, but those are extremely rare. So at least for PML, that's the way that you would diagnose it. Now, you can develop, for example, if an individual is on fingolimod, you can get a wide variety of infections. Here it's a totally different type of mechanism of action. Here the cells are trapped within the lymph nodes, so that means now your entire periphery is immune compromised, right? So here you can get viral infections, bacterial infections, fungal infections. So here, if a patient presents with new neurological symptoms, you have to have a really open mind for all these possibilities. Now, let's say a patient was on dimethyl fumarate, and dimethyl fumarate causes neutropenia early on. So here you have to worry about an individual developing bacterial infections, so latent tuberculosis or bacterial meningitis can occur in these individuals. That's something to keep in mind. It's not that other infections cannot occur with dimethyl fumarate, you can see PML and other things too, but the chances of bacterial infections are greater. So, you got to make sure that you draw all the cultures for that purpose. Similarly, if you're on a complement inhibitor, like a C5 inhibitor or the thing that I could use in NMO, there are the chances of meningococcal meningitis. So, these patients, you need to prevaccinate them before you start these kinds of treatments and look for that possibility. When you suspect bacterial infections, particularly acute bacterial meningitis, there time is of essence. Also, in some of the acute viral infections, for example---herpes encephalitis is another one---you have to be so careful, and if you suspect any of them, even if they're with possibly atypical manifestations, you treat first and then diagnose later, and draw all your cultures, whatever you need to, and just treat them. And these infections can also cause cerebral edema, so one has to be careful about doing spinal taps in these individuals. You want some kind of neuroimaging before you do them. In the days when we didn't have neuroimaging, we used to say, "Okay, if your patient has focal neurological signs or is comatose, you don't do it." But these days, you can get imaging very quickly and very easily. All the-- Because of our stroke management, we've learned how to do them so quickly. So, I think there's little excuse not to do imaging and prevent herniation from occurring. Dr Berkowitz: That's very helpful. So, using the information we know about the drug, and we're going to rapid-fire review some of that in a bit to know what infections the patient is susceptible to, but acknowledging that any patient can get any infection, right? Whether they're on particular medications or not. And then if you're not sure, based on the neuroimaging, which as you said, is helpful, but not always helpful in distinguishing between infections and flares or, as you said, in the case of meningitis, encephalitis, early on at least, especially in immunocompromised or immunomodulated, quote unquote, patient might not see the typical imaging. So really, when safe, getting CSF or cultures, PCRs, and other infectious studies too is really gonna be the definitive diagnostic maneuver here. Is that fair summary across the board? Dr Nath: I think you said that absolutely right. And you summarized that correctly. And, you know, thing about infection, a lot of neurological diseases are, you know, diagnosed by clinical acumen, like your Parkinson's and Alzheimer's and others. Think about infections is caused by an organism, demonstrate the organism, right? That should be your goal. It doesn't mean that clinical acumen is not important, but here you have an opportunity to demonstrate the organism, so you should depend upon that. Dr Berkowitz: Okay. Well, you gave us a nice segue by talking about some of the infections to worry about with some of the medications. So what I'd like to do now for the sort of second half of our interview here is to go through some of the more common medications used for MS, and if we have time, for NMO, and just sort of go kind of rapid fire here, and for each medication, if you can tell us the kind of top infectious concerns and whether when to consider them or what screening needs to take place before or during administration of the medication, and then any vaccine considerations we should be aware of. Some of these will obviously be quite short depending on the medicine. So, going back to the two medications I alluded to earlier that were the only ones in play when you and I last saw each other on the wards when I was a medical student, beta interferon, glatiramer acetate, any infections or vaccine considerations with these medications? Dr Nath: No, I think they're probably your safest medications now as far as immunomodulatory therapies are concerned. These two, and IVIG, if you ever use them, are probably the safest, do not require any vaccine considerations, per se. Dr Berkowitz: Perfect. Okay. So, moving on to fingolimod and others in the sphingosine-one phosphate receptor modulator family, what are the infectious considerations? Any prescreening or vaccination considerations? Dr Nath: I think all your patients should be prescreened for antibodies to JC virus, because there is a risk for PML, and those who are positive should be closely monitored. So, it's not an absolute contraindication for using these medications, but they just require closer monitoring. With this class of drugs, PML is of consideration. Also, these varicella-zoster virus infection, yeah, with that you can develop zoster encephalitis or myelitis. It can present with motor symptoms as well, which can be atypical. You don't usually see them otherwise in immune-competent individuals. So, varicella-zoster, sometimes you can develop encephalitis, also vasculitis with varicella-zoster, so one has to be careful. So, getting the shingles vaccine can be actually very helpful to prevent these things. And then some patients can even develop herpes simplex encephalitis also, and that can be extremely atypical. So, they don't- they can involve the basal ganglia, can involve the brain stem and cerebellum. So again, your index of suspicion should be very high. Interestingly, although HSV encephalitis has been associated with NMDA receptor encephalitis, those reports of NMDA receptor encephalitis have not been published yet with NMS patients. Not sure why, maybe they just have been missed. But that doesn't seem to be a major concern. And then there are a whole host of other infections that can occur with this class of drugs, and that can include toxo; fungal infections, particularly crypto. There's a case report of histoplasmosis; hepatitis virus, particularly hepatitis C; and then the poxvirus is a good example. You can get molluscum contagiosum; warts with papillomavirus; you can get atypical mycobacteria; and even Kaposi sarcoma, which is HHV8. So, there's a huge variety of infections with the sphingosine one phosphate receptor modulators. Dr Berkowitz: And any- aside from screening for JC virus before initiating these, any- and then continuing to monitor for JC antibody index, any other considerations as far as labs to send, monitoring before or on the drug or vaccine considerations for patients on fingolimod and the others in this category, siponimod, etcetera? Dr Nath: Yeah, there are a lot of things to consider. All the details are really available in the chapter if you look at them. But briefly, all the things that one could potentially vaccinate patients for, all these infections I mentioned, one should do so. The timing is critical so that if you can do it before treatment, I think, before starting treatment, that is absolutely important. And you got to give them at least, you know, two to three weeks for these vaccines to take effect before starting your medication. If your patient already arrives on a medication, then you got to play this game of you know, before the next dose, give them again two to three weeks before the next dose and start vaccinating them and get all the vaccines in. Broadly, about the things to worry about the vaccines are you have live vaccines, and you've got the inactivated vaccines or the subunit vaccines. You have to be careful with live vaccines, because if your patient is immunocompromised, that virus can sometimes itself cause harm. For example, you know, yellow fever is one, and there you can develop encephalitis from it. Measles, mumps, rubella, these are all live vaccines. Now, the good thing is that a lot of us have been immunized very early in childhood, but that may not be the case any longer. And so, these things, one has to be very careful with when you're giving live vaccines, that we want to avoid them as much as possible, and individuals are gonna be immune-compromised. But all the others, meningococcus, for example, you should- the HPV vaccines, the varicella zoster vaccines, all these things, you've got to pre-vaccinate and make sure that they have an antibody response to them before starting immunocompromising therapy. Dr Berkowitz: Perfect. Okay, moving on to some of the other orals. What infectious and/or vaccine considerations do we have with teriflunomide? Dr Nath: Okay, yeah. Teriflunomide is a very interesting drug. It's relatively safe. There is concern about the possibility of varicella zoster infection, people have reported that, and also tuberculosis. But PML is extremely rare, if not at all, and we haven't seen herpes encephalitis quite yet. Dr Berkowitz: Got it. How about dimethyl fumarate? Dr Nath: Yeah. So dimethyl fumarate is... as I mentioned earlier, it's interesting because it causes this neutropenia. It's transient, but it occurs early on, and these patients can be at risk of PML, although small. They can develop varicella zoster virus infection, herpes encephalitis, and also fungal infections. For example, cryptococcal infection has been reported with dimethyl fumarate. Dr Berkowitz: Okay. We've spoken a bit about natalizumab and PML, and you have extensive information on this in your article, and I'll defer the reader to that. But for natalizumab, what are the key points every neurologist should know about natalizumab and PML as far as from the practical perspective, screening, frequency of screening, when to worry, when to not use natalizumab at all in the first place based on what you find in your screening for JC virus? What are the key points every neurologist should know? Dr Nath: Uh, yes. You bring up an important point, and that is all patients should be monitored for JC virus. If they're JC virus-negative, so that's your most ideal patient to go on natalizumab, but that doesn't mean they cannot get infected with the virus. In fact, there's an interesting study claiming that, you know, patients, when they get these infusions, they're all sitting in the same room getting infused. Some have JC virus, some don't have JC virus, and so there's the potential that we may be aiding the transmission here in some way or another. The virus is an interesting one. It comes out in urine, and then it's spread through oral contamination, gets into the tonsils, and then spreads from there to your marrow and resides in the kidney and the marrow, as well as the lymph nodes, forever. So, you, you have to monitor these patients to see that during the course, even if they're negative, they could turn out positive. So, every six months or a year, an antibody test should be done on all patients irrespective. If a patient already has antibodies, that's not an absolute contraindication. It just means you've got to monitor them closely for development of new symptoms, and if, whenever there are new symptoms, don't just assume this is due to MS, but just make sure the MRI is done with and without contrast. The- and if there's still a suspicion, that you do a CSF evaluation for JC virus. Just detecting, looking for JC virus in the blood, a rising titer is another thing that can help you. And so, the titer is also important. And the reason you have rising titers is it means that there's an infection that's already occurred in the brain, and the immune system is reacting to that infection by increasing titers. But that alone is not sufficient to make the diagnosis. You still- that gives you an index of suspicion. You've got to then do the MRI and the spinal tap to, you know, be absolutely certain. So, each patient is a little bit different, so the way you monitor them is going to depend on where they are. You know, if they've had prior immunomodulatory therapy before starting natalizumab, or if they're on natalizumab for more than two years, then the chances of PML are much greater, so you may want to monitor them more closely. Uh, they never had any prior immunomodulatory therapy, you're just starting natalizumab, maybe once a year is sufficient. So, I think you've got to tailor it depending on what your risks are for each patient. Dr Berkowitz: Perfect. That's very helpful. And again, you write extensively about PML and natalizumab and PML considerations in your article. So, for a more detailed and in-depth discussion of what we just discussed, definitely hope readers will take a look at your article. Okay. Last but not least---certainly not least, 'cause we're using these probably, it seems, the most commonly in many places I've worked---rituximab, ocrelizumab are B-cell therapies for MS. What are some of the infectious and vaccine considerations related to these infusion medications? Dr Nath: So, there's concern for PML with anti-B-cell therapies also, maybe not to the same degree as natalizumab, but the same principles should be applied. A lot of people think that these are relatively safe. I don't think so. I think we see enough number of patients on B-cell therapies with PML. So, I would use the same caution because these infections are... you know, can be fatal. So, one should be very careful, even with anti-B-cell therapies. And just with natalizumab, you also have the risk of VZV infection causing shingles. HSV1 has been reported, but there's another interesting complication that has been reported with anti-B-cell therapies, and that is severe West Nile encephalitis. And as mosquitoes-borne diseases are getting more and more prevalent, and we're seeing West Nile cases erupting every summer, I think one's got to be, you know, very cognizant of the fact that this can occur. These patients should take precautions to prevent mosquito bites from occurring and not expose themselves to areas where they could be at risk for it. Unfortunately, there is no vaccine for it and no specific treatment for West Nile. So, all one can do is use prevention strategies for mosquito bites. Dr Berkowitz: Yeah, I'm glad you mentioned that. I think the only really truly severe neuroinvasive cases I've seen of West Nile virus have indeed been in patients who were being treated with B-cell therapy. Not, if I'm remembering correctly, for immune-mediated disease, but for a lymphoma, so probably other confounding factors there. But yeah, it's a disease we learn about and think about, but I've only seen the most severe cases in patients who had abnormal immune systems, so I'm glad you flagged that. This has been a very helpful discussion, and I've learned a lot from you. I learned a lot from your article, just as I did when you were my attending some 20-something years ago on the wards when I was a medical student. So, it's good to continue learning from you through your writing and research, and today from getting to talk to you again. I encourage our readers to read your article and to bookmark those tables for when these considerations come up for your patients on these immunomodulatory therapies and you're wondering which infections to worry about and how to manage vaccines in this patient population. So again, today I've been interviewing Dr. Avi Nath about his article on vaccine considerations and infection risk in multiple sclerosis and related disorders, which he wrote with Dr. Amit Bar-Or. This article appears in the April 2026 Continuum issue on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thank you again to our listeners for joining today. Dr Nath: Thank you so much, Aaron, for that wonderful interview, and I'm extremely proud of all your accomplishments over the last 20 years. You've done an amazing job, and it was such a pleasure to see you and to be able to do this interview with you. Thank you again. Dr Berkowitz: Thanks. That means a lot. I never would have imagined- we won't say 20, how many, but 20-something years ago as the medical student looking up to you and all your expertise on these infections and all of your research that led to so much of our understanding on these, that I would find myself interviewing you two decades later. So, for all the students listening, you never know where you'll end up, but I appreciate your very kind words. Dr Nath: That's what we hope for all our students. Thank you so much. Dr Berkowitz: Thanks again. Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
In this episode, Muhamed Baljevic, MD, FACP, and Johnathan Ticku, MD, discuss various strategies to optimize the use of bispecific antibodies in their practices for the treatment of R/R MM through patient monitoring, dosing in outpatient settings, and using tocilizumab and IVIG, among other management strategies. Presenters: Muhamed Baljevic, MD, FACP Associate Professor of Medicine Division of Hematology-Oncology Department of Medicine Director, Multiple Myeloma Program Director, Vanderbilt Amyloidosis Multidisciplinary Program (VAMP) Co-Chair, Scientific Review Committee, VICC Disease Team Lead, Plasma Cell Dyscrasias and Lymphomas Vanderbilt-Ingram Cancer Center Vanderbilt University Medical Center Nashville, Tennessee Jonathan Ticku, MD Medical Oncologist and Hematologist GU Oncology Lead, Mayo Clinic Health System Assistant Professor of Oncology, Mayo Clinic La Crosse, Wisconsin Link to full program: https://bit.ly/4u0xH6q Get access to all of our new podcasts by subscribing to the Decera Clinical Education Podcast on Apple Podcasts, YouTube Music, or Spotify. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.
In the last episode of this series, Dr. Justin Abbatemarco and Dr. Benjamin P. Trewin discuss how to apply this data into clinical practice. Read more about this abstract on the AAN website. Show transcript: Dr. Justin Abbatemarco: Hello, and welcome back. This is Justin Abbatemarco and I'm joined by Benjamin Trewin where we're reviewing top abstracts from the AAN annual meeting in Chicago. Today we're talking about his abstract maintenance immunotherapy and MOGAD, early steroid benefit, dose thresholds, and disability risk. Ben, we've done this really great job of dissecting the data, steroids, non-steroidal agents. How do you think about the treating MOGAD cases in clinic though? How do you try to put this data and the data we've talked about into clinical practice? Dr. Benjamin P. Trewin: It's obviously a very good and actionable question, and our research has always tried to focus on these dilemmas facing the clinician at the bedside. And so the way that we think about this is, of course, we try to come up with some rules or some guidelines to treat all patients, as that's the most effective way of giving the message, but we need to acknowledge there is variation within MOGAD patients. There are people with low relapsing propensity who will take a very long time to relapse. You'll need to follow them for a long time. And there are ones with high relapsing propensity. So some of our previous work, we actually reviewed thousands of MOGAD patients in the literature and found that if you follow them for more than five years, over 70% actually relapse. It's just a matter of following them. So acknowledging this variation in the patients is important, but at the same time, the guideline we would probably endorse based on our research is that all patients with MOGAD after a first attack should be treated with oral corticosteroid taper, including at least five months of 12.5 milligrams per day oral corticosteroids. Now, how does that work in practice? Well, you would probably start them, and I say probably here because we don't have the strength of evidence for the very start of the course and the very end. But what did we do? Well, we start them at about one milligram per kilogram. And over probably about two to three weeks, you can bring them down to about 12.5 milligrams per day, or in children, 0.16 milligram per kilogram per day. And then you'll do that four or five months. And then over two or three weeks after that, you would step them down. Of course, you want to be careful that you don't have any adrenal issues. You would want to go slow enough for that. But at the same time, you don't want to prolong the course too long and put yourself at risk of side effects. Dr. Justin Abbatemarco: I think that's really helpful and practical. And you don't need these huge doses, it looks like, to treat these patients well and trying to really be mindful of those side effects that are truly dose dependent. And then yeah, we have some really great data. We need some randomized data to help us inform next steps, but this retrospective data, we're starting to put together this picture around B-cell depleting IVIG like we talked about. So super helpful. Ben, really excited to see you at the annual meeting. And yeah, thank you for your time and expertise.
In the second episode of this series, Dr. Justin Abbatemarco and Dr. Benjamin P. Trewin discuss what was found in non-steroidal maintenance therapies. Read more about this abstract on the AAN website. Show transcript: Dr. Justin Abbatemarco: Hello and welcome back. This is Justin Abbatemarco from the Cleveland Clinic. And we're joined by Ben Trewin on his abstract maintenance immunotherapy and MOGAD, early steroid benefit, dose thresholds and disability risk. Ben, in our first episode we really talked about corticosteroids, but your paper and abstract looked at other therapies. What did you find in those non-steroidal maintenance therapies? Dr. Benjamin Trewin: In addition to looking at oral corticosteroid therapies, we also looked at B-cell depleting therapies, namely rituximab and ocrelizumab, and intravenous immunoglobulin and steroid-sparing therapies, namely azathioprine and mycophenolate predominantly, I suppose a couple on methotrexate. Now, what we found, it's important to note that we were able to tease apart the effects of all these drugs with our Cox proportional hazard model chops up, follow up into distinct intervals with different combinations and permutations of these medications and their different doses in a more granular way than is allowed by previous techniques like incident rate ratios when we compare pre and post annualized relapse rate, and we think this is a strength of the study. With this methodological strength, we were able to see that steroid-sparing therapies, despite 334 patient years of data, do not appear to have any independent benefit with respect to time to next relapse. The estimate of effect there was 1.06. And then for time to confirm sustained disability, there was also no confidence signal, the confidence interval being 0.15 to 1.4, that it actually prevented any disability despite a wealth of data, which I think is an important thing to note. And I think previous studies, particularly looking with incident rate ratios, have been a little more optimistic with that. And I think there might be misattributing some of the benefit of concomitant steroids to the steroid-sparers, but it's more complex than that, of course. And then with respect to B-cell depleting therapies, we did have 48 of 261 patients exposed, which is reasonable, but not quite enough to get the signal we're looking for. However, we found something quite interesting, because when we compared the Liverpool data to the Australasian data, the two big study groups involved, we saw that it wasn't quite as effective in Liverpool as it was in Australasia in this subgroup analysis. And so we dug a little deeper, as one should, and found that the dosing is actually different. And in Australasia, we have a tendency to just give two grams of rituximab up front, or 600 milligrams of ocrelizumab. And then six-monthly, you give a gram of rituximab without fail, without trying to watch the B cells or trying to muck around with doses in any way. And when we looked at that, the threshold dosing, as we termed it, as compared to below threshold dosing, there actually was weak evidence at a PVA of 0.08 that threshold dosing is superior to below threshold dosing. And that needs to be reproduced, but I think that was an important signal. And finally, I would say IVIG, of course, has some very strong data in this area. And I think it's important from this study at least to remain a little agnostic on that as we only had 31 patients on IVIG, and so I absolutely wouldn't say it's not effective. I would say unfortunately, we had insufficient data to make any big claims about that. Dr. Justin Abbatemarco: I think some really great data to help pick apart here and help inform practice. I think your point about looking at the previous literature and trying to tease apart these steroid-sparing agents, that corticosteroids they're not uniformly addressed, and so it's difficult to think about at those previous data points, so I appreciate that. And then this dose response to the B-cell therapies, there's been questions in the literature, because I think we've gotten a lot of mixed results on B-cell therapies. And so this to me is one of the larger studies that really help answer this question that maybe B-cell therapies are effective and maybe we need to be a little more sensitive to dose, which is the same theme we saw on IVIG. IVIG, maybe at higher doses, could be more effective for MOGAD. What do you think about that comparison? Dr. Benjamin Trewin: I like where you're going with that because we're quite interested in these dose responses as we introduce this 12.5 milligram per day oral corticosteroid dose or 0.16 milligrams per kilograms per day in kid. And so we're quite interested. And, of course, that work by Dr. Chen and Dr. Mariner has revealed that IVIG also has quite a sensitive dose threshold there at one gram every four weeks. And we followed that precinct because that research was so strong. So it's nice to feel like we're building on previous studies and then perhaps even detecting another dose threshold with respect to rituximab. And I must say, it was a little bit of a surprise, we came in and saw why is the Liverpool data moving that way and the other one moving this way? So it was a nice data-driven evolution of our multi-variable model. Dr. Justin Abbatemarco: So helpful. And I'll ask everyone to come back for the final episode, where we try to put this all together. We're going to put Ben on the spot and really understand how he approaches these cases in clinical practice. Ben, thank you. Dr. Benjamin Trewin: Thanks very much, Justin.
