S1E11 Making the right medication choices with Dr Aaron Boster

Geoff Allix  00:00

Support for the Living Well with MS podcast is provided by Overcoming MS, a global charity registered in the United States, United Kingdom and Australia, whose mission is to educate, support and empower people with MS in evidence based lifestyle and medication choices that can improve their health outcomes. Please visit our website at www.overcomingms.org to learn more about our work and hear directly from people around the world, about the positive impact Overcoming MS has made on their lives. Now, on to today’s episode. In today’s episode, we’ll be talking about medication and disease modifying therapies. Joining me today is Aaron Boster, a board-certified clinical neuroimmunologist specializing in multiple sclerosis. Dr. Boster decided that he wanted to become an MS specialist at a very young age of 12, when his uncle was diagnosed with MS. Dr. Boster runs a very popular YouTube channel, with literally hundreds of episodes and regular Q&A sessions covering every aspect of MS. I thoroughly recommend that you have a look at this excellent resource. So with that, welcome, Aaron Boster.

 

Dr. Aaron Boster  01:12

Thank you so much for having me, Geoff. It’s a pleasure to be here.

 

Geoff Allix  01:14

And just to cover your YouTube channel, it does cover really every aspect, doesn’t it? It seems to be a weekly episode you do, very regular.

 

Dr. Aaron Boster  01:29

I try to only publish a video a week. But if I’m honest, I get so excited, I can’t help myself. And when I look at my analytics, I probably publish two videos weekly, and then I try to do a live stream a couple times a month as well. So, it’s a big, really exciting piece of my life if I’m honest with you.

 

Geoff Allix  01:48

And then with Q&A sessions as well, you’re more accessible than my actual neurologist. But I mean I think most people probably see their actual neurologists probably on a six-monthly basis, but actually having that ability to connect online is very useful.

 

Dr. Aaron Boster  02:10

It struck me that if I see patients four times a year, that’s about twice as often as the the typical MS patient is seen in clinic. And yet, someone impacted by MS has the disease 365 days a year, which based on my advanced mathematics means that they’re stuck with MS, 361 days annually without a clinic appointment, without a touchpoint with their provider or their team. And so I was really looking for ways outside of the walls of the clinic to help educate and up someone’s game. And I feel as if YouTube and social media, podcasts, these are all modern modalities where we can really help provide education and energize and empower people. You know, and sometimes you need to hear about, pick a topic: bladder, at three o’clock in the morning, not at a scheduled clinic appointment. So, you know, I really appreciate you commenting on the YouTube channel. It’s been really special for me.

 

Geoff Allix  03:14

So, to talk about medication, neurologists often talk about levels of efficacy, and they group things into a low, medium or high efficacy medication. So could you describe this a little bit?

 

Dr. Aaron Boster  03:29

I’d be happy to. I’ll start by saying that there isn’t, at least in the United States, any codified formal classification. And yet, given the clinical trials data, and real world experience, we do group the MS therapeutics, the disease modifying therapies, sort of into a low, medium and high efficacy. The lower efficacy drugs tend to be the self injections. These would include products like interferon beta products, trade names in the United States would include things like Betaseron, Rebif, Extavia, Plegridy, Avonex. It would also include glatiramer acetate or codename Copaxone, and these are self injections that have largely been around since the mid-to-late 1990s. And they have a mild impact on ability to decrease annualized relapse rate, a very mild impact in the ability to slow down disability progression and to clean up the MRI, if you will. And so we would oftentimes refer to those as ‘first line therapies’ much to my chagrin, or ‘low efficacy therapies’. The second grouping, interestingly, are largely tablets or pills. And there’s several different kinds. These would include cladribine (Mavenclad) and siponimod (Mayzent),  those are the two newest entrants. They also include fingolimod, or Gilenya, and Tecfidera, or dimethyl fumarate, and lastly, teriflunomide, or Aubagio. And these pills largely have an improved ability to decrease annualized relapse rate, disability progression, and have an improved ability to impact the MRI on several metrics. Now, if you get a little bit granular, Geoff, we might look at some of the pills as being slightly higher efficacy, still within this medium category, and something a little bit lower on that same list. So one might place Gilenya and cladribine (Mavenclad) up a little bit higher, and one might place teriflunomide (Aubagio) slightly down lower. But again, you’re still dealing with sort of a medium tier, if you will, or a mid-range efficacy. The highest efficacy drugs currently available in the MS armamentarium are actually all infused agents. There’s three monoclonal antibodies, which are drugs that are infused into the vein. And these would include natalizumab, which is Tysabri, ocrelizumab, which is Ocrevus and alemtuzumab, which is Lemtrada. And these drugs, unequivocally, had the most potent ability to decrease annualized relapse rate, impact disability progression, and clean up the MRI. When you start to get into the higher efficacy drugs, you also start to introduce some really exciting metrics, things like no evidence of disease activity, really impacting the rates of brain volume loss, slowing that down, in some cases down to normal, and the most beautiful three letters that could ever be spoken in this field, CDI, or confirmed disability improvement.