Although rare, recognizing NMOSD is crucial for improving patient outcomes through correct diagnostic and treatment approaches. Reports of atypical forms and increasing knowledge of clinical, imaging, and laboratory-specific features are fundamental for the accurate recognition of this condition. Research on targeted therapies and biomarkers measuring and predicting disease activity will improve NMOSD management. In this episode, Gordon Smith, MD, FAAN, speaks with Sara Mariotto, MD, PhD, coauthor of the article "Neuromyelitis Optica Spectrum Disorder" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Mariotto is a neurologist in the Neurology Unit in the Department of Neurosciences, Biomedicine, and Movement Sciences at the University of Verona in Verona, Italy. Additional Resources Read the article: Neuromyelitis Optica Spectrum Disorder Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: Neurology is an increasingly therapeutic specialty, and across many of our subspecialty areas, lots of new drugs are being approved. Are you interested in learning more about a historically disabling disorder for which we now have a spectrum of new therapies that, if used appropriately and promptly in the right clinical situation, promise to dramatically improve patient outcomes? If so, keep listening. My name's Dr Gordon Smith. Today I'll be talking with Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today, I'm interviewing Dr Sara Mariotto about her article on neuromyelitis optica spectrum disorder or NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 Continuum issue on multiple sclerosis. Sara, welcome to the podcast, and maybe you can start by introducing yourself to our audience. Dr Mariotto: Yes. Thanks, Gordon. I'm Sara Mariotto. I'm a neurologist, and I work at the Neurology Unit, University of Verona, where I do both clinical diagnosis and research into neuroimmunology---so, in particular, autoimmune encephalitis, NMOSD, and MOGAD. Dr Smith: Well, this is a super exciting area. Whenever I hear about NMOSD, I think of one specific patient I had, and I always think of her when I come across something like your article, which is really fantastic. So, before we dive into the details, I wonder if maybe you can just explain to our listeners who aren't up to speed on what NMOSD is, what the disorder is, and maybe why it's so important that all of our listeners learn how to recognize it quickly and get people started on therapy. Dr Mariotto: Yes, sure. So, neuromyelitis optica is an inflammatory autoimmune CNS disorder usually associated with aquaporin-4 antibodies, although there are a few cases, around 10%, who can be antibody-negative. And I think it's very much important to have in mind this disease and recognize it because it can be severe, as you pointed out; can present with very severe optic neuritis, myelitis, the brain stem, or area postrema syndrome. So, it can be really severe, affect quite young people around 40 years of age---although it can affect also the pediatric population and elderly people---and, importantly, it can be treated. It's very much important to treat this patient in the acute stage very quickly with steroids or plasma exchange in addition, and then to start a chronic treatment. So, we have treatment for this condition. So, it's very much important to, to recognize it quickly and treat the patient properly. Dr Smith: So, I wonder if we can talk a little bit about the diagnostic criteria and boundaries of NMOSD, right? So, someone who comes in with bilateral op- severe long segment optic neuritis or long segment myelitis, we think about it. But what are the boundaries? Should we be looking for this, for instance, in someone who comes in with a unilateral optic neuritis or looks like typical multiple sclerosis? Is it important to get aquaporin-4 antibodies in those patients? What do the diagnostic criteria say about this? Dr Mariotto: So, I wouldn't test aquaporin-4 antibodies in all patients with demyelinating conditions because although aquaporin-4 antibody assay is very specific, as for all assay and all antibody testing---also for MOG antibodies, for example---some false positive results can come out. So, I would suggest to test aquaporin-4 antibodies not in typical MS cases but in those who could be suggestive for not being MS, so in all those cases with atypical optic neuritis and myelitis or other syndromes. For those cases, it's important to test aquaporin-4 antibodies, but I wouldn't test them in all typical, classical MS cases. As I said, it's quite specific, the assay, so it's uncommon to have false positive results, but it can be. Dr Smith: Serum, CSF, both? Dr Mariotto: So, for aquaporin-4 antibodies, they're usually present in serum. They can be positive also in the CSF. And there are a few reports of isolated CSF positivity. But if we analyze larger samples volume, then it becomes clear that isolated CSF positivity is so, so rare that it's not recommended to test them in the CSF when serum is negative. So, for aquaporin-4 antibodies, the recommended matrix of testing is serum, which is different for MOG, which is not the topic of our article but is important to mention because MOG antibodies should be tested in serum and CSF. But aquaporin-4, I would recommend to test serum. Dr Smith: What are the boundaries between MOGAD and NMOSD? And you talked about the differential testing of antibodies, which I was going to ask about. But when should we think of NMOSD relative to MOG? Dr Mariotto: Yeah. There are aspects which are the one mentioned in the criteria, highly suggestive for NMOSD. But the clinical spectrum can be similar to that of MOGAD. Usually, although there are some clinical aspect---like, for example cortical encephalitis or ADEM, which is more typical for MOGAD, or others like area postrema syndrome, which are more typical of NMOSD. The spectrum can be similar among the two conditions, so that's why in our clinical experience, usually they ask both aquaporin-4 and MOG antibodies in patients. It's- for experts, it can be easy to differentiate the two conditions, but for nonexperts can not be so easy. Dr Smith: Can you define area postrema syndrome? I think not all of our listeners see that every day. Dr Mariotto: Yeah, sure. This is a syndrome which is highly suggestive of NMOSD. That's why I mention it. And it's characterized by nausea, vomiting, hiccups are known as the syndrome. And it is very, very suggestive because of the expression of aquaporin-4 in that area of NMOSD. That's why I strongly recommend for all patients who comes out to have this syndrome to test for aquaporin-4 antibodies. MOGAD is hardly ever positive for that, so I think that whenever you see a patient with that syndrome, you should think about NMOSD. Dr Smith: I'm just curious, aquaporin-4 is a water channel, which is kind of an interesting concept. Our conversation, I really want to make sure we give clinically important information to folks, but it's so curious to me at least, how does this actually result in a inflammatory demyelinating syndrome? For a simple neuromuscular guy, what's the immunopathogenesis of this? Dr Mariotto: Yeah, the immunopathogenesis is quite complicated, as in all CNS disorders. And of course, aquaporin-4 antibodies are the main focus, but they are not the only one. As you said, aquaporin-4 antibodies have a target, this water channel, which is at the basis of the disease, and they are produced by the interplay between T cells, B cells, and plasma cells. But then also eosinophils, macrophages, cytokines, and chemokines are involved, enter the CNS, and then another important component is complement, which is highly activated in this disease. At the end, we have astrocyte damage because astrocytes are the main target of the disease, but also axon and myelin are involved. So, it's a quite complex pathogenesis based on the antibodies, but not only on that. Dr Smith: And this will become important when we start talking about treatment. There seems to be a recurring theme of long segment demyelination, right? Optic neuritis is typically a large percentage of the length of the optic nerve, and obviously the myelitis se- more than three segments. Do you see other long segment areas of CNS demyelination, corpus callosum or things like that? Any ideas why that is, if that's true? Dr Mariotto: Of note, this is quite interesting because usually when we have NMOSD, we have a longitudinal involvement, especially of the optic nerve and spinal cord, while brain lesions are quite different. Like, we usually do not have the typical Dawsen fingers-like lesions that we have in MS, for example, or the classical periventricular or subcortical extensive lesions that we can see and we have in mind when we think about MS. In some cases with NMOSD, the brain is completely negative, so we do not see anything. And Dawsen lesion's quite suggestive of NMOSD. So, you're right. I mean, this is related partially to the expression of aquaporin-4, and that's why we have this typical involvement also for area postrema, for example, and maybe also our other examples of clinical aspect that we can see in these conditions. But it's basically linked with the expression of aquaporin-4, which is the main target of the disease. And that's why usually the brain doesn't show so much involvement as we can see in MS, for example. Dr Smith: I was actually really interested in some of the unusual manifestations or phenotypes, and I don't want to get into arcadia, really, but which of these should our listeners be familiar with that would really suggest that they should be thinking about NMOSD beyond the area postrema and other features that we've already talked about that are part of the core criteria? Dr Mariotto: Yeah. I mean, I think that the encephalic syndromes or also ADEM, which is most typical of MOGAD but can be observed also in NMOSD or PRES, for example, are syndromes that can be considered in patients with NMOSD. There are the typical ones, which are the ones showed in the criteria, but whenever we have a brainstem involvement or, like, these encephalic syndromes or also PRES, we should think about NMOSD also. Dr Smith: Another area I was interested in are red flags. In your article, you talk about red flags that might suggest an alternative diagnosis, right? And then this presumably is particularly important in seronegative patients, which 10% is not a reasonably high number, I suppose. What are red flags we should be thinking about for some other diagnosis? Dr Mariotto: Yeah. I would here mention two very important red flags. The first one is a very hyperacute onset. Usually these conditions, these inflammatory conditions have a subacute onset, so whenever you have a very, very acute onset, you should think about something else. This can occur sometimes also in NMOSD, but hardly ever occur. Like, a very acute myelitis, the first thing we should think about is a vascular origin, for example, with a lot of pain and not about NMOSD, although sometimes the differential diagnosis is not so easy. The second thing is a progression independently of relapses, which hardly ever occur in NMOSD. Usually in NMOSD, we have the onset, and then we have a relapsing disease course. That's why we have to treat patients always and not to stop treatment. But we do not have progression in the meanwhile, while we can have, for example, this in MS. Same thing is for MOGAD. So, these are two things that I think is very much important to keep in mind. Dr Smith: I want to pivot to talk about treatment because that's been super exciting. But rumor has it there are new diagnostic criteria coming for NMOSD in the next year. I bet you know a bit about those. Can you give our listeners any indication about kind of where the puck is going on this? Not so much what the criteria are specifically, but what sort of diagnostic challenges are the new criteria going to help us with once they come out? Dr Mariotto: Yeah. So basically, we are working on that, so you will read them in the next future. This is the good point of the conversation on the new criteria. And we work a lot on the definition, on the new definition and nomenclature of NMOSD; on the definition of seronegative NMOSD, which is also quite tricky; and then on the assay we should use to test aquaporin-4 antibodies, and also on potentially new syndromes which should be included into the main feature of the disease. But hopefully you will read about this very soon. Dr Smith: Looking forward to it. And Continuum Audio listeners, you heard it here first, so thank you. Let's pivot to treatment. This has been super exciting, and I wonder if the way to approach this is to start with acute management and then sort of chronic management. Would that make sense? Dr Mariotto: Sure. Dr Smith: Let's say I go on service on Friday, and I have a patient who comes in with positive aquaporin-4 and bilateral optic neuritis. What's the acute approach to managing that patient? Dr Mariotto: So, the first approach is to administer intravenous steroids, but I would not wait to escalate to plasma exchange. There is quite good evidence that we should treat the patient with additional plasma exchange very quickly, and every day of delay of plasma exchange can cause increased disability. So, we should treat patients with steroids first, and then if we are not satisfied by the recovery, soon start with a plasma exchange. There is also some evidence, although less, for IVIG, but it's important to try to treat them very quickly, even if it's Friday, you know, there is the weekend and so on. But I think it's very much important to start with steroids after excluding other infectious causes or so on, and then to start quickly with plasma exchange. The main problem could be that we do not have the results of the antibody yet. Dr Smith: Right. So, let me ask that question. You know, let's say my patient comes in on Friday, and clinical syndrome that really looks like NMOSD, and we're waiting for the aquaporin-4. There are many places where it's hard to get plasma exchange over weekends. And so, in that setting, are you better off doing the steroids over the weekend then PLEX on Monday, or should we just give IVIG because maybe it's as good as PLEX? What's your advice there? I'm trying to get ready for Friday because I know one's coming in. Dr Mariotto: That's true, that's true. Usually they come on Friday or Saturday. I think it's acceptable to have three days of steroids and see how the patient improves, and then after three days to start with plasma exchange. Actually, we have a very good improvement if we start between three and five days after onset. So, I think waiting for three days is acceptable just because we can see if the steroids work properly or not, and then we can quickly start to plasma exchange. But I would not wait, like, 10 days, you know, before starting with a plasma exchange, and I would not wait for antibody results. Dr Smith: Got it. Super helpful. And I'm actually not joking around, I learned recently that I have a reputation among our residents for having lots of optic neuritis when I'm on service, which I think is sort of karmic justice for being a peripheral nerve expert. But let me ask another question. So, let's say we do that, and the patient gets three or five days of pulse methylprednisolone and five courses of PLEX, and they're not doing well. Do you then just move right along into another agent B cell depletion therapy? I mean, what's your next step in escalation in the acute setting? Dr Mariotto: I would for sure start to, as you said, with steroids, plasma exchange, and in case IVIG, and then quickly move to chronic treatment. And for patients who are not recovering well, I would think of something which has a quick effect so we can really start treating patients very quickly. There are different options. And all over the world, there are different rules for using immunosuppression in NMOSD. Like in Italy, for example, it's different from US or other countries, Germany, for example. There are different approved treatments and different rules of using them before or after rituximab, for example. We all know that there are treatments approved for NMOSD all over the world. But in some countries, like for example in Italy, we should use rituximab first, and then if it doesn't work, escalate to the approved treatment. I know in the US it's different. But anyway, for a patient who does not improve quickly, I would start with something which has a quick effect on the disease. Dr Smith: And then rituximab versus inebilizumab, you know, CD20, CD19, what's your advice there? Is one preferable to the other, you know, if we have options to do either? Dr Mariotto: Yeah. So, between rituximab and inebilizumab, we know that the target, well, is different, but is anyway B cells, so CD19 and CD20. With CD19, we can affect both plasma blast, plasma cells, and B cells. That's why the target is broader. And of note, this is an approved drug, while rituximab is, in most countries, used as off-label treatment. Dr Smith: So inebilizumab would probably be preferable if we're able to do that. Dr Mariotto: Unfortunately, there are not so many studies comparing rituximab with the approved drug, which is, of course, a pity, but that's the case. While we have clinical trials for all the approved drugs, and although the trials were designed differently, as we mentioned in the Continuum paper, we can argue something of the comparison between the approved drugs. But it is not so clear the comparison between rituximab and the new drugs, which is also something that we should work on. Dr Smith: And then for chronic suppressive management, what other options are there? Dr Mariotto: So, in addition to B cells, target can be interleukin-6, as we know with tocilizumab or satralizumab, and then complement with eculizumab. These drugs are both based on the pathogenesis of the disease. That's why we also discuss it in the paper, which shows a clear involvement of complement, and among cytokines of interleukin-6. So, targeting these made clear that could improve the disease quite well, and that's why they designed some clinical trials on these drugs, which are now approved, as we said, for NMOSD. Dr Smith: Wow, so many options, and a lot of questions, but limited time. Let me just ask a couple of more. I see a lot of myasthenia patients, and there's a lot of variability, as you know, in patients with myasthenia, the extent to which complement is an important mechanism versus other, you know, important mechanisms. To what extent is response to a complement inhibitor kind of uniform across NMOSD? Or there's some patients who just don't respond to a complement inhibitor and others that respond really well. And then just, I'll just give my second question out is, you know, what about combination therapies for patients who have particularly challenging NMOSD? Dr Mariotto: So usually these patients have a terrific response to complement inhibitors, and this is also shown by the clinical trials where we saw how eculizumab have a very impressive effect on the disease. And also, maybe this is also your experience, a very quick effect. So that's why there are also thoughts on using it in a very acute stage of the disease. That was what I was thinking about before. But then it has a very huge effect on complement, which is a major factor involved in the pathogenesis of NMOSD also in the chronic disease stage, and that's what also we see from clinical trials. Usually, we prefer to switch treatment from one to another and not to combine them. Of course, in very difficult cases, this can be considered, but the recommendation is to switch from one of these approved drugs to the other, or from rituximab to one of the approved drugs, and try to find out the best for our patient before combining them. Dr Smith: The complement inhibitor trials are breathtaking, at least for me. If I'm trying to convince students to go into neurology, I'll say, "Take a look at that paper," because anyone who claims that we're "diagnose and adios" is so wrong. It's so exciting. So, at a high level, this must have fundamentally changed outcomes for patients. I mean, it's still a difficult disease, but what is the kind of prognosis for that patient I described who comes in, gets the therapy you talked about? What does their long-term outcome look like in this modern therapeutic environment? Dr Mariotto: So, NMOSD is almost always a relapsing disease. That's why, as we mentioned, we have to treat patients always. But the prognosis changes a lot since we were also able to use all these drugs for the disease. So, the prognosis changes if we recognize it properly and early, and if we treat NMOSD properly with immunosuppressives. So, whatever we choose it's important to start it quickly, and this is the only way that we have to improve the prognosis of this disease. We have very active cases, but we have also cases who responds quite well to this immunosuppressive treatment, since now we have, as mentioned, these ones which are very impressive and show incredible results. So, the prognosis of the disease change in the last year, thanks also to the improvement of the diagnosis and of the treatment choices for the disease. Dr Smith: I'm just... I- maybe my last question, you know, just at a personal level, not only for you as an expert who's caring for these patients, but in the patient community, this must have been a pretty exciting period of time, right? I mean, these, these drugs are coming fast and furious, and what a change. What's the kind of zeitgeist in the community, both your professional community and amongst the patient community about where we are? Dr Mariotto: Yeah, you're right. The last years were defined the years of NMOSD and also MOGAD because we had finally approved drugs which is relevant for all the disease that we treat and changed the landscape of the disease for clinicians, but also for patients. And we have more than one, as we said, so we have more options that we can also discuss with patients to try to choose the best one in terms of activity, but also route of administration or time. Some years ago, we just had rituximab, which is not approved in most of the countries, and now we have different approved drugs. And we improved the diagnosis of the disease thanks to the availability of live cell-based assay. And then we are working a lot also on biomarkers like GFAP, for example, which has been shown to be a very attractive biomarker able to mark disease activity and maybe also prognosis on this disease. So, you're right. I mean, in the last years, the landscape of NMOSD changed a lot. Dr Smith: Sara, thank you so much for talking with me. I could keep going for another half an hour, but I would be in trouble with my editor, so I think we probably need to wrap it up. But thank you so much. This has been very informative. Dr Mariotto: My pleasure. Dr Smith: Mine too. Thank you. Again, today I've been interviewing Dr Sara Mariotto about her article on NMOSD, which she wrote with Dr Romain Marignier. This article appears in the April 2026 issue of Continuum on multiple sclerosis. Be sure to check out Continuum Audio episodes from this and other issues, and thanks to you, our listeners, for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
Send us Fan MailA healthy 26-year-old starts feeling “off,” and within weeks she can't walk, can't swallow, and can't trust her own body. We share a mother's firsthand account of her daughter Heather's 13-month fight with Guillain-Barré syndrome (GBS), a rare autoimmune neuropathy that attacks the peripheral nervous system and can lead to rapid paralysis, severe pain, and terrifying complications. This is a story about what GBS looks like in real life, not in a brochure: the confusion at the start, the scramble for answers, and the way everything changes when symptoms accelerate.We also talk honestly about the healthcare system from a family's point of view. You'll hear about repeated hospital visits, discharges that don't match the severity of decline, and the fight to get treatments like IVIG at the right time. We unpack the emotional weight of watching swallowing fail, nutrition drop, and rehab become a daily grind, plus the moments that raised serious questions about basic safety and attentive care. If you've ever had to advocate for a loved one, this conversation will feel uncomfortably familiar.And running through it all is faith: the prayers a parent prays, the fear of praying “the wrong thing,” the surprising people who show up with compassion, and the way hope can coexist with grief. We leave you with practical perspective on patient advocacy and rare disease awareness, and a reminder that caregiving is both relentless and sacred.If this moved you, follow the show, share the episode with someone who needs it, and leave a review so more people can find this story. What part hit you the hardest?Support the showBE PROVOKED AND BE PERSUADED!
Familiarity with the clinical, MRI, CSF, and serologic features of MOGAD can help neurologists recognize this condition in clinical practice. Awareness of the utility and pitfalls of the MOG antibody test is critical. The current therapeutic approach is guided by retrospective studies and the application of immunotherapies used in other autoimmune neurologic disorders. In this episode, Gordon Smith, MD, FAAN, speaks with Eoin P. Flanagan, MBBCh, coauthor of the article "Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease" in the Continuum® April 2026 Multiple Sclerosis and Related Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Flanagan is a professor of neurology and the division chair of the Division of Multiple Sclerosis and Autoimmune Neurology in the Department of Neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @GordonSmithMD Full episode transcript available here Dr Smith: So, what neurological disorder can cause bilateral optic neuritis, transverse myelitis, ADEM, or can mimic acute flaccid myelitis, intracranial hypertension, viral encephalitis, or cause seizures? Sounds like the great imitator, perhaps. If you want to know and learn more about this syndrome and how you can treat it---and it is very treatable---keep listening. My name is Gordon Smith, and today I have the great opportunity to talk with Dr Eoin Flanagan from the Mayo Clinic on his article on myelin oligodendrocyte glycoprotein antibody associated disease, or MOGAD, which is in the April 2026 issue of Continuum on Multiple Sclerosis and Related Disorders. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing Dr Eoin Flanagan about his article on myelin oligodendrocyte glycoprotein associated disease, or MOGAD, which appears in the April 2026 Continuum issue on multiple sclerosis and related disorders. Eoin, welcome to the podcast, and please introduce yourself to our audience. Dr Flanagan: Yeah, thanks so much. I'm Eoin Flanagan. I'm a neurologist at the Mayo Clinic. I'm originally from Ireland. I work in the neuroimmunology lab at the Mayo Clinic, and work and see patients with MS, MOG, and autoimmune disorders here in Rochester, Minnesota. Dr Smith: Your article is super interesting, I think, and this has been a really rapidly evolving area over the last, you know, many years. We have many more antibodies, and MOG is something that's been around for a while, but we've certainly learned a lot more about it. This is a topic that I think will be familiar to most of our listeners, but I wonder if maybe you can just begin by laying the foundation. Like, what is MOG? What's its typical presentation? Dr Flanagan: So, MOG is a protein on the surface of the oligodendrocyte or its CNS myelin, and it was always of interest as a potential antibody target, and initially it was investigated in multiple sclerosis. But subsequently, we recognized that the antibodies to MOG have a specific syndrome, of which about a quarter of patients are pediatric and then the remainder are adults. And they can present with a variety of syndromes, probably most commonly optic neuritis, but also acute disseminated encephalomyelitis, or ADEM. Transverse myelitis can also occur, and then some other unusual brain and brainstem cerebellar syndromes can also occur. Dr Smith: I was really impressed in the very broad phenotypic spectrum of MOG. We'll talk more about that, of course. But I wonder if maybe you can tell us when we should be ordering MOG antibody? Given this broad variability, does anyone who has a CNS demyelinating disease need a MOG assay, only specific phenotypes? What guidance do you have for our listeners? Dr Flanagan: Yeah. It's a great question. So, I think you have to be a little bit careful because the MOG antibody test is a little bit sticky. So sometimes we can see some low-positive false positives. So, we don't wanna order it in every single patient with classical MS. So, I suppose we'll start with who not to order it in. I think it's also a very optic nerve- and optic neuritis-central disease, so I think you really need to be considering this in a patient with optic neuritis who does not have lesions in the brain suggestive of multiple sclerosis. And then we think about some of the features: if the lesion, the enhancement along the optic nerve is long, if it's bilateral, if there's a lot of optic disc edema accompanying that, we tend to think about MOG antibodies. And then children with demyelinating disease, MOG is over-represented in that cohort, so it accounts for about a third of those. So, if you have a child with CNS demyelinating disease, particularly if they're under twelve, with ADEM presentations or other presentations, you probably want to be ordering the MOG antibody test. And then a longitudinally extensive transverse myelitis in adults, certain types of cerebral phenotypes that we can get into, you would want to consider ordering MOG antibodies too. Dr Smith: Now, you point out in the article that it's really important that laboratories use the cell-based assay for MOG as opposed to an ELISA, for instance. Is this something folks need to be very attentive to, or are all of the commercial laboratories now using a cell-based assay? Dr Flanagan: Yeah. I think all of the commercial labs are using cell-based assays, so we don't really get into much of an issue. There are some differences between serum and CSF, so really, serum is the optimal sample to order. There is also some differences between the live cell-based assay and the fixed cell-based assay, where the live cell-based assay may have some advantages in terms of sensitivity. And then CSF is kind of still under evaluation about its role in the condition. So in general, it's a serum test. And then we have to remember that the antibody tends to be highest at the onset, and then it goes down over time. So, if you delay your testing or you're testing a patient long after the condition, it can go negative, for example. So it tends to be highest both around the relapses and particularly at the onset of the condition. Dr Smith: You mentioned earlier that the test is sticky, which I take to mean that there is some risk for low-titer false positives. How do you navigate that situation? When should we be suspicious about a false positive? Dr Flanagan: Yeah. I think there's some very useful features that can help you. You know, the main differential diagnosis is going to be multiple sclerosis, particularly in the US, in regions of the northern US where MS is particularly common. So, you really wanna be making sure that if you get a positive result, low positive, that it's not multiple sclerosis. And some of the best discriminating features are CSF oligoclonal bands. They're about 85% in MS and about 15% in MOG, so an easy number to remember, 85 and 15. And then the lesions in MOG, the brain lesions, tend to disappear over time. So, if you have the advantage of that follow-up MRI a year down the line, about 70% of lesions in MOGAD will resolve, while in MS, as we know, the term means multiple scars, so the MS lesions tend to persist over time. So, they are two quite useful features that can help discriminate. Dr Smith: And how about specific phenotypes or areas of involvement or imaging abnormalities that suggest MOG? One of the things I found really interesting in your article is there are a host of different syndromes that I think had largely been previously described, many of them, that became clear later that these were really tied to MOG antibodies. Presumably, that's helpful in interpreting the antibody assay in that patients who have, perhaps, a borderline low titer, for instance, but have a very typical phenotype are more likely to have MOG than those who have a more clearly MS-type phenotype. Dr Flanagan: Yeah, absolutely right. Yes. So, there's certain phenotypes that we don't tend to see with MS. The acute disseminated encephalomyelitis, or ADEM, is one that's particularly common in children. And about half of people that have ADEM will be positive for the MOG antibody. So that's a syndrome you need to look out for, which would be often in children, encephalopathy, and they would have multifocal white matter lesions, sometimes involving the gray matter. A second syndrome that was an interesting discovery from a Japanese group was this unilateral cerebral cortical encephalitis, where patients can have this swelling and T2 hyperintensity, often just on one side of the brain. And it's in the cortex, and some of those patients won't have any white matter lesions. And in that situation, it's important to order the MOG antibody, and that seems to be a specific phenotype of MOGAD. But sometimes people don't think about it because the white matter is not involved. So, if you see these patients, they often present with seizures, sometimes they even have fever accompanied by it. And if you see those patients and see this radiological feature, then you really want to consider ordering the MOG antibody too. Dr Smith: Yeah, I found that really interesting. And I- actually, my next question is perhaps a good follow-up on that, is, what are the diagnostic pitfalls? You give a lot of examples of situations and I think some cases where it's easy to get tripped up and misdiagnose someone who has MOG with another fairly common neurological problem. Dr Flanagan: Yeah, I think some of the things that can help you when you're determining if the MOG is a true positive or false positive is the level of the antibodies. The super high titers, if it's a clear positive or very strong positive, the likelihood is that that is much more likely to be MOGAD than those low positives just above the cutoff. So that can be useful to help you discriminate from false positives. Those lesions, again, if all the lesions persist over time, that's going to be more suggestive of multiple sclerosis. Other diagnostic pitfalls, I suppose, if it's a syndrome that's not really associated with MOG, like peripheral neuropathy or other syndromes where we'll see some case reports, but usually I would be very cautious about those kind of presentations. So usually, having the antibody at a high level, and then also if they've had other symptoms suggestive of MOGAD, like if a patient has had recurrent optic neuritis and then they have an unusual brain syndrome, or they start out with an unusual brain syndrome and then have recurrent optic neuritis. You know, there are situations that make it more likely if they're having other typical phenotypes of the MOGAD where we can kind of expand the spectrum, but we have to be careful. Dr Smith: I was really curious about the dynamic imaging findings. And you point this out both in terms of the resolution of imaging findings, but also in that patients who have an acute MOG syndrome often have very rapid evolution of the imaging abnormalities. I'm just curious, you know, why is that, and what do you make of it? Does it have a mechanistic implication, do you think? Dr Flanagan: I don't think we know for sure. I think there's probably a lot more happening than we see on MRIs sometimes. What sometimes can happen in about 10% of patients is the initial MRI can be normal. We don't tend to see that with multiple sclerosis or NMOSD. Then what we see is it evolving over time. So, at that time, if you do a CSF, you'll often see inflammation, but we don't see the lesions. Now, that might be because the MRI is not very good at picking up cortical involvement. That can be difficult to see in MRI. Or there could be other factors. It could be a functional effect on the MOG but without frank demyelination yet, for example. Or there could be edema that you- myelin edema that you can't see as a lesion yet on MRI. But we do see that if you repeat the MRI, sometimes it'll change a lot. So, you may go from one or two lesions on the first MRI to twenty lesions on the second MRI a week later. So, it does tend to change a lot. And then over time, those lesions also resolve. So, what I say is if it's a very suspicious situation---like a child comes in with new-onset encephalitis, has inflammatory CSF---you might wanna consider repeating that MRI down the line and seeing if it's changing. And then over time, you know, a repeat MRI a year after the onset when there's brain or spinal cord lesions can be very helpful just to make sure you're on the right track, because lots of those lesions will then disappear, and that's a very clear discriminator from multiple sclerosis. Dr Smith: Yeah, thanks. I mean, I was wondering the same thing about whether that particular feature might imply, you know, a functional abnormality as opposed to more of a structural abnormality. So probably a lot more to learn as we move forward. There are now consensus diagnostic criteria that were published a couple of years ago. I think you've already touched on kind of the general approach, but do you want to speak to those? I found your summary pretty helpful. Dr Flanagan: Yeah, I think that those criteria are quite useful. They have three main parts to them. The first part is having a characteristic clinical syndrome. So, we talked about ADEM, we talked about cerebral cortical encephalitis, transverse myelitis that's often longitudinally extensive, and optic neuritis being the main syndromes, but sometimes other brainstem or cerebellar involvement can be seen. And then the second part is having a positive MOG antibody. And then there's some caveats there. So, if you have a high positive, then you don't really need any additional supportive criteria. On the other hand, if you're low positive, to get at those sticky antibodies that make sure it's not a false positive, you need some additional supportive clinical or MRI criteria. Or if you're only positive in CSF, you need that additional criteria. You also need to be negative for the aquaporin-4 antibody, because they can overlap clinically. And some of those supportive criteria are things that we talked about a little bit earlier, longer lesions within the optic nerve, bilateral involvement, involvement of the nerve sheath or optic disc edema. This is a situation, MOG antibody disease, where your fundoscope is useful and looking in the back of the eye and seeing swelling, because we don't tend to see that quite as often. It's less common in multiple sclerosis, but we often see prominent edema in MOGAD. And then in the spinal cord, the lesions tend to be central in the cord. Sometimes they form this H sign where it's restricted to the gray matter, and they tend to be longer, sometimes involving the conus. Patients will often have neurogenic bowel or bladder. And then in the brain, deep gray involvement, those large lesions along the cortex with swelling are some of the typical features. And then the final step is exclusion of another diagnosis. Just like with any test that we do in neurology, our final step is going to be to put that into context. So that's just a normal thing that we will always do when we get a group of test results back that we don't know what it means. We have to put it into context. So, make sure it's not multiple sclerosis, everything else does not look like multiple sclerosis, and then you can be on your way to make a diagnosis. Dr Smith: Definitely encourage listeners to read your article. I guess I say that with every time I- or with everyone I talk to for Continuum Audio, but the images are really fantastic and the cases are fantastic. So, everything you've described is well-illustrated, including really nice schematic sort of diagrams that help differentiate NMO from MOG and MS. So, if you like MRI scans and good imaging frameworks, then this is the article for you. Dr Flanagan: I think that's true, and the other thing is that the imaging is quite helpful because it takes a while for that antibody to come back. We're lucky at Mayo Clinic, if you work here, it, it comes back faster for you. But for many places, that time of sending it in, so a lot of times you don't know right away. So, looking at scrutinizing that MRI can be very helpful to guide you on your way and to know what you're dealing with and how to approach both the acute treatment and plans to have potentially a steroid taper after the acute treatment and those kind of things that can help guide you in that regard. Dr Smith: Yeah. So, let's talk about treatment. You know, what's your approach to treating a patient who has an acute demyelinating syndrome related to MOG? Dr Flanagan: So similar to other things, MOG is very steroid responsive. So, we use high-dose IV methylprednisolone in adults. That would be one gram IV for five days. And then we also will sometimes use oral steroids, twelve hundred and fifty milligrams. That's a bit of a hassle because it's twenty-five fifty-milligram tablets, it doesn't come in a larger tablet version. But it's very helpful to patients because they can get started on it right away. You don't have to set up an infusion center. So, we have used those oral steroids often in people who don't have access to an infusion center, are not in the hospital. And particularly as it's often optic neuritis, some of those patients are seen in the outpatient setting, so we can get in with treatment quickly. In patients where it's more severe, it doesn't recover quickly with steroids, then we would consider escalating to plasma exchange as our second-line treatment, and there's some retrospective data that suggests that plasma exchange can be useful. That's gonna be particularly for those people who don't have that quick response to steroids, or maybe more severe phenotypes like that brain involvement with ADEM or cerebral cortical encephalitis, where those patients might be in the hospital and quite unwell. I will say, we might get on to this, that sometimes MOG can be very, very severe and even fulminant, where there can be increased intracranial pressure, and these patients can be in the ICU, and it can be life-threatening. And so, it's really important to treat those patients aggressively, and some patients have even required hemicraniectomy or additional treatment. Sometimes IL-6 blocking medications have been used in that situation. So, monitoring and treating increased intracranial pressure in those rare patients, probably 2 or 3% that have the very severe attack, is important. Dr Smith: I think one of the things I found interesting, and then I'd love to get your feedback on this, is that most patients with MOG seem to have a very readily treatable disorder that's monophasic, right? You treat them with steroids, and they do well. On the other extreme, there are these patients that have a much more malignant presentation, and there are some that sound like they benefit from prophylactic or some chronic therapy. What's your approach, right? In MS, we do serial scans to monitor, and obviously, our patients are on, you know, chronic disease-modifying therapy. How do you decide when you're going to provide some sort of prophylactic therapy? How do you monitor it? How long do you continue it? Dr Flanagan: That's a great point. We don't know for sure yet, but I think for the most part, our approach has been if the patient has a single episode, they recover well from that episode. So, if that's optic neuritis, they're back to twenty/twenty vision. They have recovered well. We don't tend to use chronic maintenance immunotherapy. Sometimes after the first attack, we'll do a little bit of a slow taper, maybe over four, six weeks. We have done longer than that. And then we won't place them on any long-term treatment, because it's about 50% of patients that may have a monophasic disease, so we don't want to treat all those people who are destined never to have another relapse. On the other hand, if a patient had a very severe episode, they're in the ICU, they're intubated, some of those patients then afterwards we will start them at least temporarily on an attack prevention medication for at least a few years to get them through. Some patients will be very fearful of future relapses in that situation. Or if they don't recover well, if they're blind in one eye after an episode and then their other eye is vulnerable, or they're left with some residual deficits neurologically from a myelitis, then we would often sometimes put those patients after the first attack. But most of the time, we're gonna wait and see if they get that second attack, and then once they have the second attack, that is when we would consider a steroid-sparing medication. But I will say that there's no proven medications. We don't have any clinical trial data available yet. So some of those patients with relapsing disease, we'll either try to enroll them in a clinical trial, or we'll use an off-label treatment to try and manage their disease based on what we've learned from neuromyelitis optica or from multiple sclerosis. A few different options seem to be better, and we can maybe get into that too. Dr Smith: Yeah, let's go there. So, what options are there? You mentioned in more fulminant disease IL-6 inhibitors, and by that I assume you mean tocilizumab, but what are the options when you want to use prophylactic therapy? Dr Flanagan: So, that tocilizumab can be beneficial in the very acute situation, in that malignant situation. But also as an attack prevention treatment, the IL-6 blockers seem to- some of the retrospective data seems to look like it works reasonably well, so we work and see if we can get that approved. Another medication that can work well is IVIG or subcutaneous immunoglobulin as a maintenance treatment, so we would sometimes give that, like, at least one gram per kilogram once a month. The benefit of that is it doesn't lower your immune system, so there's some advantages there, particularly in people who may be more prone to infections, older people. So, we'll sometimes use that. But we do get into a lot of challenges with insurance coverage, and it can be difficult to get these approved by insurance because we only have retrospective data out there. So then for some patients, if they're in a region where there's a clinical trial available, we might try to enroll them in a clinical trial. And there are some clinical trials underway now, so hopefully in the future we'll be able to have some FDA-approved medications that can have some Class 1 data that we can follow. Because it's hard when you're just following retrospective data or anecdotal reports, it's a little bit difficult to know exactly how well you're doing with your treatments. Dr Smith: Well, Eoin, I wonder if we could finish up by just looking into the future, right? I mean, it sounds like a fun patient population to take care of because you've got lots of great therapies and can have a durable impact. But sure would be nice to have more evidence-based therapies and an FDA approval. What trials are going on? What's the future look like? Dr Flanagan: Yep. So, there's some trials going on in the- a couple of worldwide trials. One is on an FCRN blocker called rozanolixizumab, which is kind of like a plasma exchange-type treatment which removes your antibodies, and it's a weekly subcutaneous treatment where adults are enrolled. And the second one is called satralizumab, which is another IL-6 blocking medication. And again, that one's given once monthly under the skin. And the trial for that also includes children down to age eighteen, so for adolescents, too, that can be an option. There are trials, I believe, in Asia for tocilizumab too, and there's one starting in Australia for rituximab. So, the good news is that we're going to have some really good data down the line for lots of different agents, and we'll be able to figure out which treatments work. And this will be really of great benefit to our patients when we get that Class 1 data to kind of guide us on what we should be using and really build on the success of some of the other conditions like neuromyelitis optica spectrum disorder, where we now have four or five approved, medications that work very well. Dr Smith: Well, Eoin, thank you. This is a great conversation. I will say that it... the topic that I was a little intimidated about. I'm a simple peripheral nerve guy, as you know. But I think moreso than any other Continuum article I've read recently, I'm, like, loaded for bear. I can't wait to go back on the inpatient service and look for some MOG patients, because your article really left me feeling kind of prepared to think through this in a clinical setting. So, thank you for the conversation, and congratulations on a really wonderful piece for Continuum. Dr Flanagan: Yeah, thanks so much. Always a great honor to be involved in the Continuum, and thanks to all the readers out there. Dr Monteith: This is Dr. Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
Hosts: Dr. Daniel Ennis, Dr. Janet PopeGuests: Dr. Marinka Twilt (Pediatric Rheumatologist, University of Calgary; ASM Program Committee Chair), Dr. Mo Osman (University of Alberta; Abstract Chair & ASM Planning Committee Co-Chair)We're coming to you almost live from Halifax for Day 2 of the Canadian Rheumatology Association ASM. The day featured diverse podium science, practical workshops, and a lively Great Debate on DMARD tapering.Podium sessions highlighted lupus research on cancer risk, rising costs and work disability in RA, and new biologic insights into flares, with B-cell changes supporting patient-reported disease activity in lupus.Workshops focused on practical tools, including capillaroscopy for early CTD detection, pediatric updates on neonatal lupus risk (anti-Ro vs anti-La), and a structured lab-based approach to unexplained lymphadenopathy.The Dunlop-Dottridge Lecture reviewed statin-associated myositis, emphasizing delayed onset, persistence after discontinuation of the statins, and early IVIG-based treatment.The Great Debate explored DMARD tapering, reinforcing that while guidelines are cautious, real-world care requires shared decision-making and a focus on the lowest effective dose rather than full discontinuation.Main TakeawaysRising costs and ongoing work disability remain significant in RAPatient-reported flares have a clear biological basisStatin-associated myositis can occur years after statin use and requires early IVIGDMARD tapering should be individualized, with focus on lowest effective doseWhat to Watch for on Day 3State-of-the-art lecture on Still's disease across the lifespanMore high-impact podium presentationsClinical workshops, including one on topical therapiesGala dinner and closing eventsMore highlights coming tomorrow—stay tuned!
Behind every kidney cancer diagnosis is a person navigating difficult decisions about treatment and care. Today, we're diving into how to navigate the side effects of kidney cancer treatments and how to tell the difference between side effects and warning signs. This episode is supported by Exelixis. In this episode we heard from: Andrew Allers was diagnosed incidentally with clear-cell Renal Cell Carcinoma (RCC) in 2015 after a soccer injury. After a radical nephrectomy and four years of monitoring, Andrew's stage IV diagnosis was made in 2019 with metastases in his rib, hip, lungs and lymph nodes. The bone tumors were radiated, and after two rounds of an immunotherapy combination, a serious auto-immune reaction necessitated a pause in treatment while Andrew's care team figured out a solution. With regular IVIG infusions to manage the adverse reactions, a single-agent immunotherapy was restarted in early 2020 and within a few months a set of scans showed remarkable improvement -- tumors still visible, but "clinically unmeasurable" in the words of his oncologist. Just over a month later, a vision issue took Andrew to the local ER where he was diagnosed with two brain metastases, one of which was in the occipital lobe. The following day an emergency craniotomy was performed, followed by a round of brain radiation. Over the next 18 months, a series of 4 more brain tumors were discovered, radiated and added to the monitoring schedule. Since beginning a TKI in 2022 Andrew has been free of new brain metastases, and the immunotherapy continues to keep the lung and lymph node tumors at bay. After retiring in 2023, Andrew has become active in the Kidney Cancer community, participating in the research grant review process in the CDMRP & KCRP and as a Legislative Advocate for KidneyCAN, an advocacy group that campaigns for federally funded research into Kidney Cancer treatments. Julia Stevens, PharmD, BCOP is a Clinical Pharmacy Specialist in Ambulatory Oncology at Beth Israel Deaconess Medical Center in Boston, MA. She collaborates with medical oncologists to care for patients with kidney cancer. Her primary clinical responsibilities include educating patients and caregivers, monitoring and supporting those on oral therapies, minimizing the financial toxicity of treatment, and providing drug information and treatment recommendations to her team. Dr. Stevens is also a member of the Kidney Cancer Association Clinical Advisory Board. Rimda Wanchoo, MD is a Professor of Medicine at the Zucker School of Medicine and full time nephrologist at Northwell Health in NY. She graduated from medical school in India followed by residency at St. Barnabas in New Jersey and fellowship at NY Presbyterian at Weill Cornell. Her interests are taking care of patients with cancer and kidney diseases, glomerular disease and end stage kidney disease. She has been at Northwell for the last 14 years . She also serves as director of quality for the division and medical director of the largest joint venture dialysis unit in the health system. She has published and spoken on several onconephrology topics internationally. She serves as an associate editor for JON and CKJ. She is one of the founding members of American Society of Onconephrology (ASON). Additional Resources Kidney Cancer Kidney Cancer: Treatment and Living Well Voices for Kidney Health Kidney Cancer Association (KCA) KidneyCAN Do you have comments, questions, or suggestions? Email us at NKFpodcast@kidney.org. Also, make sure to rate and review us wherever you listen to podcasts.
Leslie Kenny was told in her 30s that she had five years to live. Diagnosed simultaneously with lupus, rheumatoid arthritis, and Hashimoto's thyroiditis — and told to give up her dream of having children — she did what true Betties do: she refused the prognosis, threw everything she had at it, and got to work. Now 60 years old, Leslie reports a biological age of 21. She is autoimmune disease-free. And she naturally conceived a child at 43. Her recovery journey led her to collaborate with University of Oxford scientists and to discover spermidine — a naturally occurring, food-derived longevity compound that was hiding in plain sight. It's been in our food for millennia, it's in breast milk, and it's in every plant on earth. And it addresses 9 of the 12 hallmarks of ageing identified by science as the root causes of why we get older. For 20% off Primeadine, go to: https://www.oxfordhealthspan.com/DRSTEPHANIE Episode Overview (timestamps are approximate): (0:00) Intro/Teaser (4:00) What Is Spermidine and Why Do We Lose It? (8:00) Autophagy, Hair, Nails & the Biological Dashboard (17:00) The 12 Hallmarks of Ageing, Explained for Real Life (23:00) mTOR, Muscle Loss, and Why Spermidine Is Different (27:00) Food Sources, Dosage & Lifestyle Levers (38:00) Leslie's Story: The Diagnosis, the Prognosis, the Refusal (55:00) IVIG, Trauma Therapy & the Surprise Pregnancy at 43 (1:18:00) Femspan, Future Research & Where to Find Leslie (1:22:00) The After-Party Thoughts with Dr. Stephani Resources mentioned in the Episode can be found at: https://drstephanieestima.com/podcasts/ep464 We couldn't do it without our sponsors: JUST THRIVE HEALTH - Take the Just Thrive FEEL BETTER challenge today, and save 20% on your first order. Go to https://justthrivehealth.com/better and use the code BETTER to see the difference for yourself. BON CHARGE - Achieve glowing skin, gain more energy, and uplevel your recovery practice with a suite of red light products. Get 15% off at https://boncharge.com/better with code BETTER. HIGHER DOSE - If you're noticing thinning, shedding, or simply want to support scalp and hair health proactively, this is a powerful addition to your routine. Get 15% off the Red Light Hat at https://higherdose.com with code BETTER at checkout. KENETIK - You think carefully about how you fuel your body but are you fueling your brain? Learn more about Kenetik and try it for yourself by going to https://drinkkenetik.com/BETTER and use code BETTER for 15% off QUALIA LIFE - Boost energy, DNA health, and cellular protection. Save 15% at https://qualialife.com/better with code BETTER. ****************************P.S. When you're ready, here are two ways Dr. Stephanie can help you:Subscribe: The Mini Pause — My weekly newsletter packed with the most actionable, evidence-based tools for women 40+ to thrive in midlife.Build Muscle: LIFT — My progressive strength training program designed for women in midlife. Form-focused, joint-friendly, and built for real results. Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.
In this SRNA "Ask the Expert" episode moderated by Krissy Dilger, Dr. John Chen of the Mayo Clinic answered audience questions about MOG antibody disease (MOGAD). He discussed diagnosis and the importance of titers and live cell-based assays given possible false positives [00:02:42]. Dr. Chen reviewed acute management with early high-dose steroids, prolonged tapers, and escalation to plasma exchange for severe or steroid-refractory attacks, as well as evolving long-term options including IVIG/subcutaneous IG and IL-6 blockade [00:04:14]. Audience questions covered relapse prediction, vision recovery timelines, fatigue, pregnancy, heredity, symptom interpretation, and whether to stop immunotherapy when antibodies become undetectable [00:12:13]. Finally, Dr. Chen described current and upcoming research, including a trial that is currently enrolling participants, and future prospects for optic nerve regeneration while cautioning against unproven stem cell clinics [00:41:37].John J. Chen, MD, PhD attended the University of Virginia for his undergraduate and combined MD/PhD degrees and completed his Ophthalmology residency and Neuro-Ophthalmology fellowship training at the University of Iowa. He then took a position at the Mayo Clinic in 2014 where he specializes in Neuro-Ophthalmology. Currently, he serves as a Consultant and Professor of Ophthalmology and Neurology, and Neuro-Ophthalmology Fellowship Director at the Mayo Clinic. Among Dr. Chen's awards and honors are the AAO Senior Achievement Award, Top Doctors in Minnesota, the Heed Fellowship, Real World Ophthalmology Inspiring Academic Leader Award, Ophthalmology Teacher of the Year Award four times leading to induction to the Educators Hall of Fame, and the Mayo Clinic Distinguished Educator Award – awarded to the top educator at Mayo Clinic in Rochester. He is an Associate Editor for Ophthalmology and the Journal of Neuro-Ophthalmology, has authored more than 250 peer-reviewed publications, and focuses his research on ophthalmic imaging, idiopathic intracranial hypertension, and optic neuritis, particularly NMOSD and MOG antibody–associated disease.00:00 Welcome and Introductions01:08 What Is MOGAD?02:42 Causes and Triggers03:23 How MOGAD Is Diagnosed04:14 Acute Attack Treatments06:35 Steroid Side Effects08:13 Testing During Treatment09:09 Long Term Therapies12:13 Interpreting MOG Positivity16:51 Eye Symptoms and Vision Fluctuations20:12 Antibody Titers and Severity21:19 Relapse Risk After First Attack23:09 Seizures and Encephalitis24:17 Vision Recovery After Optic Neuritis25:13 Acute Treatment Window25:57 Hereditary Risk Questions26:35 Stopping Azathioprine Safely29:56 Managing Post Attack Pain30:16 Steroids IVIG and Plasma Exchange32:08 Infections as Triggers33:01 Retesting MOG Antibodies35:01 Fatigue and Workup36:23 Prognosis and Life Expectancy37:45 Tinnitus and Brain Pressure39:05 Pediatric and Pregnancy Concerns41:37 Trials and Future Regeneration46:05 Research Resources and Wrap Up
In his weekly clinical update, Dr. Griffin and Vincent Racaniello are aghast at the CDC's decision to no longer test for rabies and mpox and the revised charter for its the advisory committee on immunization practices, an outbreak of E. coli illness in raw cheese, before Dr. Griffin then deep dives into the measles outbreak, recent statistics RSV, influenza and SARS-CoV-2 infections, the Wasterwater Scan dashboard, Johns Hopkins measles tracker, clinical practice guidelines for treating COVID-19, PEMGARDA authorized use for certain immunocompromised individuals where to find PEMGARDA, how to access and pay for Paxlovid, if the nasal microbiome modulates COVID-19 disease severity, reviews the use of steroid, antibiotics, anticoagulants and IVIG for treating COVID-19 including long COVID, and contacting your federal government representative to stop the assault on science and biomedical research. Subscribe (free): Apple Podcasts, RSS, email Become a patron of TWiV! Links for this episode State public health labs step up as CDC pauses testing for various pathogens, including rabies, mpox (CIDRAP) Infectious Diseases Laboratories : Test Directory (CDC) Kennedy rewrites the rule for membership on US vaccine advisory panel (Reuters) Advisory Committee on Immunization Practices (ACIP): ACIP charter (CDC) Quick takes: More E coli tied to raw cheese, drug-resistant Shigella in UK, TB funds for Sudan (CIDRAP) Voluntary Recall (FDA) E. coli Outbreak Linked to Raw Dairy (CDC: E.coli Infection (Escherichia coli)) We 100% disagree with the FDA's false "possible link", and extreme allegations (RawFarm USA) Risk of Multiple Sclerosis Among Persons With Epstein-Barr Virus–Positive Mononucleosis(Neurology) US Scientists Sequence 1,000 Genomes From Measles, a Disease Long Eliminated With Vaccines (KFF HealthNews) Wastewater for measles (WasterWater Scan) Measles cases and outbreaks (CDC Rubeola) Big outbreak, bright lights…Measles Dashboard (South Carolina Department of Public Health) Utah measles outbreak response (Utah Department of Health and Human Services) UtahMeasles Dashboard (Utah Department of Health and Human Services) Tracking Measles Cases in the U.S. (Johns Hopkins) Measles vaccine recommendations from NYP (jpg) Weekly measles and rubella monitoring (Government of Canada) Measles (WHO) Get the FACTS about measles (NY State Department of Health) Measles (CDC Measles (Rubeola)) Measles vaccine (CDC Measles (Rubeola)) Presumptive evidence of measles immunity (CDC) Contraindications and precautions to measles vaccination (CDC) Adverse events associated with childhood vaccines: evidence bearing on causality (NLM) Measles Vaccination: Know the Facts(ISDA: Infectious Diseases Society of America) Deaths following vaccination: what does the evidence show (Vaccine) Influenza: Waste water scan for 11 pathogens (WastewaterSCan) USrespiratory virus activity (CDC Respiratory Illnesses) Respiratory virus activity levels (CDC Respiratory Illnesses) Flu vaccine recommendations: Vaccines and Related Biological Products Advisory Committee March 12, 2026 Meeting Announcement (FDA) WHO updates all 3 viral strains to be included in fall flu shots (CIDRAP) FDA vaccine advisers recommend adding subclade K to fall shots (CIDRAP) Weekly surveillance report: cliff notes (CDC FluView) OPTION 2: XOFLUZA $50 Cash Pay Option(xofluza) RSV: Waste water scan for 11 pathogens (WastewaterSCan) Respiratory Diseases (Yale School of Public Health) USrespiratory virus activity (CDC Respiratory Illnesses) RSV-Network (CDC Respiratory Syncytial virus Infection) Vaccines for Adults (CDC: Respiratory Syncytial Virus Infection (RSV)) Economic Analysis of Protein Subunit and mRNA RSV Vaccination in Adults aged 50-59 Years (CDC: ACIP) Respiratory Diseases (Yale School of Public Health) Waste water scan for 11 pathogens (WastewaterSCan) COVID-19 deaths (CDC) Respiratory Illnesses Data Channel (CDC: Respiratory Illnesses) COVID-19 national and regional trends (CDC) COVID-19 variant tracker (CDC) SARS-CoV-2 genomes galore (Nextstrain) 2025 Clinical Practice Guideline Update by the Infectious Diseases Society of America on the Treatment and Management of COVID-19 (CID) 2025 Clinical Practice Guideline Update by the Infectious Diseases Society of America on the Treatment and Management of COVID-19: Baricitinib vs. Tocilizumab (CID) ImmunobridgingAnalysis of Pemivibart for the Treatment of COVID-19 – A Therapeutic Gap for the Immune Compromised Remains (OFID) PEMGARDA® is authorized for use in certain moderately to severely immunocompromised patients to help prevent COVID-19 (Pemgarda) Where to get pemgarda (Pemgarda) EUAfor the pre-exposure prophylaxis of COVID-19 (INVIYD) Infusion center (Prime Fusions) CDC Quarantine guidelines (CDC) NIH COVID-19 treatment guidelines (NIH) Drug interaction checker (University of Liverpool) Help your eligible patients access PAXLOVID with the PAXCESS Patient Support Program (Pfizer Pro) Understanding Coverage Options (PAXCESS) Infectious Disease Society guidelines for treatment and management (ID Society) Molnupiravir safety and efficacy (JMV) Convalescent plasma recommendation for immunocompromised (ID Society) What to do when sick with a respiratory virus (CDC) Managing healthcare staffing shortages (CDC) Anticoagulationguidelines (hematology.org) Daniel Griffin's evidence based medical practices for long COVID (OFID) Long COVID hotline (Columbia : Columbia University Irving Medical Center) The answers: Long COVID Association of nasopharyngeal Dolosigranulum pigrum and Corynebacterium species with post-acute sequelae of SARS-CoV-2 in a longitudinal cohort (Microbiology Spectrum) The effect of corticosteroids, antibiotics, and anticoagulants on the development of post-COVID-19 syndrome in COVID-19 hospitalized patients 6 months after discharge: a retrospective follow up study (Clinical and Experimental Medicine) Intravenous immunoglobulin treatment for long COVID: a case report of clinical and immunological findings (LANCET: Infectious Diseases) Management of Orthostatic Hypotension (JAMA: Internal Medicine) Reaching out to US house representative Letters read on TWiV 1312 Dr. Griffin's COVID treatment summary (pdf) Timestamps by Jolene Ramsey. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv Content in this podcast should not be construed as medical advice.
In this powerful in-person interview at the Tick Boot Camp studio, Matt Sabatello sits down with Dr. Somer DelSignore, DNP, a board-certified pediatric practitioner specializing in Lyme disease, tick-borne co-infections, PANS/PANDAS, autoimmune and neuroimmune disorders, autism-like regression, and congenital tick-borne illness. This episode is essential listening for parents who have been told to “wait and see,” families who have seen multiple specialists without answers, and anyone trying to understand how infection, inflammation, immune dysfunction, and nervous system imbalance can impact a child's brain and development.
Featuring an interview with Dr Hanny Al-Samkari, including the following topics: Case: A woman in her early 70s incidentally diagnosed with immune thrombocytopenia (ITP) experiences a suboptimal response to prednisone and IVIG — Bhavana (Tina) Bhatnagar, DO (0:00) Case: A man in his early 50s with a long history of ITP undergoes splenectomy — Neil Morganstein, MD (5:06) Case: A woman in her mid 50s with symptomatic iron-deficiency anemia who was found to have ITP has received corticosteroids, rituximab and IVIG — Jennifer Yannucci, MD (12:25) Case: A woman in her early 30s who previously received ABVD (doxorubicin/bleomycin/vinblastine/dacarbazine) and autologous stem cell transplant for Hodgkin lymphoma is diagnosed with ITP 5 years later that is refractory to high-dose prednisone, IVIG and rituximab, then romiplostim — Priya Rudolph, MD, PhD (18:19) CME information and select publications
Measles is back in the headlines, and with it a wave of fear, confusion, and half-answers. This episode looks past the rhetoric to a question that matters deeply to families and clinicians alike: What does the evidence actually say about treating measles once someone is sick, in both children and adults?Sign up for weekly webinars: Weekly Webinars - Independent Medical Alliance Host Dr. Elizabeth Mumper, Senior Fellow, Pediatrics at the Independent Medical Alliance, is joined by two co-authors of a new peer-reviewed systematic review in Antiviral Research titled “Acute Management of Measles: A Systematic Review of Therapeutic Strategies.” Her guests are Dr. Joseph Varon, IMA President, and Matthew Halma, IMA Director of Research.Together, they walk through what decades of published research already tell us about measles treatment and why so few parents and even clinicians have heard about it.They cover:• Why this systematic review was needed and what question it set out to answer• Key findings on Vitamin A, ribavirin, interferon-alpha, IVIG, and supportive nutrients• What measles tends to look like clinically in children and how it can differ in adults• Whether treatment-focused research has been overlooked or crowded out by vaccine-only messaging• How to think clearly about immunity from infection versus immunity from vaccination• Practical, evidence-informed steps families can take if measles is circulating, including when to seek urgent medical care• For parents, pediatricians, and front-line clinicians, this conversation offers a calm, evidence-based look at what can be done during measles illness, not just before it.Aired Wednesday, March 11, 2026.Also:• Donate: https://imahealth.org/donate/• Follow: https://imahealth.org/contact/• Webinar: https://imahealth.org/category/weekly-webinars/• Treatment: https://imahealth.org/treatment-protocols/• Medical Disclaimer: https://imahealth.org/about/terms-and-conditions/About IMA (Formerly FLCCC Alliance)The Independent Medical Alliance™ is a nonprofit, 501(c)(3) organization and coalition of physicians, nurses, and healthcare professionals united by a mission to restore trust and transparency in healthcare. The organization's mission is one driven by Honest Medicine™ that prioritizes patients above profits and emphasizes long-term wellness and disease prevention through empowerment of both physicians and their patients. With a focus on evidence-based medicine, informed consent, and systemic reform, IMA is driving a movement to create a more compassionate and effective healthcare system.For more information about the Independent Medical Alliance, visit www.IMAhealth.org
About Farrah Woodall: Farrah Woodall is a registered nurse, esthetician, and holistic wellness entrepreneur who blends medical experience with natural solutions to help people prioritize “well care” over “sick care.” With nearly 30 years in nursing—from neonatal intensive care to concierge IVIG infusions—she respects Western medicine for acute care while championing proactive health through detoxing, blood type–specific nutrition, CBD, functional mushrooms, and botanical skincare. Through her brand, My Earthly Essentials, her work in network marketing, and her involvement with BNI and her local Chamber of Commerce, Farrah empowers individuals and small businesses to take ownership of their health and build sustainable, legacy-focused lives. In this episode, Jennie and Farrah Woodall discuss: Farrah's background and philosophy on health Balancing nursing with network marketing and direct sales Building a holistic wellness business (My Earthly Essentials) Leveraging networking platforms: Chamber of Commerce & BNI How caring for mind, body, and spirit helps entrepreneurs show up stronger in life and business Key Takeaways: Proactive “well care” beats reactive “sick care.” Farrah urges people to focus on detoxing, nutrition, and daily habits that help prevent illness rather than waiting for a diagnosis. Your body is your business asset. As an entrepreneur, when you care for your mind, body, and spirit, you show up better for your clients, family, and opportunities. Network marketing success is built on relationships and time, not quick wins. Strategic networking multiplies your impact. Combining BNI, Chamber of Commerce, and business collaborations lets her leverage other people's networks and create win‑win referrals. Multiple aligned income streams can fit under one clear brand. "My vision is to offer healing trust and togetherness with a mission of providing services and products that are disruptive to the mainstream constructs that ail us." – Farrah WoodallConnect with Farrah Woodall: Website: https://myearthlyessentials.com/ LinkedIn: https://www.linkedin.com/in/myearthlyessentials1/ Facebook: https://www.facebook.com/MyEarthlyEssentials1 Instagram: https://www.instagram.com/MyEarthlyEssentials1 TikTok: https://www.tiktok.com/@MyEarthlyEssentials1 YouTube: https://www.youtube.com/@MyEarthlyEssentials1/posts CONNECT WITH JENNIE: Facebook:https://www.facebook.com/badassdirectsalesmastery Instagram: https://www.instagram.com/badassdirectsalesmastery/ Website: https://badassdirectsalesmastery.com/ Show: https://badassdirectsalesmastery.com/blog/ YouTube: COMING SOON! LinkedIn: https://www.linkedin.com/in/badassdirectsalesmastery/ Email: jennie@badassdirectsalesmastery.com Audio production by Turnkey Podcast Productions. You're the expert. Your podcast will prove it.
In his weekly clinical update, Dr. Griffin and Vincent Racaniello talk about the health misconceptions that RFK Jr continues to perpetuate and how to combat them, first cases of highly pathogenic influenza in the California elephant seal population before Dr. Griffin deep dives into economic costs of not vaccinating against measles, the measles outbreak in South Carolinaand Utah, ICE detention centers, lack of accurate reporting may prevent the US from losing its status as a country that eliminated measles, immune amnesia from measles infection, influenza strain selection for the 2026-2027 vaccine, recent statistics for RSV, influenza and SARS-CoV-2 infections, the Wasterwater Scan dashboard, Johns Hopkins measles tracker, where to find PEMGARDA, how to access and pay for Paxlovid, when to use steroids for treating influenza, long COVID treatment center, where to go for answers to your long COVID questions, clinical trials for long COVID treatment including GLP-1 inhibitors and IVIG and contacting your federal government representative to stop the assault on science and biomedical research. Subscribe (free): Apple Podcasts, RSS, email Become a patron of TWiV! Links for this episode Kristen Panthagani, MD, PhD (Substack) You can know things! (Substack) Kmpanthagani: Kristen Panthagani, MD, PhD Instagram) Kristen Panthagani, MD, PhD kmpanthagani (Threads) Psychological inoculation improves resilience against misinformation on social media (Science) 5 Logical fallacies in the era of RFK Jr. (Substack) Tecovirimat for the Treatment of Mpox (NEJM) California records avian flu in northern elephant seals (CIDRAP) First Cases of Highly Pathogenic Avian Influenza in Northern Elephant Seals Confirmed in California (UC Davis) Wastewater for measles (WasterWater Scan) The health and economic repercussions of declining MMR coverage in the United States (medRxiv) 2025 measles resurgence carries estimated $244 million price tag (CIDRAP) US builds case to retain measles elimination status as infections mount (Reuters) Expert meeting on US measles elimination status delayed to November (Reuters) 'Nearly Every' Child With Measles Suffers This Hidden Threat (Medscape) CDC acting director Bhattacharya urges use of measles vaccine (Reuters) Measles cases and outbreaks (CDC Rubeola) Measles Dashboard (South Carolina Department of Public Health) Utah measles outbreak response (Utah Department of Health and Human Services) Utah Measles Dashboard (Utah Department of Health and Human Services) Escobar: ICE sending sick migrants to El Paso hospitals for quarantine (BorderReport) Tracking Measles Cases in the U.S. (Johns Hopkins) Measles vaccine recommendations from NYP (jpg) Weekly measles and rubella monitoring (Government of Canada) Measles (WHO) Get the FACTS about measles (NY State Department of Health) Measles (CDC Measles (Rubeola)) Measles vaccine (CDC Measles (Rubeola)) Presumptive evidence of measles immunity (CDC) Contraindications and precautions to measles vaccination (CDC) Adverse events associated with childhood vaccines: evidence bearing on causality (NLM) Measles Vaccination: Know the Facts(ISDA: Infectious Diseases Society of America) Deaths following vaccination: what does the evidence show (Vaccine) Influenza: Waste water scan for 11 pathogens (WastewaterSCan) US respiratory virus activity (CDC Respiratory Illnesses) Respiratory virus activity levels (CDC Respiratory Illnesses) Flu vaccine recommendations: Vaccines and Related Biological Products Advisory Committee March 12, 2026 Meeting Announcement (FDA) WHO updates all 3 viral strains to be included in fall flu shots (CIDRAP) Weekly surveillance report: cliff notes (CDC FluView) OPTION 2: XOFLUZA $50 Cash Pay Option (xofluza) RSV: Waste water scan for 11 pathogens (WastewaterSCan) Respiratory Diseases (Yale School of Public Health) US respiratory virus activity (CDC Respiratory Illnesses) RSV-Network (CDC Respiratory Syncytial virus Infection) Vaccines for Adults (CDC: Respiratory Syncytial Virus Infection (RSV)) Economic Analysis of Protein Subunit and mRNA RSV Vaccination in Adults aged 50-59 Years (CDC: ACIP) Respiratory Diseases (Yale School of Public Health) RSV Detection and Antibiotic Prescribing Decisions for Pediatric Respiratory Tract Infections (JAMA Network) Waste water scan for 11 pathogens (WastewaterSCan) COVID-19 deaths (CDC) Respiratory Illnesses Data Channel (CDC: Respiratory Illnesses) COVID-19 national and regional trends (CDC) COVID-19 variant tracker (CDC) SARS-CoV-2 genomes galore (Nextstrain) Where to get pemgarda (Pemgarda) EUAfor the pre-exposure prophylaxis of COVID-19 (INVIYD) Infusion center (Prime Fusions) CDC Quarantine guidelines (CDC) NIH COVID-19 treatment guidelines (NIH) Drug interaction checker (University of Liverpool) Help your eligible patients access PAXLOVID with the PAXCESS Patient Support Program (Pfizer Pro) Understanding Coverage Options (PAXCESS) Infectious Disease Society guidelines for treatment and management (ID Society) Molnupiravir safety and efficacy (JMV) Convalescent plasma recommendation for immunocompromised (ID Society) What to do when sick with a respiratory virus (CDC) Managing healthcare staffing shortages (CDC) Anticoagulationguidelines (hematology.org) Daniel Griffin's evidence based medical practices for long COVID (OFID) Long COVID hotline (Columbia : Columbia University Irving Medical Center) The answers: Long COVID SARS-CoV-2Persistence and the Gut Microbiota: New Insights into Long COVID Pathogenesis (MDPI) Neither Metformin nor Ursodeoxycholic Acid Effectively Treats Postacute Sequelae of COVID-19 (Annals of Internal Medicine) Long COVID: RECOVER-TLC Clinical Trials (Foundation for the National Institute of Health) Design and rationale of RECOVER-AUTONOMIC: A randomized platform trial evaluating interventions for Long COVID postural orthostatic tachycardia syndrome (American Heart Journal) Dr. Ruth's Newsletter: COVID, Flu & Health News, 3/1/26 (Substack) Reaching out to US house representative Letters read on TWiV 1302 Dr. Griffin's COVID treatment summary (pdf) Timestamps by Jolene Ramsey. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv Content in this podcast should not be construed as medical advice.
In this episode of the Oncology Brothers podcast, we dived deep into the complexities of multiple myeloma treatment, focusing on the groundbreaking MajesTEC-3 trial. We had the pleasure of welcoming Dr. Luciano Costa from the University of Alabama, who shared insights on the combination of teclistamab and daratumumab for relapsed refractory multiple myeloma. Listen us on: Spotify: https://open.spotify.com/show/31BXhY9FM4gPWG10WgE11o Follow us on social media: X/Twitter: https://twitter.com/oncbrothers Instagram: https://www.instagram.com/oncbrothers Website: https://oncbrothers.com/ Key topics discussed included: The impressive progression-free survival (PFS) rates observed in the MajesTEC-3 trial, with a PFS of 83.4% at three years. The mechanism of action of teclistamab as a bispecific antibody targeting BCMA and its synergy with daratumumab. Safety profiles, including the management of cytokine release syndrome (CRS) and infection risks, along with the use of IVIG for prophylaxis. The evolving landscape of multiple myeloma therapies, including the role of CAR T-cell therapy versus bispecific antibodies. Join us for this informative discussion that aims to keep healthcare professionals updated on the latest advancements in multiple myeloma treatment. Don't forget to like, subscribe, and check out our other episodes for more insights on oncology! #MultipleMyeloma, #MajesTEC3, #Teclistamab, #Daratumumab, #BispecificAntibody, #OncBrothers
Pediatrics Now: Cases Updates and Discussions for the Busy Pediatric Practitioner
Link for CME credit coming soon! This episode follows Lisa and Craig Wilkerson as they share their son Ryan's sudden, severe decline from sudden-onset OCD-like symptoms to full disability caused by PANS/PANDAS, and the family's multi-year struggle to get proper medical care. They describe repeated misdiagnoses, traumatic hospital experiences, and even CPS involvement, until Dr. Anthony Infante used specialized testing and prescribed IVIG immunotherapy. The treatment gradually restored Ryan's sleep, hygiene, social life, and independence. Listeners and viewers will hear clinical pearls about listening to families, considering autoimmune causes for acute neuropsychiatric changes, and the role of multidisciplinary care and targeted immune testing and treatment.
Dr. Alex Menze and Dr. Divyanshu Dubey discuss the clinical insights into autoimmune nodopathies, particularly focusing on CASPR1 and CASPR1/CNTN1-complex-IgG. Show citation: Paramasivan NK, Basal E, LaFrance-Corey RG, et al. Clinical Insights Into CASPR1 and CASPR1/Contactin-1 Complex Autoimmune Nodopathies. Neurology. 2026;106(5):e214403. doi:10.1212/WNL.0000000000214403 Show transcript: Dr. Alexander Menze: Hi, this is Alexander Menze. I just finished interviewing Divyanshu Dubey for the Neurology podcast. For today's Neurology Minute, I'm hoping you can tell us the main points of your paper. Dr. Divyanshu Dubey: Our paper talks about a rare form of autoimmune neuropathy associated with antibodies, CASPR1, as well as CASPR1/Contactin-1 complex IgG. These patients present with similar to CIDP, IDP, but tend to have more rapid progression, often a lot of sensory features preceding motor deficits including sensory ataxia in the contact and CASPR complex cases and presence of neuropathic pain in some of the CASPR1 cases. These patients, similar to other neuropathies are refractory to IVIg, but respond relatively well to rituximab. Dr. Alexander Menze: Thank you. Be sure to download this week's podcast to hear our full interview.
Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions: S: What's the deal with smoothies? Why are they recommended so much? Not just by Equilife but from a lot of other wellness practitioners. In general I find they don't satiate me for long and could end up causing me to overeat in the long run. But more than that, I developed a different issue. I found Equilife, as it seems many have, when experiencing gut issues (probably post infectious IBS) and looking for answers. My issues kept coming and going. Then I started to realize it was aggravated during detoxes. (This all evolved over a year and a half.) I finally discussed with AI. In a nutshell, AI suggested I eat warm foods only, cooked veggies. Eat foods in a particular order. This wasn't high risk so I tried this advice. It helped so much. So now I wonder, is it really best to recommend smoothies for everyone? Especially when the detox with shakes or smoothies are recommended as a starting point before other protocols? Seems like if smoothies were to be recommended, it might be better post gut healing? (I now remember a Chinese medicine practitioner telling me years ago that warm food is better for a sensitive gut. I had forgotten that temporarily.) Btw - it's all cold or raw food that can be too much for me right now. Not just shakes or smoothies but I also tested these things alone, outside of the detox. I just see smoothies recommended as nutrition for all kinds of reasons and to people with all kinds of gut issues and don't really hear anyone discuss when it is not good for some of us. Now I just need to figure out how long to heal before I can add back cold food and raw veggies at times. I miss my carrot sticks but glad my gut is happier. So why are smoothies such a thing in the wellness community? Katie: Thank you for everything you have done and taught me. I had a Prenuvo scan done (thank you for the code) and found that I have a small pineal gland cyst, multiple kidney cysts, a syrinx in my spinal cord and a cyst on my cervix. I lived a very unhealthy first 33 years, but have been living clean the last 3. Big 5 showed bacterial overgrowth, mold, candida, heavy metals, mitochondrial dysfunction, high manganese, high bedtime cortisol, and low T3. Hormones and omegas were optimal. What is the root cause of cyst formation? Besides going through protocols and proteolytic enzymes is there anything else I should do? Of course, not looking for diagnosis or treatment plan. Liz: Hi Dr. Cabral, I am a 36 year old female with no history of health problems before the last 2 years. On June 26, 2024 I underwent an XILF lumbar fusion surgery to fuse my L4/L5 because of chronic back pain. I soon found that this was the biggest mistake of my life. I haven't been the same since. I have been experiencing unrelenting, chronic nausea and abdominal discomfort on a daily basis. I also experience brain fog and chronic fatigue. As such, my performance at work has significantly decreased, my mood has been at an all time low, some days I can't even get out of bed. I wish I never had the surgery, had I known my quality of life would have plummeted so drastically. I've gone to countless specialists (a gastroenterologist, endocrinologist, rheumatologist, an ENT, neurologist, OBGYN, Accupuncture, even tried Reiki, and every test result shows unremarkable/normal results. I recently went to pain management and they gave me an epidural after seeing significant scar tissue around the surgical site. I am not experiencing any relief. In fact, I think I feel worse. I am getting married in May and want to start a family but have not been able to get myself right since my surgery. I'm scared I'll never be able to find relief. I don't know where else to turn or what else to do. I just want to get back to normal again and enjoy my life. If there's anything you can think of that I can try, I'll do it. I'm at my wits end. Please help me. Rebecka: Hi Dr. Cabral. I have recently been diagnosed with Anemia. I have not been told the specific type of Anemia. I feel terrible 24/7. My symptoms include fatigue, weakness, dizziness, chest pain and shortness of breath. I feel this is an off and on chronic problem as I have realized I've been having these symptoms for years. My RBC are low, my retic is low and low lymphocytes. Mcv and mch values were high on my CBC. Vitamin b12 and folate normal and my TSH was what I considered low normal. I also experienced a hot flash after lunch every day. I am very petite at 5ft 1 and 95-100lbs and I am 43 years old. What tests should I be doing to figure out the root cause of my anemia? I know hormones and stress can play a role as well. I live a very stressful lifestyle working full time with 2 young daughters. On top of all this, I had an ultrasound of my abdomen in December. It showed biliary sludge and a 2cm hemangioma on my liver. Are there and herbs to dissolve the sludge before it causes any more pain or complications? I would just like to feel "good" again and live a somewhat normal life. Please help me. Renee: Hi Dr Cabral, Firstly thank you for your dedication to helping people globally find answers to their health challenges. I am an IHP lv 2 and would greatly appreciate any advice on a client with CIDP (MADSAM syndrome) — Chronic Inflammatory Demyelinating Polyradiculoneuropathy. A 62 yr old male, fit, dealing with symptoms for 2 yrs, legs are weak and seem to be getting weaker, continues to experience widespread fasciculations (nerve twitching), which are now also affects his hands. His neurologist has recommenced treatment with IVIG (Intravenous immunoglobulin) to address what body is doing to the nerves. I will be having him on the DESTRESS protocol and highly recommending the Big 5 to get to the root cause. Your thoughts on using IVIG along with removing toxicities and replacing deficiencies would be extremely appreciated as I am very keen to help him reverse this and get his life back. Thanking you in advance. Renae Thank you for tuning into today's Cabral HouseCall and be sure to check back tomorrow where we answer more of our community's questions! - - - Show Notes and Resources: StephenCabral.com/3662 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!
In this episode, Danielle shares her heartbreaking journey from a dedicated hospice nurse to a vaccine injury survivor, detailing the devastating impact of the COVID-19 vaccine on her health, career, and family. She joins us from her hospital room as she fights not only for her life, but for justice, for help in covering the treatment that is actually keeping her out of Hospice (yes, Hospice!), and for the acknowledgement from the government, the medical community, and insurance companies, some of whom STILL will not acknowledge the cause of her injuries. Her story underscores the urgent need for recognition, support, and systemic reform, and we encourage everyone to listen, to share, and to go to www.react19.org to help Danielle and thousands like here who need us. Timestamps00:00 - Introduction and Danielle's background as a hospice nurse 02:11 - Danielle's testimony to the FDA and life-changing vaccine injury 04:46 - The story behind Danielle's decision to get vaccinated 08:07 - The progression of her health decline over four years 09:51 - The systemic neglect and lack of treatment options 12:54 - The role of organizations like React 19 in finding help 15:16 - The importance of recognition and medical advocacy 17:04 - The treatment: IVIG, costs, and barriers to access 20:21 - The ongoing fight for medical acknowledgment and insurance coverage 23:36 - The necessity of treatments like IVIG for survival 26:14 - Systemic failures and the need for reform in healthcare and insurance 28:37 - The mental health toll and community support 31:01 - Danielle's heartfelt letter to her son and the personal toll 32:25 - The call to action: educate, donate, share, and advocate 34:30 - The importance of community and systemic change 37:00 - Sharing stories to create awareness and push for justice 40:26 - The ongoing hope for healing and systemic acknowledgment 43:11 - Connecting with Danielle: social media and activism 44:03 - Closing remarks and encouragement to spread awarenessResources & Linkswww.React19,orgDanielle's Twitter - @thecoercednurseJust Think: The Podcast on Instagram - JustThink_ThePodcastSupport the CausePlease visit React 19 to learn more, donate, and share Danielle's story. Your support can help bring systemic change and provide life-saving treatments for vaccine-injured individuals.
In this powerful and deeply moving episode of the Tick Boot Camp Podcast, we sit down with Julia Bruzzese, a 22-year-old Lyme disease survivor, disability advocate, and future physician whose life was forever changed by an untreated tick bite in childhood. After developing a classic bull's-eye rash at age 9, Julia went undiagnosed for nearly two years, despite textbook symptoms of Lyme disease. By age 11, she experienced a catastrophic neurological decline that left her paraplegic and wheelchair-bound. Over the next decade, Julia saw more than 100 doctors, endured profound medical gaslighting, and navigated an exhausting journey through antibiotics, IVIG, IV antibiotics, plasmapheresis, stem cells, ozone therapy, and integrative care. Julia's story became internationally known after a moment with Pope Francis on the JFK airport tarmac went viral in 2015—an event that opened doors to care, advocacy, and awareness. She later became the emotional centerpiece of the award-winning documentary The Quiet Epidemic, appeared at New York Fashion Week as a Lyme disease advocate, and was profiled by renowned journalist Mary Beth Pfeiffer. Today, Julia is finishing her undergraduate degree and has been accepted into medical school, determined to become the kind of doctor she needed when the system failed her. This episode is a masterclass in: Pediatric Lyme disease Medical gaslighting vs. lack of education Clinical diagnosis vs. unreliable testing The patient-doctor relationship Chronic illness, disability, and purpose Why Lyme disease changes lives—and why early treatment matters Childhood Lyme Disease & Missed Diagnosis Tick bite and bull's-eye rash dismissed at age 9 Two years of worsening symptoms labeled as “growing pains,” viruses, or psychological Why early Lyme treatment saves lives Neurological Collapse & Hospital Trauma Sudden onset of paralysis, vision loss, fevers, hair loss, and weakness at age 11 Over 100 doctors and repeated hospitalizations Being accused of malingering and conversion disorder The devastating impact of medical disbelief on children The Quiet Epidemic Documentary How Julia became the heart of the film at age 12 Why she initially hesitated to share her story The emotional impact of seeing her illness reflected on screen How the documentary helps families explain Lyme disease to others Meeting Pope Francis & Global Awareness How a school principal secured last-minute tickets The Pope walks directly to Julia's wheelchair The moment that changed everything Media coverage that led to access to lifesaving care Treatment Journey Lyme-literate diagnosis by NP Somer DelSignore Oral and IV antibiotics IVIG (including under-dosing issues) Plasmapheresis POTS, Babesia, Bartonella, and autoimmune complications Stem cell therapy abroad Ozone and integrative protocols Why there is no single silver bullet for Lyme disease The Medical System & Lyme Denial Why doctors often say “it's all in your head” The difference between malice and lack of training How medical education fails chronic illness patients Fear of insurance companies, lawsuits, and “accepted guidelines” Why Lyme is a clinical diagnosis, not a test result Reframing “Medical Gaslighting” Why anger is understandable—but not always healing How patients and doctors can become better partners Understanding doctors' limitations without excusing harm Advocacy with clarity, not hostility Disability, Identity & Resilience Navigating life and education as a wheelchair user Accommodations, accessibility, and invisible illness “I have Lyme. I am not Lyme.” Learning when to rest, when to fight, and when to live Becoming the Doctor She Needed Working as a medical assistant and hospital volunteer in a wheelchair Applying to and being accepted into medical school Becoming the first wheelchair-using medical student at her institution Why lived experience belongs in medicine Medical Malpractice Lawsuit Lawsuit filed in NYC (March 2021) against multiple doctors and hospitals Failure to diagnose and treat Lyme disease despite clear evidence Why Lyme malpractice cases are rare—and necessary Seeking accountability, not revenge Purpose, Faith & Meaning From “Why me?” to “Why not me?” How suffering clarified her calling The role of faith, family, and community Why Julia wouldn't give this journey back—even now Memorable Quotes “I was criminalized as an eleven-year-old child for being sick.” “It actually was in my head—the bacteria was in my brain.” “I have Lyme disease. I am not Lyme disease.” “There is no silver bullet for Lyme. Healing is trial and error.” “I wouldn't be who I am—or know my purpose—without this journey.” Why This Episode Matters This episode is essential listening for: Parents of children with unexplained symptoms Lyme disease and chronic illness patients Medical professionals and students Advocates fighting for better diagnostics and care Anyone who has ever felt dismissed, unseen, or unheard in healthcare Julia Bruzzese's story is not just about Lyme disease—it's about truth, resilience, accountability, and hope.
Featuring perspectives from Dr Sagar Lonial and Dr María-Victoria Mateos, including the following topics: Introduction (0:00) Best of ASH Multiple Myeloma (1:56) Case: A man in his late 50s with t(11;14) IgA kappa myeloma discovered during workup for new Stage IV kidney disease who has a chest wall plasmacytoma receives daratumumab with CyBorD and radiation therapy to the plasmacytoma with minimal response — Jeremy Lorber, MD (8:35) Antibody-Drug Conjugates and Other Emerging Novel Therapies for Relapsed/Refractory (R/R) Multiple Myeloma (MM) — Dr Lonial (16:58) Case: A man in his mid 80s with severe obesity and coronary artery disease, chronic heart failure and sleep apnea receives belantamab mafodotin with low-dose pomalidomide for multiregimen-relapsed myeloma — Neil Morganstein, MD (27:57) Case: A man in his mid 60s with a history of stroke with aphasia receives teclistamab for multiregimen-relapsed MM after daratumumab, proteasome inhibitors, immunomodulatory drugs and selinexor — Justin Favaro, MD, PhD (34:42) Integrating Chimeric Antigen Receptor (CAR) T-Cell Therapy and Bispecific Antibodies into the Management of R/R MM — Dr Mateos (39:09) Case: A man in his early 70s with kappa light chain myeloma experiences complete response on cilta-cel CAR T-cell therapy with hypogammaglobulinemia requiring IVIG and develops melanoma of the abdominal wall — Bhavana (Tina) Bhatnagar, DO (52:07) Case: A man in his mid 50s with heavily relapsed MM who received multiple prior lines of therapy, including CAR T-cell therapy, receives talquetamab — Priya Rudolph, MD, PhD (55:44) CME information and select publications
Better Edge : A Northwestern Medicine podcast for physicians
Oncologist George Georges, MD, moderates a discussion with Christine Hsieh, MD, rheumatologist, and Arjun Seth, MD, neurologist, on advancing care for inflammatory myopathies. The panel introduces the Northwestern Medicine Myositis Clinic, a one-stop model that simplifies diagnostics and connects patients to clinical trials. They review current treatment strategies — steroids, IVIg, steroid-sparing agents, rituximab, and JAK inhibitors — along with approaches for refractory disease. The panel also explores cellular therapies, including CAR-T cell trials.
In this episode of ASTCT Talks, host Terri Lynn Shigle, PharmD(The University of Texas MD Anderson Cancer Center; Pharmacy SIG Immediate Past-Chair), sits down with Zainab Shahid, MD (Memorial Sloan Kettering Cancer Center; ID SIG Chair), and Gabriela Maron, MD (St. Jude Children's ResearchHospital). As coauthors of the ASTCT Practice Guidelines, "American Society for Transplantation and Cellular Therapy Best Practice Considerations for the Prevention and Management of Infections After Chimeric Antigen Receptor T-Cell Therapy for Hematological Malignancies," recently published in Transplantation and Cellular Therapy, they discuss the implementation of critical strategies for safeguarding CAR T recipients.The conversation explores the nuances of the manuscript,providing a practical perspective on translating these consensus recommendations into clinical operations.Assessing the Burden of Immunosuppression: Evaluating the cumulative risk factors that predispose CAR T recipients to infection, including heavy pretreatment and the effects of lymphodepletion.Prophylaxis Optimization: Critical considerations regarding the timing, selection, and duration of antimicrobial regimens in the post-CAR T setting.Managing Hypogammaglobulinemia: A pragmatic look at IVIG replacement strategies, balancing emerging clinical evidence with institutional protocols and global product shortages.Addressing Evidence Gaps: Insider insights into the expert panel's deliberations on "grey areas," such as the management of CMV reactivation and optimal post-therapy vaccination schedules.The Pediatric-Adult Continuum: Ensuring that prevention and management strategies are robust and applicable across the full age spectrum of CAR-T recipients.This episode provides essential context for cliniciansseeking to move beyond the published guidelines and operationalize these bestpractices with greater precision and confidence.Thank you to Johnson & Johnson and Legend Biotech forsupporting this episode.
Listen to the episode Treating Side Effects of Intravenous and Subcutaneous Immune Globulin hosted by patient advocate Abbie Cornett. In this episode, we'll be exploring what the side effects of IG treatment are and how to manage them. Our guest today, Michelle Greer, RN, is executive vice president of sales at Nufactor, a specialty infusion company. Michelle has had years of experience working with both patients and clinicians to help people manage IG therapy safely and effectively. Support the show
Can a COVID-19 infection flip a hidden switch in your immune system—triggering arthritis or other autoimmune conditions? Dr. Isabelle Amigues explains what she's seeing in clinic, the science behind post-infection immune shifts, and why treatment and vaccination choices must be tailored to you.What You'll Learn:From infection to inflammation: Real cases of new-onset inflammatory arthritis (rheumatoid, psoriatic) and PMR emerging soon after COVID-19—and how clinicians decide if it's causation or coincidence.The “two-hit” model: Genetics and risk factors (family history, smoking, stress, adiposity) can lie dormant until an infection like COVID-19 triggers overt autoimmunity.Immune overdrive & treatment overlap: Why severe COVID-19 sometimes responds to steroid/IL-6/TNF-blocking therapies—tools also used for autoimmune disease—plus what that tells us about shared pathways.Treat what's in front of you: If your labs/exam meet criteria for RA/PMR/vasculitis/lupus, treat per standard rheumatology care—regardless of whether COVID was the spark.Post-COVID (long COVID) nuance: Dysautonomia, fatigue, exercise intolerance often require team-based care (coaching, nutrition, PT, psychotherapy) to rebalance sympathetic/parasympathetic systems.Vaccination decisions: Not one-size-fits-all. Context matters—prior reactions, exposure risk, location, and current therapies (e.g., IVIG may already provide community antibodies)—so decide with your rheumatologist.Science evolves, partnership endures: Cutting through misinformation with clear, individualized education and a strong patient-physician relationship.What's next: Details on Dr. Amigues' upcoming holistic inflammation webinar and group coaching designed to speed remission and build resilience.If an infection can nudge a predisposed immune system into autoimmunity, which lever will you pull this week to lower baseline inflammation—sleep, stress care, movement, nutrition, or community support?
If you're wondering which therapies may influence care delivery, budgets, and decision making in 2026, the pipeline offers an early preview and it points to a year defined by innovation. We're seeing new first in class treatments, thoughtful next generation agents, and a biosimilar market where fewer launches are offset by important competitive shifts driven by recent approvals. John Schoen and Heather Pace from the Center for Pharmacy Practice Excellence join Stacy Lauderdale, Associate Vice President of Evidence-Based Medicine and Drug Information and your Verified RX program host to highlight pipeline agents worth watching and discuss what they may mean for care delivery and spend management in the year ahead. Guest speakers: John Schoen, PharmD, BCPS Senior Clinical Manager of Drug Information Vizient Center for Pharmacy Practice Excellence Heather Pace, PharmD Senior Clinical Manager of Drug Information Vizient Center for Pharmacy Practice Excellence Host: Stacy Lauderdale, PharmD, BCPS Associate Vice President Vizient Center for Pharmacy Practice Excellence Show Notes: 01:01 — Episode Scope The focus is non-CGT therapies; CGT pipeline will be covered in Part 2. 01:50 — Therapeutic Areas With the Most Approvals Oncology leads the pipeline. Others include infectious disease, neurology, rare disease, endocrine, hepatology, dermatology, and rheumatology. 02:37 — Biosimilars in 2026: Momentum or Headwinds? Discussion of potential “biosimilar void”—only 10% of expiring biologic patents have biosimilars in development. Emerging role of PBM private-label biosimilars. 03:51 — FDA Draft Guidance on Interchangeability FDA exploring interchangeable designation for all biosimilars. Potential shift away from clinical efficacy studies in favor of analytical comparisons. Guidance still in draft and open for public comment. 05:34 — John's Top Picks for First-in-Class Agents 06:11 — Orviglance First manganese-based, oral MRI contrast agent. Advantages for patients with kidney impairment. Used for liver imaging. 06:20 — Why Non-Gadolinium Matters Lower risk of nephrogenic systemic fibrosis. 06:46 — Tabelecleucel First allogeneic EBV-specific T-cell therapy. For EBV-positive PTLD post-transplant. Could become new standard of care. 07:42 — Tanruprubart First therapy specifically for severe Guillain-Barré Syndrome (GBS). Shows improved outcomes over IVIG and plasma exchange. 08:20 — Comparing to Standard of Care Review of improved real-world data outcomes. 09:03 — Therapies That May Shift Care Delivery 09:32 — Icotrokinra: First oral IL-23 antagonist for plaque psoriasis. 10:00 — Insulin Icodec First once-weekly basal insulin for type 2 diabetes. Resubmitted after safety concerns in type 1 diabetes. 10:59 — Honorable Mentions Camizestrant SERD for ER+/HER2– metastatic breast cancer. Ensitrelvir (COVID-19) Oral option for pre-exposure prophylaxis. Also being evaluated for treatment. Doravirine + Islatravir (HIV) Introduces new NRTTI class. Cefepime + Zidebactam Active against metallo-β-lactamase–producing organisms. 14:05 — Key Biosimilar Launches Omalizumab (Xolair) First biosimilars in asthma/allergy space. Aflibercept (Eylea) High competition expected pending litigation. Pertuzumab (Perjeta) First biosimilar anticipated in oncology. 15:31 — Biosimilars Approved in 2025, Impacting 2026 Ustekinumab (Stelara): first full year of competition Denosumab (Prolia/Xgeva): 10–15 biosimilars expected Eculizumab (Soliris): notable for rare disease market entry 17:17 — John's Closing Thoughts Strong mix of first-in-class advances and next-gen convenience therapies. 17:36 — Heather's Closing Thoughts 2026 will focus on speed and scale after the 2025 biosimilar wave. Pharmacists pivotal in ensuring smooth patient transitions. VerifiedRx Listener Feedback Survey: We would love to hear from you - Please click here Subscribe Today! Apple Podcasts Spotify YouTube RSS Feed
Send us a textWhat happens when we challenge our long-standing assumptions about phototherapy in the NICU? In this special installment of our Rethinking Phototherapy series, Ben and Daphna are joined by Dr. Deepak Manhas to examine one of the most complex questions: how should we manage hyperbilirubinemia in preterm infants?Unlike term babies, preemies face unique risks—shorter red blood cell lifespan, immature bilirubin conjugation, lower albumin binding, and increased blood-brain barrier permeability—all of which make them more vulnerable to bilirubin-induced neurologic dysfunction. This conversation explores why traditional guidelines cannot simply be applied to preterm infants and why clinicians often initiate phototherapy earlier.Dr. Manhas discusses the creation of gestation-specific treatment charts, the challenges and dangers of exchange transfusion in this fragile population, and the uncertain role of therapies such as IVIG, albumin, and phenobarbital. The team also unpacks practical issues: what “double phototherapy” should really mean, how to order irradiance and body surface area coverage with precision, and the role of bili blankets in promoting family bonding.By situating this discussion in the broader Rethinking Phototherapy series, the episode highlights both the progress and the unanswered questions in caring for preterm infants.
CME credits: 0.50 Valid until: 29-10-2026 Claim your CME credit at https://reachmd.com/programs/cme/mechanism-driven-gmg-therapy-fcrn-antagonists-and-the-rise-of-precision-neurology/36277/ This Clinical Countdown addresses key challenges in diagnosing and managing generalized myasthenia gravis (gMG), with a focus on FcRn antagonists. Drs. Edmundson and Goyal review diagnostic challenges in gMG, along with the mechanism of FcRn blockade and how it compares to traditional therapies such as corticosteroids, IVIG, and plasma exchange. The discussion highlights pivotal phase 3 trials (ADAPT, MycarinG, and VIVACITY MG), evaluating differences in efficacy, dosing schedules, and administration routes for agents like efgartigimod, rozanolixizumab, and nipocalimab. Faculty discuss how data from these trials informs individualized treatment planning and facilitates shared decision-making. =
Welcome to the Oncology Brothers podcast! In this Challenging Cases episode, we take a deep dive into thrombocytopenia management—a common yet often perplexing topic in everyday hematology and oncology practice. We are joined by Dr. Ronak Mistry, hematologist at the University of Pennsylvania and co‑host of Fellows on Call, to walk through real‑world cases spanning ITP, anticoagulation with low platelets, and HIT. We covered essential topics such as: • Workup of thrombocytopenia and confirming the diagnosis of ITP • First‑ and second‑line ITP therapy—steroids, IVIG, TPO receptor agonists, and splenectomy • Managing anticoagulation in thrombocytopenic patients with cirrhosis and DVT • Step‑by‑step approach to suspected HIT in the inpatient setting • Rapid‑fire tips—transfusion thresholds, chemo‑related thrombocytopenia, and medication culprits Whether you're a hematologist, oncologist, or internal medicine resident, this episode is packed with case‑based teaching points, practical pearls, and the latest guidance from ASH and NCCN for non‑malignant hematology. Follow us on social media: • X/Twitter: https://twitter.com/oncbrothers • Instagram: https://www.instagram.com/oncbrothers • Website: https://oncbrothers.com/ Don't forget to like, subscribe, and tune in for more challenging case discussions, treatment strategies, and expert insights from the world of hematology and oncology! #Thrombocytopenia #HematologyPodcast #ITP #HIT #OncologyBrothers
Host: Jennifer Caudle, DO Guest: Katie Beadon, MD, MASc, FRCPC Multifocal motor neuropathy (MMN) is a chronic, immune-mediated motor neuropathy that can mimic other neuromuscular disorders1-3 and is one of the few motor neuron disorders that is treatable.4 However, disease severity correlates with the length of time a patient remains untreated, which is why early recognition and treatment initiation is essential for preserving long-term motor function.5-6 Joining Dr. Jennifer Caudle to discuss the diagnosis and management of MMN is Dr. Katie Beadon, Co-Director of St. Paul's Hospital Immunotherapy in Neurology Clinic and an Assistant Clinical Professor at the University of British Columbia in Vancouver. References: Guimarães-Costa R, Bombelli F, Léger JM. Multifocal motor neuropathy. Presse Med. 2013;42(6 Pt 2):e217-24. doi:10.1016/j.lpm.2013.01.057 Beadon K, Guimarães-Costa R, Léger JM. Multifocal motor neuropathy. Curr Opin Neurol. 2018;31(5):559-564. doi:10.1097/WCO.0000000000000605 Vlam L, van der Pol WL, Cats EA, et al. Multifocal motor neuropathy: diagnosis, pathogenesis and treatment strategies. Nat Rev Neurol. 2011;8(1):48-58. doi:10.1038/nrneurol.2011.175 Yeh WZ, Dyck PJ, van den Berg LH, Kiernan MC, Taylor BV. Multifocal motor neuropathy: controversies and priorities. J Neurol Neurosurg Psychiatry. 2020;91(2):140-148. doi:10.1136/jnnp-2019-321532 Cats EA, van der Pol WL, Piepers S, et al. Correlates of outcome and response to IVIg in 88 patients with multifocal motor neuropathy. Neurology. 2010;75(9):818-25. doi:10.1212/WNL.0b013e3181f0738e Van …
Host: Jennifer Caudle, DO Guest: Katie Beadon, MD, MASc, FRCPC Multifocal motor neuropathy (MMN) is a chronic, immune-mediated motor neuropathy that can mimic other neuromuscular disorders1-3 and is one of the few motor neuron disorders that is treatable.4 However, disease severity correlates with the length of time a patient remains untreated, which is why early recognition and treatment initiation is essential for preserving long-term motor function.5-6 Joining Dr. Jennifer Caudle to discuss the diagnosis and management of MMN is Dr. Katie Beadon, Co-Director of St. Paul's Hospital Immunotherapy in Neurology Clinic and an Assistant Clinical Professor at the University of British Columbia in Vancouver. References: Guimarães-Costa R, Bombelli F, Léger JM. Multifocal motor neuropathy. Presse Med. 2013;42(6 Pt 2):e217-24. doi:10.1016/j.lpm.2013.01.057 Beadon K, Guimarães-Costa R, Léger JM. Multifocal motor neuropathy. Curr Opin Neurol. 2018;31(5):559-564. doi:10.1097/WCO.0000000000000605 Vlam L, van der Pol WL, Cats EA, et al. Multifocal motor neuropathy: diagnosis, pathogenesis and treatment strategies. Nat Rev Neurol. 2011;8(1):48-58. doi:10.1038/nrneurol.2011.175 Yeh WZ, Dyck PJ, van den Berg LH, Kiernan MC, Taylor BV. Multifocal motor neuropathy: controversies and priorities. J Neurol Neurosurg Psychiatry. 2020;91(2):140-148. doi:10.1136/jnnp-2019-321532 Cats EA, van der Pol WL, Piepers S, et al. Correlates of outcome and response to IVIg in 88 patients with multifocal motor neuropathy. Neurology. 2010;75(9):818-25. doi:10.1212/WNL.0b013e3181f0738e Van …
What happens when your capacity looks different every single day, but your business still has to keep moving forward?In this episode of Business with Chronic Illness, I'm joined by Ashley Carlson, an agency owner, mom of two, and chronic illness advocate, to talk about the hard but freeing truth: you can do anything, but you can't do everything.Ashley opens up about building and growing her agency while navigating multiple chronic illness diagnoses, monthly IVIG infusions, and the everyday realities of parenting. She shares how she's redefined productivity, learned to ask for help, and built systems that allow her business to run even when she needs to rest.By the end of this episode, you'll walk away with:Practical systems for sustainability – why delegation, accountability, and team support make your business more resilient.A new way to define success – learning how to honor today's 100% (even if it looks different from yesterday).Permission to rest without guilt – shifting out of the perfectionism trap and embracing flexibility in life and business.Ashley's story is a reminder that running a business with chronic illness is not about pushing harder—it's about creating support, sustainability, and joy along the way.Connect with Ashley:Website: https://www.elevatevbsolutions.comInstagram: https://www.instagram.com/elevatevbsolutions/LinkedIn: https://www.linkedin.com/in/ashleymcarlson/Leave us a Review and share this episode with a friend.Send Me A Text & Share Your QA's or ThoughtsJoin The 5-Day Audio Series - Rooted Sales Loved this episode? Leave a review: https://www.craftedtothrive.com/reviews/new/Products We Love + Special Guest Gifts → Want to support the show and treat yourself? We've created a quick-access list of products I personally use and love, exclusive savings from podcast guests, and other gems that can help you live well and do business with chronic illness. Explore our faves + savings here!Subscribe HERE to Chronically Profitable, A free, exclusive email series that shows you how to sell with self-trust, create content that converts, and use long-form strategies, especially podcasting, to attract dream clients consistently, even during the ups and downs of business and life. You'll learn how to build a rhythm that helps you sell even while you rest.To Start and Grow A Creative or Service-Based Business with Chronic Illness, Join
Kaitlyn Oleinik is a chronic illness advocate and the author of Revival: My Journey with Neuropsychiatric Lyme Disease. She was bitten by a tick at age six and spent much of her life fighting an invisible illness while being dismissed by the medical system. Diagnosed with Lyme disease and co-infections in her teens, Kaitlyn has endured everything from hallucinations and involuntary psych holds to IVIG and stem cell treatments. Her book and voice give a name to the unspoken pain of countless others living with Lyme.
Dr. Joseph J. Burrascano Jr., a pioneer in the field of Lyme, began his practice in East Hampton, NY, in 1981, where he identified and detailed the clinical aspects of Lyme in a high-prevalence area. Renowned for his groundbreaking diagnostic and treatment guidelines since 1984, he has advised the CDC, NIH, and U.S. Senate, authored extensive publications, and is a founding member of ILADS, continuing to educate globally.
Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions: Will: Dr. Cabral, I am trying to get information on a healthy all natural substitute for alcohol. I have stopped drinking since I've been actively using your products and enjoying my new lifestyle. Still sometimes I have the need/urge to relax in the evenings or while out with friends and family. What can you tell me about this product? https://www.calmingco.com/?srsltid=AfmBOor6Jl5JF5dSf0ia1k1GSuWSMLPznoChs_nnnV8LQr88V4C7yR6u Christin: Can you speak to some ways to support a child (11 yrs) with type 1 diabetes? My daughter was diagnosed 3 years ago with autoimmune T1D. I've looked into stem cell therapy as one option to restore pancreatic function and several of the protocols include an IV detox prior to the therapy. Some of them can be done with children and others cannot. I would love to help her body every way possible, but it seems options are often limited for children. What can I do to help her body function optimally? Patrick: Hey dr I just listened to your podcast on kidney stones. I believe you mentioned before that you could do a shot of olive oil and lemon but you didnt mention it this time is it still something you recommend. Thanks Andy: Hi dr c, we love all you do. Post jab in 2021, and almost immediately, I developed burning all over my body which has now culminated in a diagnosis of small fiber neuropathy and pots. Perhaps the worst symptom has been my intolerance to exercise in the form of rapid heart rate and headaches post exercise. I have had done all types of functional medical tests including stool tests, organic acid tests, mould tests and listened to all your pots podcasts. Nothing major ever shows up. I did you mould protocol which helped some underlying gut issues. I have qualified for IVIG treatment. Do you suggest running the big 5 or proceeding with the IVIG and do you have any views on long term effects of IVIG. I am 33, healthy and was a long distance runner before all this. Love from down under. Kim: Hi Dr. Cabral, My 13 year old son has HSP which is inflammation of the blood vessels. That's what I gather anyway. We found out he had it after coming down with a virus and/or food poisoning. He had red dots all over the lower legs which turns out was due to the capillaries breaking. He has high amounts of protein in his urine. We are going to meet with a specialist for it but I was wondering if you could help me figure out what supplements to have him take? They're probably going to want to put him on a small dose of blood pressure medication to relieve some stress on his blood vessels but he doesn't have high blood pressure. I know there are things I can do to help his body but I just don't know what that is. Any advice you have for me to help my child, I would really appreciate it! Thank you for tuning into today's Cabral HouseCall and be sure to check back tomorrow where we answer more of our community's questions! - - - Show Notes and Resources: StephenCabral.com/3438 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? The best way to help me spread our mission of true natural health is to pass on the good word, and I read and appreciate every review!
In his weekly clinical update, Dr. Griffin with Vincent Racaniello bewail the attack on science within the US and withdrawal from the global health communities, association between the shingles vaccine and reduced dementia occurrence, ending of Uganda's ebola outbreak, undermining effective responses to human bird flu infections, growing measles outbreak in the US and dire predictions of the return of vaccine preventable diseases including polio if vaccination rates continue to decline, before Dr. Griffin reviews recent statistics on RSV, influenza and SARS-CoV-2 infections the WasterwaterScan dashboard, how HHS is undermining the Novavax COVID-19 vaccine, if Paxlovid reduces stroke, where to find PEMGARDA, provides information for Columbia University Irving Medical Center's long COVID treatment center, where to go for answers to your long COVID questions and contacting your federal government representative to stop the assault on science and biomedical research. Subscribe (free): Apple Podcasts, RSS, email Become a patron of TWiV! Links for this episode Lab animal RIFFing (NY Times) Herpes zoster vaccination and dementia occurrence(JAMA) The recombinant shingles vaccine is associated with lower risk of dementia (Nature Medicine) Uganda declares end to latest ebola outbreak (Reuters) Enhancing the response to avian influenza in the US and globally (LANCET: Regional Health-Americas) H5 Bird Flu: Current Situation (CDC: Avian Influenza Bird flu) Measles Update — United States, January 1–April 17, 2025 (CDC: MMWR) Measles in Europe……..but greater in the US (CIDRAP) Measles – Annual Epidemiological Report for 2024 (ECDC: European Center for Disease Prevention and Control) Measles (ECDC: European Center for Disease Prevention and Control) Measles cases and outbreaks (CDC Rubeola) Measles 800 in Texas…. (Texas Health and Human Services) 2025 Measles outbreak guidance (New Mexico Health) On the precipice of disaster': Measles may be endemic in 25 years if vaccine uptake stays low, model predicts (CIDRAP) Modeling Reemergence of Vaccine-Eliminated Infectious Diseases Under Declining Vaccination in the US (JAMA) Measles vaccine recommendations from NYP (jpg) Get the FACTS about measles (NY State Department of Health) Measles (CDC Measles (Rubeola)) Measles vaccine (CDC Measles (Rubeola)) Presumptive evidence of measles immunity (CDC) Contraindications and precautions to measles vaccination (CDC) Measles (CDC Measles (Rubeola)) Measles (CDC: Measles Rubeola) Adverse events associated with childhood vaccines: evidence bearing on causality (NLM) Measles Vaccination: Know the Facts(ISDA: Infectious Diseases Society of America) Deaths following vaccination: what does the evidence show (Vaccine) Influenza: Waste water scan for 11 pathogens (WastewaterSCan) US respiratory virus activity (CDC Respiratory Illnesses) Weekly surveillance report: clift notes (CDC FluView) Respiratory virus activity levels (CDC Respiratory Illnesses) 200 children die from flu (CIDRAP) Weekly surveillance report: clift notes (CDC FluView) FDA-CDC-DOD: 2025-2046 influenza vaccine composition (FDA) RSV: Waste water scan for 11 pathogens (WastewaterSCan) US respiratory virus activity (CDC Respiratory Illnesses) RSV-Network (CDC Respiratory Syncytial virus Infection) Waste water scan for 11 pathogens (WastewaterSCan) COVID-19 deaths (CDC) COVID-19 national and regional trends (CDC) COVID-19 variant tracker (CDC) SARS-CoV-2 genomes galore (Nextstrain) Health secretary RFK Jr. declares certain vaccines have ‘never worked,' flummoxing scientists…..what certain vaccines?(STAT News) More FDA uncertainty roils full approval for Novavax COVID vaccine (CIDRAP) FDA Punts on Major Covid-19 Vaccine Decision After Ouster of Top Official (WSJ) U.S. health officials inject new uncertainty into approval process for Covid boosters (STAT News) Interim Clinical Considerations for Use of COVID-19 Vaccines in the United States (CDC: COVID-19) Where to get pemgarda (Pemgarda) EUA for the pre-exposure prophylaxis of COVID-19 (INVIYD) Infusion center (Prime Fusions) CDC Quarantine guidelines (CDC) NIH COVID-19 treatment guidelines (NIH) Drug interaction checker (University of Liverpool) Infectious Disease Society guidelines for treatment and management (ID Society) Molnupiravir safety and efficacy (JMV) Convalescent plasma recommendation for immunocompromised (ID Society What to do when sick with a respiratory virus (CDC) When your healthcare provider is infected/exposed with SARS-CoV-2 (CDC) Managing healthcare staffing shortages (CDC) Steroids, dexamethasone at the right time (OFID) Anticoagulation guidelines (hematology.org) Into the Unknown: Practical Remdesivir Restriction in the Era of Widespread SARS-CoV-2 Seropositivity (CID) Tocilizumab and IVIG experience during the service follow-up in patients with severe COVID-19 pneumonia(Rev Insti MedTrop Sao Paulo) Daniel Griffin's evidence based medical practices for long COVID (OFID) Long COVID hotline (Columbia : Columbia University Irving Medical Center) The answers: Long COVID Risk of New-Onset Type 2 Diabetes Among Vaccinated Adults After Omicron or Delta Variant SARS-CoV-2 Infection(JAMA) Reaching out to US house representative Letters read on TWiV 1214 Dr. Griffin's COVID treatment summary (pdf) Timestamps by Jolene Ramsey. Thanks! Intro music is by Ronald Jenkees Send your questions for Dr. Griffin to daniel@microbe.tv Content in this podcast should not be construed as medical advice.
This AANEM podcast features Dr. Joome Suh, a neurologist and neuromuscular specialist at Brigham and Women's Hospital, interviewed by neuromuscular fellow Dr. Nadia Khalil. They discuss HMG-CoA reductase immune-mediated necrotizing myopathy (HMGCR IMNM), a rare autoimmune muscle disease often associated with statin use. The discussion covers clinical presentation, epidemiologic considerations, histopathologic findings, and treatment approaches, with special focus on Dr. Suh's recent research published in Muscle and Nerve with co-author Dr. Anthony Amato. Their study found that patients receiving maintenance IVIG as part of their regimen were more likely to have a normal CK at 6 months and the daily prednisone-equivalent was lower. A sub-group analysis suggested IVIG as monotherapy is effective.
The inflammatory and infectious optic neuropathies are a broad, heterogeneous, and common group of diseases producing visual loss. Although many now-distinct syndromes have been previously combined as “typical or atypical optic neuritis,” recent developments highlight the importance of precision terminology as well as an individualized evaluation and treatment approach. In this episode, Gordon Smith, MD, FAAN speaks with Eric Eggenberger, DO, MS, FAAN, author of the article “Optic Neuritis” in the Continuum® April 2025 Neuro-ophthalmology issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Eggenberger is a professor of ophthalmology, neurology, and neurosurgery at the Mayo Clinic in Jacksonville, Florida. Additional Resources Read the article: Optic Neuritis Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing someone who really needs no introduction, Dr Eric Eggenberger, about his article on optic neuritis, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Eric, welcome to the podcast, and maybe you can introduce yourself to our audience. Dr Eggenberger: Thank you. Thanks for having me. So, my name is Eric Eggenberger. I work at Mayo Clinic Florida, and I am involved exclusively in neuro-ophthalmology. Dr Smith: I just had the pleasure, Eric, of talking yesterday with Lindsey De Lott about non-optic neuritis causes of optic neuropathy. And so, I'm going to kind of reference a little bit what I learned yesterday. She was great. I wonder if you might begin by talking a little bit about nomenclature. You talk about the need for use of precise terminology in your article. And yesterday she taught me a lot about the risk of misdiagnosis and other causes of optic neuropathy, and the two seem related. So, I wonder if you can maybe lay the foundation for our conversation by talking about terminology? Dr Eggenberger: I think that's a great point. So, we are in an era now where, instead of lumping all these different diagnoses together, we have learned to split apart some of these clinical entities. And so, I think it's really important that we focus on precise terminology and recognize that all optic neuritis is not the same. And we have very different, distinct clinical pathways for these imaging pathways, treatment pathways, for these different types of optic neuritis, whether that's MS related, whether it's MOG related or aquaporin-4 related. Dr Smith: So, I wonder maybe we can begin by just, you know, giving our listeners wisdom, pearls, and pitfalls about, how do you recognize when someone with a suspected optic neuropathy has optic neuritis versus a noninflammatory optic neuropathy? Dr Eggenberger: So, that's a really important issue because there's a lot of clinical overlap in terms of exam findings. So, for instance, in any optic neuropathy, let's say it's unilateral, you typically are going to see decreases in acuity and field and color, and you're going to see a relative afferent pupillary defect. And then it's really the context that that occurs in that helps us distinguish different disease entities. So, with optic neuritis, typically you're going to have pain. And that's oftentimes going to be in the younger populations compared to some of the other common optic neuropathies we see, like ischemic optic neuropathy, for instance. Dr Smith: Right. So maybe we can talk a little bit about, kind of, your overall diagnostic approach, right? A lot of this is, of course, based on age and context, but young people get ischemic lesions and older people can have inflammatory lesions. So, what's your overall approach to the patient you just described? Let's say it's a forty-eight-year-old woman who comes to the emergency department with subacute unilateral vision loss and there's dyschromatopsia, APD, reduced acuity. And, you know, let's just say a fairly, you know, benign-looking fundoscopic exam. What do you do to evaluate that patient? Dr Eggenberger: In that particular context, I think we're looking at other contextual clues. Is there other vascular risk factors or other things to point you in one direction or the other? One of the important parts you mentioned was the fundus exam. So, we know with ischemic optic neuropathy, 100% of the time with AIOM, you're going to see disc edema. And so, in the context of that story, we want to confirm on our exam an optic neuropathy, and then we can kind of focus on the retrobulbar courses or different types of optic neuropathies. From an exam perspective, in that particular patient we'd be looking to measure the acuity, quantify that. And in the ER, you're not going to be able to do a perfect field, but you'll get some sense of the field and how much field loss there is. And then as you mentioned, the afferent pupillary defect is critical. And we're going to get a little bit of the historical features in terms of pain. With typical retrobulbar optic neuritis, most of those patients are going to experience some pain, and usually it's pain on eye movements. And those would be the clinical things to focus on. Other exposures the patient may or may not have had, any other concomitant conditions, would all help point you in different directions, perhaps, and then we're probably on towards imaging. Dr Smith: Yeah, maybe you can talk a little bit about that? What's the appropriate use of imaging? I mean, presumably the patients, like the one I just threw out there, are pretty much all going to get neuroimaging. What's your approach to that? How do you protocol the study? What should we be looking for? Dr Eggenberger: In our clinic, we would typically be ordering an MRI orbit and brain, and each of those has a specific purpose. The orbit is going to show us the extent of the optic neuropathy. So, we're particularly looking for a longitudinally extensive optic nerve lesion or more than half of the optic nerve involved. And most patients acutely, if it isn't an “itis" situation, we'll see enhancement. And then the MR brain is going to be useful for looking for other evidence of demyelination within the central nervous system. We may at some point get down to doing an MR cord, but I think acutely it's going to be brain and orbit that most of our patients are getting. Dr Smith: Let's say that we did the scan and, sure enough, there's sort of a shorter segment, so less than half the length of the nerve region of enhancement. What's the rest of your diagnostic evaluation look like for that patient? Dr Eggenberger: So, in that particular case, we would look at the remainder of the brain. So, we're looking for other evidence of demyelination and any other contextual clues, systemically that would point you one direction or another. But with a shorter segment involved, one of the more common things we might encounter would be multiple sclerosis-related optic neuritis. Dr Smith: Would you look for aquaporin-4 and MOG in a patient with what appears to be an isolated, uncomplicated short segment optic neuritis? Dr Eggenberger: So, I think it really depends a bit on the context. I would never fault anybody for looking at MOG or an aquaporin-4 in that context because those are really treatment-altering diagnoses, but the yield in this particular case with a short segment involved and depending on the acuity and other features is probably going to be pretty low. Dr Smith: I really liked as an aside- I wasn't going to go there next, but you kind of got me thinking about it, you have a really nice section in your article. Which, all of it's great, but talking about how to manage low titer MOG antibodies. I wonder if you could talk about that because I think that's a lesson, maybe, that is transferable to a lot of other testing that we do. in terms of pre-prior probability and titer and so forth. Dr Eggenberger: Yeah, that's really an important point. So, we've seen this come up a number of times where the MOG antibody is a very good test, but in low titer it has a relatively low positive predictive value, perhaps 50%. In those cases, particularly without a classic clinical context, you have to be extremely alert for some other diagnosis that could mimic what you think is inflammatory demyelinating optic neuritis, but in fact is infectious or some other cause. Dr Smith: Yeah, super, super important and helpful. In terms of aquaporin-4, how does that compare in terms of predictive values, lower titer positive results? Dr Eggenberger: So aquaporin-4, the test has a very high specificity. So, it's quite useful if positive. You have to keep in mind there can be some false negatives, but the test otherwise is quite specific. And that is a diagnosis, you know, we never want to miss. It's a vicious disease. It tends to be a blinding disease, particularly without treatment. Bad things happen when we miss that, and we want to get on that diagnosis early and do pretty aggressive early and prophylactic treatment. Dr Smith: Your article covers not only the common causes of optic neuritis and, you know, MS, isolated optic neuritis, MOGAD NMO, you talk about a bunch of other things. I wonder, in this patient that we've been discussing, in the absence of any other historical information that seems relevant---or maybe you can define what would seem relevant---would you do other evaluation in that individual, other serologic evaluation and so forth, just in terms of diagnosis? Dr Eggenberger: In that particular case, without other red flags, I don't think I would initially. And follow-up is going to give you a lot of this context. So, you'd be on the lookout for other systemic conditions. So, if the patient had some arthropathy, if the patient had any pulmonary disease hints, if there was anything else that could lead you on a broader expedition. But I think in the context of this case, acutely in the ER, I probably wouldn't do a big lab plug for this. I probably would kind of go down the most likely road and start our treatments, and then follow that patient up. Dr Smith: Yeah, I know your article does a really great job, I think, of outlining when do you need to think about some of these less common causes. Well, can we talk about treatment, Eric? Because I want to move on to some other things. But- so, we've got a patient with isolated optic neuritis, nothing else, you know, in terms of the other antibodies we've talked about. What state-of-the-care- or, state-of-the-art treatment for that patient? Dr Eggenberger: So, the acute treatment for these inflammatory, optic neuritis-type cases is very similar Initially. High dose steroids remains kind of the standard. And then, in MS-related optic neuritis, we may or may not see a taper. So many times it's just an acute treatment of three to five days high dose. Whether that's oral or PO, we could institute either depending on the particular case. And then the taper would depend on the potential cause. So, for instance, with these antibody-driven diseases---so with MOG- or particularly with aquaporin-4---if it's a longitudinally extensive region of optic nerve involved, we tend to use a longitudinally extensive taper. And so, we use prednisone in those cases for several months while we're getting everything else set and deciding what the overall course is going to bring. Dr Smith: What about IV versus oral? There must be something about my practice. I was telling this to Lindsey. Every time on our hospital service, we seem to have at least two patients with optic neuropathies, which I always enjoy, but I find it's a little weird to admit someone who's doing just fine otherwise to the hospital with three days of IV SOLU-MEDROL. So, I'm always trying to figure out, like, how can I get this patient home? And your article had the best term I've heard in a long time, which is “SOLU smoothies.” I mean, are there other strategies that you sometimes use, other than just high-dose IV methylprednisolone? Dr Eggenberger: So, I agree with you. It's sometimes hard to admit somebody for just an IV therapy. And we'll do this as an outpatient, high-dose IV, but we'll also use high-dose orals. And in times in the past when there's been methylprednisolone shortage, we've used high-dose oral or IV dexamethasone as well. I think the IV form, although it's the gold standard, the high-dose oral forms have pretty equivalent bioavailability and are pretty tolerable in my experience. And certainly more convenient. Dr Smith: I wonder if we should switch and maybe talk a little bit about aquaporin-4, I mean, you emphasized that this is a vicious disease---I love the way you describe that---and often blinding. What updates do you have in terms of our therapeutic approach to NMO? That's been rapidly evolving of late. Dr Eggenberger: Right, so these are cases we're always going to share with neuroimmunology. And it requires kind of a multidisciplinary approach, in my opinion, for ideal or for best outcomes. And so, all of these patients are going to get put on prophylactic medications. So, this is a disease you just can't leave untreated. Bad stuff will happen for sure. And we now, fortunately, have some approved, FDA-approved medications that can positively impact the course of this disease. So, that's been a welcome addition. Dr Smith: What are the FDA-approved medications at this point for NMO? Dr Eggenberger: So, there are several at this point, and this is an area that's in growth, fortunately. And again, these are cases we're going to be sharing with our neuroimmunology colleagues. So, these are IV medications typically aimed at complement or CD19. And they all are relatively effective at quieting the course of the disease. Dr Smith: Maybe we can talk a little bit about MOG? I think that most of our listeners are probably pretty familiar with aquaporin-4 and NMO, what- maybe you could describe MOG a little bit and the therapeutic approach for patients with MOG-associated disease? Dr Eggenberger: So, MOG has been a real interesting kind of condition to learn more about. We certainly see a lot of MOG, and I'm sure we saw MOG before it was formally described, but I think we just thought it was kind of a benign, maybe monophasic MS type of presentation. But MOG tends to come in with a loss of acuity that kind of rivals aquaporin-4. So, the acuity tends to be pretty, pretty depressed, but it's very steroid-responsive. So, a lot of times these are the patients, you'll see that their vision will start to improve even when they're on the initial few days of the high-dose steroids. And many times we can get their vision back to 20/20 or very close to that. Dr Smith: And do these patients need chronic management? Dr Eggenberger: So, that's an area of controversy to some degree. About 50% of the optic neuritis MOG-related cases are going to have a relapsing course. And because the disease is steroid-responsive, many times we'll follow these patients after a first attack to see if this is the condition that's going to declare itself to be relapsing or if this is just going to be a monophasic kind of presentation of optic neuritis. We don't have great biomarkers to separate patients who are going to be in that 50% monophasic course versus the other half. It'll be relapsing. And so, it depends on the patient. If there's somebody that's, as many of these patients are, been very steroid responsive, they get back to 20/20, we can teach them about the disease so that if they do have a relapse, we can get them high-dose steroids in a relatively rapid fashion and they're otherwise healthy, we're probably going to watch that patient. And if it's somebody that doesn't recover 100%, there's other issues with treating them with high-dose steroids potentially in the future, then we may learn more towards an earlier prophylactic approach in that patient. Dr Smith: And what would that approach look like? Is it different from NMO or using more IVIG or B cell depletion as opposed to complement inhibition, for instance? Dr Eggenberger: In MOG, we know that the B cell depletion strategies don't work as well. And so most times we're turning to IVIG, and we found that pretty effective. That's kind of our go-to at this point. Dr Smith: Eric, it's a joy talking to you and I'd love to keep going about content, but I'll refer our listeners to your outstanding article. I mean, you're such a highly regarded neuro-ophthalmologist and educator. I wonder if you could talk to us about why you've done neuro-ophthalmology, and maybe this is an opportunity for you to convince all of our great residents that are listening or students what's great about being a neuro-ophthalmologist. Dr Eggenberger: I think neuro-ophthalmology is by far the most interesting part of neurology. So, it's an area that I think a lot of general neurologists, in my view, don't get enough of in their residency. But it's kind of the essence of neurology, where in neurology you're localizing down to the millimeter and in neuro-ophthalmology, we're localizing down to the micron level. We have several new emerging diseases like these varieties of optic neuritis we're focused on. We're learning lots about those. You get to be involved in lots of different areas of neurology. So, we'll see not just demyelinating conditions, we'll see trauma as it relates to the visual system. And we'll see tumor, and we see all different flavors, stroke, and in any piece of neurology, commonly we'll have some vision aspect that we that we get involved in. So, we see a wide variety of conditions. So, I think it's been a really exciting place to be within neurology. And it's rapidly changing at this point. We're getting new therapeutics. So, it's, I think it's a great time to be a neuro-ophthalmologist. Dr Smith: Yeah, listening to you talk and just reflecting on it, it's really true. Neuro-ophthalmology does cover the entire span of neurology, right? I'm a neuromuscular guy and we see a lot of ocular myasthenia, which is another super exciting area. But we've been talking about optic neuritis, and your article talks about infectious causes and the paraneoplastic and a whole host of things. So, you're a great advocate and salesperson for your field. You convinced me. Dr Eggenberger: Efferent neuro-ophthalmology we love, we could talk about ocular myasthenia and other aspects for another hour. And we get involved in all kinds of cases: third nerve palsies, ocular myasthenia, trauma that involves the efferent system, all different aspects. It's really a great subspecialty, and you get to see a bit of all of neurology. Dr Smith: I'm trying to remember who it was, Eric. It was an attending of mine at medical school. I went to medical school at the Mayo Clinic in Rochester, and I want to say it was Manny Gomez, who was a very famous tuberous sclerosis person, who told me that neuro-ophthalmology was the most elegant specialty within neurology. That stuck with me. Thank you so much for joining me today. I really appreciate it. Dr Eggenberger: Thank you. I appreciate it as well. Dr Smith: So again, today I've been interviewing Dr Eric Eggenberger about his really wonderful article on optic neuritis, which appears in the most recent issue of Continuum on neuro-ophthalmology. Be sure to check out Continuum audio episodes from the neuro-ophthalmology and other issues. And listeners, thank you very much for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.
In this vital and technically complex presentation, Dr Scott Antoine explains why PANS (Pediatric Acute-Onset Neuropsychiatric Syndrome) and PANDAS (Pediatric Autoimmune Neuropsychiatric Disorder Associated with Streptoccocal Infection) are common and overlooked root cause of psychiatric symptoms in children (such as OCD, restrictive eating, anxiety, emotional distress, depression, dramatic mood swings, psychosis and suicidal ideation). In doing so, he encourages physicians to explore mental health in an entirely new way, especially in the treatment of children. Dr Scott Antoine completed his undergraduate training at the University of Scranton, after which he completed his doctorate at the Philadelphia College of Osteopathic Medicine. He later served in active duty with the United States Army as an Emergency Physician and worked as an Emergency Physician at St. Francis Hospital until 2019. In addition to his board certification in Emergency Medicine, he achieved board certification in Integrative Medicine and holds certifications in Functional Medicine through the Institute for Functional Medicine (IFM) and A4M. His book The Comprehensive Physicians Guide to the Management of PANS and PANDAS was released in February 2024 to excellent reviews. He discovered his calling when he and his wife Ellen, also a Functional and Integrative Medicine physician, battled to correctly diagnose the root-cause of their 12 year old daughter's sudden-onset OCD, insomnia, rage, as PANS. Since then, he has helped hundreds of children recover from PANS and PANDAS, and in 2019 helped to pass a law which prohibits insurance companies in Indiana from denying coverage for medical care (including IVIG) for children with PANS and PANDAS. In this richly informative personable interview, he presents an evidence-based outline of the successful ways to both diagnose and treat PANS and PANDAS, and stresses that they are not nearly as rare as mainstream medicine seems to believe. He decodes complex medical expertise, referencing over 300 clinical studies and peer-reviewed medical literature, that identify biological mechanisms and the root causes that underlie PANS and PANDAS. In this episode, Dr Antoine unravels why PANS/PANDAS can have such a profound, often sudden impact on Children's psychiatric health, and demands that PANS and PANDAS be considered more broadly in psychiatric diagnoses. In this episode you will learn how infections, toxins and the immune system interplay in the expression of harmful psychiatric symptoms, why they cause PANS and PANDAS, and how they can be successfully treated. In this episode learn about: Why PANS and PANDAS are hidden and common root cause of OCD, violent mood swings, depression, anxiety and suicidality, how they are diagnosed, and the role of testing. Why physicians routinely overlook and even deny PANS and PANDAS as a cause of mental health symptoms. Why toxins and infections can trigger PANS and PANDAS and their associated neuropsychiatric symptoms. How Strep is related to autoimmunity and why to treat it even if strep tests are negative. Why a range of infections - not just strep or Lyme borrelia - can trigger neuropsychiatric symptoms (OCD, attention issues, hallucinations, psychosis, depression, suicidal ideation), including other tick-borne co-infections, influenza, Epstein Barr, chlamydia pneumonia and Covid. Ways environmental chemicals, heavy metals, pesticides and mycotoxins (mould) can lead to inflammation and autoimmunity. The concrete link between rheumatic fever and OCD, ADHD, mood issues and psychosis. Other causes of autoimmunity, including genetics, intestinal permeability, infection/T-cell activation and molecular mimicry (the mechanism by which microbes can induce autoimmunity). The 4 vital components of treatment: 1) find and treat infections 2) find and remove toxins 3) re-regulate the immune system 4) break neurological loops (OCD, anxiety). How to treat infections using prolonged use of antibiotics, and which antibiotics to choose. Why herbs (isatis, baicalensis, cat's claw etc) can reduce the duration of antibiotic use, and the studies that prove it. The binders (activated charcoal, zeolites, humic acid) and bitters that help remove toxins. Ways medications (naltrexone and steroids) can help re-regulate the immune system. Why and when IVIG is used for the treatment, why it can relieve and cure symptoms (OCD, anxiety and tics) quickly. How Exposure Response Prevention (ERP) and hypnosis outperforms medications in breaking neurological loops (OCD, anxiety, intrusive thoughts) Other helpful interventions that assist healing; nutrients, diet changes and probiotics.
Renee improved CIDP, gastroparesis, anxiety, depression, migraines, eczema, and perimenopausal symptoms. Instagram: @eatingmeattowalk YouTube: @eatingmeattowalk Timestamps: 00:00 Trailer 01:14 Introduction 05:34 Overcoming setbacks with IVIG treatment 09:53 Healing with carnivore diet 13:36 Medication weaning and lifestyle changes 15:12 Drug company influence and desperation 18:22 Normal EMG results discussion 21:38 Diet regret: harmed husband's health 26:09 Choosing health over heart risk 29:11 Reevaluating veganism and health 30:16 Veganism and misdiagnosed grip issues 34:16 Oncology: a revolving door experience 36:50 Struggles with suicide and anxiety 40:41 Vaccination experience and COVID challenges 44:54 Demyelination and nerve recovery process 48:31 Carnivore diet for chronic illness 51:57 Diagnostics beyond MRIs 52:51 Where to find Renee Join Revero now to regain your health: https://revero.com/YT Revero.com is an online medical clinic for treating chronic diseases with this root-cause approach of nutrition therapy. You can get access to medical providers, personalized nutrition therapy, biomarker tracking, lab testing, ongoing clinical care, and daily coaching. You will also learn everything you need with educational videos, hundreds of recipes, and articles to make this easy for you. Join the Revero team (medical providers, etc): https://revero.com/jobs #Revero #ReveroHealth #shawnbaker #Carnivorediet #MeatHeals #AnimalBased #ZeroCarb #DietCoach #FatAdapted #Carnivore #sugarfree Disclaimer: The content on this channel is not medical advice. Please consult your healthcare provider.
In this episode of the Bendy Bodies Podcast, Dr. Linda Bluestein welcomes Dr. Ilene Ruhoy, a board-certified neurologist and environmental toxicologist, for an in-depth discussion on brain fog, cognitive dysfunction, and chronic fatigue in conditions like Ehlers-Danlos Syndrome (EDS), Mast Cell Activation Syndrome (MCAS), and dysautonomia. Dr. Ruhoy shares insights on the immune system's role in neurological symptoms, the impact of mast cell activation, and the role of treatments like peptides, IVIG (intravenous gammaglobulin), plasmapheresis, and immune modulators. They also discuss the hidden effects of histamine on the brain, how sensory sensitivity contributes to fatigue, and the role of regenerative medicine in connective tissue healing. This episode is packed with cutting-edge research and practical solutions for improving cognitive function and energy levels. Takeaways: Brain Fog & Fatigue Are Linked to Immune Dysfunction: Cognitive dysfunction in conditions like EDS, MCAS, and POTS is often tied to inflammatory responses and immune dysregulation rather than just histamine alone. Plasmapheresis & IVIG Can Help Some Patients: For severe cases, plasmapheresis removes inflammatory mediators from the blood, and IVIG helps regulate immune function, leading to cognitive and fatigue improvements. Histamine Plays a Complex Role in Brain Function: While histamine can trigger symptoms in MCAS patients, it also has neuroprotective effects, making antihistamine overuse a potential issue for some. Sensory Sensitivity Increases Cognitive Load: Many people with EDS and related conditions experience hypersensitivity to light, noise, and smells, which can overwhelm the nervous system and worsen fatigue. Regenerative Medicine May Support Connective Tissue Repair: Peptides, stem cell therapy, and targeted immune modulation are promising areas of research to help strengthen connective tissue and reduce systemic inflammation. Connect with YOUR Hypermobility Specialist, Dr. Linda Bluestein, MD at https://www.hypermobilitymd.com/. Thank YOU so much for tuning in. We hope you found this episode informative, inspiring, useful, validating, and enjoyable. Join us on the next episode for YOUR time to level up your knowledge about hypermobility disorders and the people who have them. Join YOUR Bendy Bodies community at https://www.bendybodiespodcast.com/. Learn more about Human Content at http://www.human-content.com Podcast Advertising/Business Inquiries: sales@human-content.com YOUR bendy body is our highest priority! Learn about Dr. Ilene Ruhoy Instagram: @IleneRuhoyMDPhD TikTok: @IleneRuhoyMDPhD Podcast (YT): @Unraveledpod Twitter: @RuhoyMD Bluesky: @ruhoy.bsky.social Keep up to date with the HypermobilityMD: YouTube: youtube.com/@bendybodiespodcast Twitter: twitter.com/BluesteinLinda LinkedIn: linkedin.com/in/hypermobilitymd Facebook: facebook.com/BendyBodiesPodcast Blog: hypermobilitymd.com/blog Part of the Human Content Podcast Network Learn more about your ad choices. Visit megaphone.fm/adchoices
Welcome to another episode of the Oncology Brothers podcast! In this episode, hosts Drs. Rahul and Rohit Gosain are joined by Dr. Robert Orlowski from MD Anderson Cancer Center to discuss groundbreaking studies presented at ASH 2024 focused on multiple myeloma. We dived into four key studies: 1. AQUILA: Explore the impact of early intervention using daratumumab for smoldering myeloma, which showed improved progression-free survival (PFS) and overall survival (OS). 2. Dara Based Quad Therapy: We discuss a meta-analysis reaffirming the use of quadruplet therapy with anti-CD38 for newly diagnosed multiple myeloma as the standard of care. 3. CARTITUDE-4: study highlights the benefits of CAR-T therapy in earlier lines of treatment for patients with lenalidomide-refractory disease. 4. Role of IVIG with BCMA Bispecific Antibodies: Discover how IVIG can reduce infection rates and improve overall survival when used alongside BCMA-targeted therapies. Tune in for an insightful discussion that will enhance your understanding of the latest advancements in multiple myeloma treatment. Don't forget to check out our other episodes on CLL, myeloma, and lymphoma from ASH 2024! Subscribe to the Oncology Brothers for more updates and expert insights in oncology! Website: http://www.oncbrothers.com/ X/Twitter: https://twitter.com/oncbrothers Contact us at info@oncbrothers.com
In this powerful Tick Boot Camp Podcast episode, Lindsey Shaker shares her inspiring journey of overcoming Lyme disease and multiple co-infections. From battling years of misdiagnosis to navigating aggressive treatments, Lindsey's story highlights resilience, resourcefulness, and the importance of maintaining hope. She also emphasizes the role of movement, such as yoga and hiking, and the necessity of community and self-care in the healing process. Tune in for invaluable insights into managing chronic illness and learning how to advocate for yourself and others in the Lyme community. Introduction to Lindsey Shaker • Background: Director of Marketing for Shaker Auto Group and Lyme disease advocate. • Diagnosed with Lyme disease and multiple co-infections at age 31 after years of misdiagnosis. Lindsey's Early Life and Onset of Symptoms • Born with Lyme and Bartonella through maternal transmission. • Early symptoms: Full-body paralysis during high school track practices, emotional instability, memory loss, and balance issues in college. • Misdiagnosed with depression, ADHD, and Lyme carditis before her eventual diagnosis. The Turning Point • Mother's diagnosis prompted Lindsey to seek further testing. • Diagnosed with Lyme disease, Bartonella, Babesiosis, Typhus, Rocky Mountain Spotted Fever, Ehrlichiosis, and Anaplasmosis via blood tests conducted by Dr. Bouboulis. The Treatment Journey • Initial treatments: A combination of antibiotics, anti-parasitic medication (Mepron), and IVIG therapy. • Challenges: Managing severe Herxheimer reactions and navigating insurance for IVIG approval. • Milestones: Significant improvements in mobility and overall health over seven years of treatment. The Role of Mindset and Self-Care • Tools for resilience: Yoga, probiotics, CBD oil, and communication with Lyme-literate professionals. • Addressing environmental factors, such as mold exposure, through diet, sleep, and movement. Movement as Medicine • Physical activities: Hiking and yoga played crucial roles in her recovery journey. • Emotional benefits: Restored confidence and emotional well-being through consistent movement. Life After Lyme • Nearly 99% recovered but emphasizes the importance of continued vigilance. • Reflects on lost time but remains grateful for the progress made and the strength gained. Advice for Listeners • For Lyme patients: “Your outlook is everything. Fight for your recovery and never give up.” • For prevention: “Assign a tick-checking buddy and never skip tick checks after outdoor activities.” Lindsey's Call-to-Action • Follow Lindsey on Instagram: @LMshaker to learn more about her journey and advocacy work. • Explore Tick Boot Camp resources for tools and strategies to overcome Lyme disease and chronic illnesses. Conclusion: Lindsey Shaker's journey reminds us that recovery is possible with persistence, education, and support. Her story is a beacon of hope for others navigating the challenges of chronic Lyme and other tick-borne diseases Keywords: Lyme disease, Tick Boot Camp, Lindsey Shaker, Resilience, Misdiagnosis, Co-infections, Herxheimer reactions, IVIG, Movement, Mindset, Immune system, Chronic illness, Recovery, Advocacy, Tick-borne illnesses, Treatment journey
On today's episode of The Wholesome Fertility Podcast, Caryn Johnson of @_bondlife shares her personal journey through infertility, detailing her struggles with unexplained infertility and the eventual discovery of autoimmune issues affecting her reproductive health. She emphasizes the importance of understanding the immune system's role in fertility and the impact of lifestyle factors such as diet, stress, and environmental toxins. Caryn advocates for women to take charge of their health by educating themselves and seeking out supportive healthcare practitioners. She also discusses her supplement line, Bond, which aims to address these issues holistically. Takeaways Caryn's journey began with unexplained infertility. She experienced multiple failed IVF attempts. The immune system plays a crucial role in fertility. Many women with unexplained infertility have underlying immune issues. Stress and lifestyle factors significantly impact reproductive health. Gut health is linked to fertility and autoimmune conditions. Caryn's research led her to create a supplement line, Bond. Advocacy and education are essential for women facing infertility. Environmental toxins can affect fertility outcomes. Women should empower themselves with knowledge about their health. Guest Bio: Caryn Johnson is the Co-Founder and CEO of BOND, an innovative line of supplements reimagining hormone and reproductive health, inspired by her experience with infertility. The former Vital Proteins Chief Marketing Officer launched BOND in the Fall of 2023, fusing her professional expertise with her passion to help women take a more proactive and empowered approach to caring for their cycle and reproductive health. In 2017, when trying to start a family, Caryn learned she was autoimmune infertile. What she discovered was a stark reality - the lack of open conversations and support for women facing similar struggles. The doctor's office often left much unsaid, and the information available was surprisingly scarce. Shocked by the limited support system in place, Caryn recognized the need for a change. She leaned on her industry knowledge and contacts to advocate for herself and uncover invaluable resources. Her personal journey became a catalyst for a larger mission to make her learnings accessible to women everywhere. It was this experience that led her to create BOND. A natural born innovator, Caryn is disrupting the marketplace with this new line of products that offers women the opportunity to take control of their reproductive health before it's too late. BOND's proprietary formulations, designed to preserve fertility potential and lay the foundation for a healthier body, feature science-backed ingredients that work together to balance hormones, protect egg health, and provide cycle support. With BOND, Caryn aims to address women's health more holistically and encourage a more proactive conversation around reproductive wellness. Caryn's career began in marketing and public relations where she worked with many notable beauty brands and PR firms before being recruited as the fifth employee at then startup, Vital Proteins. She was the first marketing hire at the organization and ultimately, became the company's Chief Marketing Officer leading the team through the brand's acquisition by Nestle Health Sciences. Following her tenure at Vital Proteins, Caryn took on the challenge of leading Owlet, a baby monitor company focused on preventing SIDS, where she served as Chief Marketing Officer and successfully guided the company through its initial public offering. Caryn lives in Chicago with her husband and two children Elijah and Ruthie. You can use coupon code THEWHOLESOME for 20% off all products. https://bond.life For more information about Michelle, visit: www.michelleoravitz.com The Wholesome FertilityFacebook group is where you can find free resources and support: https://www.facebook.com/groups/2149554308396504/ Check out Michelle's Latest Book: The Way of Fertility! https://www.michelleoravitz.com/thewayoffertility Instagram: @thewholesomelotusfertility Facebook: https://www.facebook.com/thewholesomelotus/ Transcript: Michelle (00:00) Welcome to the podcast, Karin. Caryn Johnson (00:02) Thank you. Thank you for having me. Michelle (00:05) It's so nice to meet you. And I know that you do a lot of amazing work helping women I also know that you have your own story that you can share. And I would love to hear your story and really what got you inspired to do the work that you're doing. Caryn Johnson (00:21) Yeah, absolutely. So I'm here to share really the start of how I got to where I am today. And that really is rooted in finding out that I couldn't get pregnant. So we can start there and then we can get into all of the details together. But my husband and I met when I was young, early 20s. And by the time we got married many years later, we were already most right away to start having a family. There was a piece of me inside that knew that I was gonna have some sort of issue. I don't know, you already mentioned that you do visualizations to me before we started. So, you know, like I just had this feeling whether I manifested it for myself or not. I, you know, we did the full year of trying to get pregnant to no success and then went back to our doctor. Michelle (01:03) Yeah, yeah. Caryn Johnson (01:18) my typical OB-GYN and started the path of IUIs, did four IUIs, had beautiful eggs, each IUI, and reacted to the medicine quite well, but never got a positive from any of those. So we were recommended to move towards IVF. found a reproductive endocrinologist in Chicago, which is where I was located at the time. started the path to IVF and went through the process of an egg retrieval. Ended up seeing similar to what we saw in the IUIs, which was that my reproductive system performed quite well. And I was able, they were able to retrieve just about 30 eggs from one retrieval, which is quite high, borderline too high, but. just shows like the reaction to the medicine and the overall viability of my reproductive system. Of that, I had really normal odds and was able to bank close to 14, I believe, quality grade embryos. So I was really excited to move into implantation because at that point, I just really thought like whatever was unexplained is just kind of, you know, over to the side now. you know, all these things are just working out in my favor. So this is gonna be, you know, it for me, which a lot of women I feel like go into IVF feeling like the IVF center is like the place where you get your baby, which isn't always true. So. I started doing implantations and I started losing babies. Prior to that point, I had never even tested positive in any sort of like regard for a pregnancy test. And I wasn't one of those that, you know, jumped right off birth control, you know, to move into conception. I hadn't been on birth control for many, many, many, many years, you know, prior to this point. But the implantations started failing and My doctor said, this embryo was only attached for two hours, maybe a couple of hours is what they said. I just thought, how on earth, like why on earth would something attach for just a couple of hours and then that be the situation where It just doesn't work out from there. Like what is happening? And you know, got immediately, the immediate response was bad odds. You know, this happens, miscarriage happens. Just keep going. You know, one in four, in eight, you you get all the stats and there's definitely a piece of that when you're not working with really good quality embryos. But you know, I was, I knew that everything was genetically great. knew. and had no reason to believe that my body wasn't in working order to, you know, produce a pregnancy. So I just started pushing harder and getting a little bit more more fearful of continuing down the path of losing babies because I just, it hit me so hard. Even the loss of two hours, I mean, I just like, I've never felt sorrow like that. And I didn't, I just didn't feel like myself or really anyone should have to like continue down that path for like the sake of odds. So I started doing my own research and I was at the time experiencing some issues in my digestive system. I also now looking back had a definite cortisol issue. which relates into the picture, but I was a CMO at Vital Proteins at the time, which is that blue tub collagen company. And so I had a high stress level and I knew that something was going on in my digestive system. This was, you know, 2016, 2015, 2016, 2017. So. Michelle (05:39) yeah. Caryn Johnson (05:58) almost prior to when we really started, you know, as a world, as a community talking about the microbiome and gut health. But I sought out a naturopath who ended up doing a blood panel on me and told me that I had, you know, hundreds of food sensitivities, which is a a classic sign of gut dysbiosis, but at the time it wasn't translated back to like an issue in the microbiome. It was treated as like, yes, you have all of these, you have all of these issues with, you know, different foods, just avoid them. And that will be the solve versus, why do you have like, you know, why do you have a hundred things that you can't eat? Michelle (06:42) Hmm. Caryn Johnson (06:46) like watermelon seeds up to your typical gluten, et cetera. So I just started doing my own research online and I found a book called, Is My Body Baby Friendly? It's written by Dr. Alan Beer, who is now deceased, but it's over 700 pages of the science of how the immune system works with your reproductive system, your hormones, et cetera. in order to effectively procreate or in order for conception and implantation to occur. And that's when I realized there was something greater going on in my body outside again of just my reproductive system that we just hadn't figured out yet. So I read the book Front to Back. It's a very science heavy book. So I had to do a lot of like thinking about new terms and figuring and trying to remember what I was learning. At the end of the book, there was a recommendation at the time, there are more doctors now, but at the time for three doctors that practice this type of medicine, which is the field of reproductive immunology. And so, Michelle (08:01) Mm-hmm. Caryn Johnson (08:03) One of those doctors, Dr. Joanne Kwok-Kam of Rosalind Franklin ended up being in my backyard essentially 45 minutes away in the Chicago area. So I took that as a sign that I needed to call and get additional help above and beyond my RE who was doing the IVF. And I called over there and was immediately put on a six month wait list. So proceeded with the next round of IVF because I was already on some hormones. So I was already going through the round. I had at that point only done my own research. So I wasn't really sure what was going on in my body or if I could believe what I had read because my doctors that were helping me with the IVF weren't really like saying that They believed in the immunology side of things. They hadn't seen enough research, et cetera. So I wasn't really getting support on what I was researching. So it was around the holidays, October-ish, when I ended up calling into the clinic and I ended up getting a call right around Thanksgiving that they had a cancellation and I got moved up on the wait list. So I ended up getting into the reproductive immunology clinic many months before they said I would two weeks before my next IVF transfer and that was just an awesome Hail Mary. They did a full ultrasound. So tip to toe thyroid, you know, your whole stomach area inside and outside. And then they do the craziest blood panel that I've ever done. don't know how you can even draw that much blood, but vials and vials of blood to look at immune markers in addition to hormone markers, vitamin markers, and your typical blood panel. And they called me back 48 hours later and said, need to cancel this implantation. You have the highest level of antibodies that we've ever seen. not that we've ever seen, but that we're able to track. So you're past like where the chart goes essentially. So if you proceed with your implantation, it's almost definitely gonna end in a miscarriage because your body is gonna fight it off. And at that point I was terrified because that was like the first real something's actually wrong with you that I had heard. Michelle (10:21) wow. Wow. Caryn Johnson (10:50) Everything else was just unexplained, unexplained, unexplained. And I just went into shock. I didn't know what to do. I didn't know who to believe. You know, I had two sets of doctors saying different things. So I proceeded with the implantation and I ended up implanting both a boy and a girl embryo. And then started treatment right away on my immune system through the reproductive immunologist. So what they did was they put me on a series of pretty intense medications to quiet my immune system. And then I did what is called IVIG, which are blood transfusions or infusions that essentially look to wash your blood of the antibodies that are over protecting the immune system. So I went into this protocol and I ended up getting pregnant. It was positive right away. we saw, so the clinic ended up treating me one to three times a week with this IVIG infusion, which they're about two to three hours long based on, they're based on body weight. Michelle (11:50) Mm-hmm. Caryn Johnson (12:14) I was in their office, you know, at least one to two times a week, also for an ultrasound. So I knew by five weeks that both embryos had attached. you know, at that point, my immune markers were even more all over the place. We couldn't get my immune system to a stable level by any means. And I ended up losing the girl embryo at seven weeks. her heartbeat slowed and then ultimately it stopped, which is one of the symptoms or issues when you have an autoimmune issue going into a pregnancy. So, you know, that was so sad and devastating and she was higher up in the womb than the boy embryo. So at that point, It was pretty much 50-50 odds of if she was going to end up coming out and bringing him with her or if she was going to be what's called a vanishing twin, which is when your body reabsorbs the pregnancy for the sake of the other pregnancy, which is really the best case scenario because then you don't lose the other baby. Michelle (13:18) my gosh. Caryn Johnson (13:36) I was put on bed rest. This was the start of my bed rest between six and seven weeks, which continued until I gave birth, basically. I was able to go to work, but that was pretty much it. And I lived in fear that we were going to lose a little boy, but I ended up reabsorbing the girl embryo. So she never came out and we just really aggressively treated my immune system. which held on until 34 weeks when I went into basically how the immune system works during the pregnancy is during the first trimester, there is more inflammation that can be in the body and then it has to subside for the second trimester to continue successfully and then your inflammation increases and that's eventually causes or is part of why you go into labor. But my inflammation and my immune system increased really fast. my water broke early and I ended up having him, you know, early but he was healthy because some of the immune medications included steroids. So he was a little bit bigger than, you know, your typical 34, 35 weaker. But I was able to carry my son and that really started my story of what the heck happened and why is autoimmunity so under researched when it comes to your reproduction and your fertility chances and how can I actually do more now that I have my children here. Michelle (15:06) Mm-hmm. Mm-hmm. Mm-hmm. Caryn Johnson (15:33) to support other women so they don't have to go through this amount of trauma, right? But also this amount of like research and advocacy for themselves because at the end of the day, like we just can't expect that from everyone and we shouldn't. We should be able to support. Yeah, so I'll take a breath there. Michelle (15:40) Mm-hmm. Yeah. Wow, that's incredible story. And I mean, it's it's mind boggling, you know, that, nobody really talks about something that is so prevalent. And I do see that a lot, actually. And it could be the reason why you have unexplained infertility or why transfers don't work. And I speak to Amy Ralph, Amy Ralph, she's a Caryn Johnson (16:19) Yeah. Michelle (16:20) she does the same thing, Chinese medicine. And she talks about this a lot. She says, if you miscarry or you have repeated transfer failures with a good embryo and your doctor doesn't look into like what your lining is doing and how your immune system is working, then go to a different doctor because it's so important to look into that because you could spend so much time. and you can spend so much money and just so many precious years going through so much loss for something that could be treated but can also be prevented. So I'd love to actually get your input on what you've discovered and how the gut relates to it but maybe other things that you've noticed or learned for the listeners. Caryn Johnson (16:59) Absolutely. Yeah, absolutely. And I think what you're saying is just incredibly important. Like the immune system, I feel like is the secret starting point to a lot of issues. And what's happening in medicine right now is a lot of women are walking away with an unexplained infertility diagnosis, but they're accepting that as a diagnosis, right? When it's not, it's just, it's not an answer. And if you look underneath kind of that answer, you see a lot of crazy statistics, such as over 65 % of women who have unexplained infertility actually have an issue in their immune system. And then similarly over 60 % have an issue in their metabolic system. So blood sugar, insulin, know, early signs of PCOS, et cetera. And then. Michelle (18:05) You Caryn Johnson (18:10) When you look, you see that there are deep, deep nutrient deficiencies happening in this group of women as well. So you're looking at vitamin D deficiencies, vitamin B deficiencies, magnesium, omegas. All of these start with modulations that occur in the immune system as well. So when you think about it on a deeper level and from the research that I've done, Michelle (18:23) Mm-hmm. Mm-hmm, yeah. Caryn Johnson (18:39) you're looking at something that's happened to you before it's affecting your hormones and triggering one of these other issues in your reproductive system. So like for instance, not only do I have, you know, autoimmune infertility, I do carry PCOS and adenomyosis as well. And for me, and based on the research that I've done, those are secondary factors. to my immune system modulating and creating an overly inflammatory environment in my body, which then produced those issues. So we're not going up far enough in the chain of our bodies as to understanding our full systems. And again, it kind of goes back to like what's happening in medicine, which is that our doctors are Classically trained in our reproductive organs, right? So they know our uterus they know our ovaries they understand how those work, but we need to get into you know, a new phase where we have Practitioners that understand how all of the systems are working together in our body Including our immune system and our endocrine system because they do have such a big and almost starting impact Michelle (19:57) Mm-hmm. Yeah. Caryn Johnson (20:07) on what's happening with our fertility. Michelle (20:10) yeah, I completely agree. And I also I'm wondering, like, what have you seen? Because I think that when you talked about the food sensitivities, you were saying that it's okay, I'm allergic to so many things, or I'm sensitive to so many things, but why? So like, what are the things that you've seen that cause it to begin with? Caryn Johnson (20:28) Yeah. Yeah. So there are a couple of things that I see as a starting factors. One is overall stress. So if you can't keep your stress in check, you can't keep your cortisol levels in check, then your adrenal function will not perform in the rest of your hormones will not function correctly, which then trickles into some of these other problems. and then you get into other factors like what you're putting in your body. the nutrition that you have or you don't have. They're saying the American diet is still between 60 and 80 % processed food. So we're putting still mostly junk into our systems that's modulating and creating these environments that we don't want. Number three is dysbiosis of the gut, right? Which is a huge factor in Michelle (21:13) Mm-hmm. Yeah. Caryn Johnson (21:31) overall well-being and then your chances at fertility because what happens is that if your gut is in dysbiosis, your mucosal lining is disrupted and all of the toxins that are supposed to be in this like, think of it like pipe in your body, piped to get to the outside are now permeating that pipe and moving into your system and causing again, these major inflammation issues. these, this uproar of immune response that is hard to counteract. You know, once you have that level of bacteria and then toxins that are entering the bloodstream. And then the last kind of reason that you would be kind of in this situation is just based on what's going on in your environment. So are you living in a city, you know, that a lot of people in Detroit, for instance, there's a bigger rate of infertility there versus, you know, your non-city residents. It's also based on the toxins that enter your home. So are you getting rid of your plastics? Are you looking at the cleaning supplies you're using, the makeup you're putting on your face? It seems simple, but this toxic overload, again, Michelle (22:52) Mm-hmm. Caryn Johnson (22:55) creates this inflammatory response, which modulates your immune system. So those are really the four categories that kind of put you in this place. And then it kind of gets into epigenetics, which is like, you know, you've created this new world for yourself that your body has become. And, you know, is it going to be like that or are you going to be able to get yourself out of it? Michelle (23:23) Yeah. my God. It's so important and it's true. We hear all the different factors and actually those toxins and the endocrine disruptors can be found in food, I mean, through pesticides and that can also impact your gut dysbiosis. so it's just, it's like an entangled web and it really is like a reflection of how we're living today and what's allowed in this country, which Caryn Johnson (23:38) Yeah. Yeah. Michelle (23:50) I'm starting to get more and more frustrated with, you know, the fact that other countries are protecting their citizens more from chemicals and pesticides and things that are harming not only our health and chronic disease, also future. it's, it's unbelievable. And for that reason, I often tell people just go gluten free. It's not that. Caryn Johnson (23:58) Yeah. Gosh, get me started on glyphosate. It's so sad. Mm-hmm. Michelle (24:16) It's not that wheat is bad. And actually, as a matter of fact, a lot of people don't have those same responses if they go to Spain or Italy, even though it's not considered GMO, they have genetically modified it over the years. So there's so many aspects. So sometimes I'm just like, just remove it, And I see people feeling a lot better. Caryn Johnson (24:26) Right. Yeah. Michelle (24:41) just from that, and especially with autoimmune conditions, actually that like going gluten free can really help. That's what I've seen. Caryn Johnson (24:50) Yeah, no, definitely. It's just our food source is really sad. And it's just, it's so hard to pinpoint at the end of the day because no one really has the exact answer. But I just like, you see the data, like women who are eating on a Mediterranean diet have a lower risk of endometriosis. Michelle (24:55) Yeah. Mm-hmm. Caryn Johnson (25:15) women who have like vitamin sources through green leafy vegetables don't have as much PMS. So like the correlations are there. It's just like, how do we get people to make better decisions for their body and understand like, don't be me, don't make bad decisions and then get into a position where you can't have the life that you wanted or dreamed of, or you have to fight so hard for it because Michelle (25:16) Right. Yes. Mm-hmm. Caryn Johnson (25:43) of choices you made earlier in your life from lack of knowledge, you know? Michelle (25:47) Right. Yeah, totally. And then I also look at the nervous system, which is what you're, I feel like it's really linked to the cortisol issue, like the high stress, because we're constantly being bombarded with too much information. Really, I think too much information that our nervous system is able to translate. And I think that takes a trickle down effect into our bodies. I'm very big on like mind body because of that, you know, like that, that's one aspect, but of course, I mean, there's so many Caryn Johnson (26:02) Mm-hmm. Yeah. Michelle (26:16) Like I said, it's like a web and every single piece matters. And that's what you were talking about before with medicine, looking at the body as a whole, as a functioning system, rather than just one part. Caryn Johnson (26:21) you Right, right. And just going back to your comment on cortisol, you know, a lot of it does start with cortisol because if you put yourself into too high of a cortisol state, your body doesn't produce enough hormones. It basically triggers all of your other hormones to act inappropriately. It goes into your progesterone receptor. Michelle (27:00) Mm-hmm. Yeah. Caryn Johnson (27:00) pretends it's progesterone and then it goes on your thyroid and says slow down, slow down. Your body doesn't have enough energy for this and your thyroid slows. So it's really like easy to dismiss like, yeah, I'm so stressed but I don't have to be stressed today and to understanding like if your body is in a constant state of stress, like the impact it can truly have on your system and on your hormones because Michelle (27:27) Mm-hmm. Caryn Johnson (27:30) I guess also people think of like cortisol is like over here and then estrogen and progesterone as like over here because they work through different axes of the body, right? But it's all related because if you knock one off, you're messing with the others. So I just, I wish people ultimately would understand that cortisol is a huge starting factor to their fertility journey as well. Michelle (27:38) Mm-hmm. Right. Yes. Caryn Johnson (27:57) and to a hormone journey if they're not on the road to fertility. Michelle (28:02) Yes, because ultimately the body's always going to favor survival. And when you're in high cortisol, your body's basically or something is signaling your body to let it know it's not safe. So when you're constantly in this state of feeling unsafe, your body's going to worry about other things and put off other factors that it would normally pay attention to when you do feel safe. Caryn Johnson (28:08) Yeah. Right. Michelle (28:32) And being in this chronically is just not conducive to high vitality period. Caryn Johnson (28:32) Right. Yeah, I feel like at least we're in a better state of mind, like as a world where, you know, 10 years ago it was chic and cool to be like chronically stressed and like drinking like three cups of coffee in the morning and like running yourself ragged. Like I feel like everyone understands a little bit more that they shouldn't. It's just about like knowing your body and actually being able to say to yourself like, no, this isn't how I should. Michelle (28:52) It's true. Yeah, that's a good point. Yeah. Caryn Johnson (29:09) be feeling. This isn't how I want to keep stress or maintain like my day-to-day life. Michelle (29:17) No doubt that we are getting educated like never before. like, it's, it's one of those things that when like the information comes out and we start to open our eyes, it's painful because we're realizing things that are not working. However, even though it's painful, it's actually helping us in the long run. And it's kind of like the, blessing and the curse of social media and all of the technology, but the blessing is information. Caryn Johnson (29:28) Right. Yeah. Michelle (29:45) that is very important for us to know it's important for us to receive. So that aspect of it is really important. And then talk to us about your supplement product bond. And I know that you created that based on really your own frustration and it's become your baby. And I want to know what specifically or how does that address autoimmunity conditions for people who are going through that or? Caryn Johnson (30:03) Yeah. Michelle (30:14) least thinking maybe to look into their immunity in regards to their fertility, listening to this. Caryn Johnson (30:21) Yeah, absolutely. So I launched Bond just about a year ago. I concepted it. took a year prior to that from concept to launch. So really it started in the world of advocacy for me. I was just really looking to help other women getting involved in some Facebook groups, some communities. you know, there's not a lot of knowledge, a lot of people talking about this yet. There certainly wasn't, you know, even just a few years ago. so I, I took a speaking opportunity in Detroit and I went to Wayne State University, which is where they do a lot of the research for autoimmune infertility. the main head of that clinic asked me to come and speak to the researchers because they do all of this research and it's isolated into their facility. They don't actually see the impact of what's going on with women who are going through this. Michelle (31:24) Mm-hmm. Caryn Johnson (31:25) so I got to share my story and, you know, had a really nice day there learning and seeing their facility, their lab, what's going on. And on the drive home is really when it clicked for me that there's a lack of, or there's a gap in what's going on research wise and, know, what's being discussed and what's being carried out and brought to. the consumer or the public's attention. And I just felt like if I didn't take a larger stand to do something bigger to help women, that we'd be many, many more years behind even. So I went back to my house in Chicago, sat in my basement and did just clinical research for months. And I logged over 300 clinical studies, all centered around the immune system and how it relates to hormones to the reproductive system and built my thinking for original skews, which were, which are daily balance, which is our best seller conception boost, vitality, and cycle care on this thinking first. so it really started with research before it was brought forward to healthcare practitioners and then formulated out. And a lot of the research that went into each of the products is above and beyond supporting the reproductive organs. So when you look at daily balance as a whole, it has 15 vitamins and nutrients in it. And a lot of those vitamins and nutrients were chosen to not only support hormone balance, but to take that up a level and to support the immune system as it relates to being a predecessor to hormone balance. So adding a vitamin D, which is a huge hormone regulator, putting fiber, five grams of it into a supplement so that women are potentially protecting their gut lining better and producing those short chain fatty acids that are going to protect their gut in a way that just probiotics don't. Adding in a probiotic blend that we studied as being healthy strains, or not healthy strains, but strains from healthy fertile women. So really focusing on these immune factors and how they pull into the world of fertility. But to the public now, you know, almost simplifying that message and making it more of like the underlying theme because we're still not necessarily totally there. so the ingredients exists in these formulas with so much thinking and thought as it relates to the whole body. and then the formulas come out and, they're focused on hormone balance, right? As well as we have a conception product, and then we have our cycle care product, which is focused on, PMS support. So PMS, symptom alleviation, and then hormone detoxification. Michelle (34:16) Mm-hmm. Caryn Johnson (34:44) So they all have an immune angle, also address a hormonal need. And the other great thing too is that you can shop at a discount as a special thanks for listening to us here. You can head over to the link. We'll link it here with this podcast episode and use the code, the wholesome to get 20 % off your order. Michelle (34:54) Awesome. And do you have information on your site, just like support for people wanting to learn more? Caryn Johnson (35:00) Yeah. Yeah, absolutely. we're starting to add more and more to our site. I wrote a white paper on how the microbiome affects fertility that you can download off of our website as well to get more information. And yeah, we share a lot on social too with, you know, article connections there. So that's another great way to keep up with kind of like up and coming research that we're seeing. Michelle (35:32) Mm-hmm. Caryn Johnson (35:33) But yeah, I would say too, just going back to one other thing you mentioned earlier on the, on the doctor front, the best thing to do as a consumer, like when you're hitting these issues is to bring the articles in and show them to your doctor and choose advocacy for yourself. Because I found that the response from them is far greater when you have data in your hands as to why you want to. Michelle (35:51) Mm-hmm. Yeah. Caryn Johnson (36:03) add a supplement, think about a different form of medication, think about a different program that might make sense for your system. So I would say, you know, that is as important as ever. And, you know, what we try to do more and more is link that PIMD article, like when we post something so that you can find the actual source and see for yourself, you know? Michelle (36:24) Mm-hmm. Yeah. Caryn Johnson (36:31) read the information and make smart decisions. Michelle (36:31) Mm-hmm. I love that. That's great. I'm all about empowerment. think that we need a lot of that now. So this is great information. I really appreciate you sharing your story for people listening. And for people who want to find you and learn more, how can they find you? Caryn Johnson (36:41) Yeah. Thank Sure, so our website is bond.life. Our Instagram is underscore bond life and we're, you know, a newer company. I'm still really involved on our social. So we love to take DMs and interact with people one-on-one that way. If you have any questions or want to get into, you know, what you might be experiencing and what our different products are, like we're happy to get into it with you and. I will say for anyone that wants to shop on bond on our website, absolutely love to support you. And again, really the place to start with, with us is our daily balance product. has the baseline of nutritionals you need to support your nutrients stores, your hormonal balance, and of course, your immune system. that is our purple bag on the website there. But Michelle, thank you so much for having me. I really appreciate this opportunity. Michelle (37:57) Yeah, it was great having you on and having this conversation, which I feel like is so important because it is kind of like the big question mark that a lot of people are facing when they're trying to conceive. So thank you so much for coming on. Caryn Johnson (38:09) Yeah, you're welcome.
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