 

Geoff Allix  07:05

So that’s actually someone’s symptoms getting better.

 

Dr. Aaron Boster  07:13

You’re right. You know, when my uncle was diagnosed with multiple sclerosis, the assumption by the clinicians taking care of him and conveyed to us (his family) was that the only option was for him to get worse over time. And it is such a joy that in my own career, I have seen that change. We now are allowed, in some cases, to look for confirmed improvements, where people – it’s kind of like going up the down escalator – where people literally lose disability and they maintain that for quite some time. So it’s, very, very exciting when we see that.

 

Geoff Allix  07:55

And so when people go to the neurologist, either initially, or if they need to change medication, they’re often given a choice within one of those boundaries: low, medium or high efficacy medication. So, could you give us a description of the most commonly prescribed disease modifying therapies to help someone make a choice?

 

Dr. Aaron Boster  08:21

Absolutely. And this is a moving target, if you will. Up until relatively recently, the most commonly used drugs were the injections. And in my personal opinion, this is very much for the wrong reasons. The injections were the first to come out, we’re talking about the early 1990s here in the United States. And I think a lot of doctors, for better or worse, have grown very comfortable with them. The side effect profiles of those drugs, all things considered, are pretty palatable, and they’re relatively safe products. So, I think that it’s an easy choice, it may not be the best choice, if I’m honest, as far as goals of efficacy and and limiting someone’s disability. And yet, that’s done all too often. I’m here in the United States and until very recently, one of the pills had really picked up a lot of steam and dimethyl fumarate, or Tecfidera, was the market leader. And that actually changed this year, when one of the highest efficacy drugs, that’s ocrelizumab, took over the American market. Now, that’s really exciting for me as an MS treater, because as we’ve talked before, it’s my goal to put you on the single most effective drug that you’re comfortable with as early as possible.

 

Geoff Allix  09:40

Because if someone is given a choice, what’s the best things that they could do? Would they would they be able to find out about potential side effects and efficacy levels?

 

Dr. Aaron Boster  09:52

Certainly. You know, I think in order to match the right drug to the right person at the right time, we have to have a very, very candid discussion, where we talk about two things: the first thing that I think we must talk about is the disease itself. The natural history of multiple sclerosis is insidious, and this is a disease measured by decades. The impact that we have on the disease early on, resonates for years to come – or another way of saying that is – sets a trajectory for disability over time. All too often, I think that a discussion about picking a drug starts with side effects of the drug, completely ignoring the disease itself. So what I would rather do, is place the risk/benefit of a drug inside the context of the risk of the disease process. I think if we start talking about the reality of untreated or undertreated MS, it helps the patient and the family, it helps the entire village come to terms with why we need to be considering more efficacious medicines. And so once we’ve talked about the reality of what happens if MS goes untreated or undertreated, only then do I think it’s most appropriate to discuss the the actual details of the drugs. So the second piece of this, of course, is a very open, honest discussion about the good, the bad, and the ugly of each of the products. And so, by good I mean, what is the efficacy or potency of the drug? What are the expectations for future relapses, future disability, future brain volume loss, future new spots on the MRI, with a given product, and then you must talk about the tolerability of the product. It’s really easy for me to tell you, you should inject yourself or take a pill twice a day, or sit in an infusion chair, but it’s your body and your brain. I’m not the one going through it. And so we have to talk about that tolerability. I also point out, we’re asking someone impacted by MS to take a therapy for the rest of their life. And so if they’re uncomfortable with the tolerability, that’s really a no go. We also have to discuss the safety, and we have to discuss the safety as it relates to the patient when they start the drug and the safety long term. It’s only then can someone be empowered with enough knowledge to make an informed decision. You know, it hurts my heart when I hear a patient share that when it came time to talk about drugs, the doctor handed them a bunch of packets and said ‘read this and pick one.’ It also really upsets me when I hear ‘well, the doctor said that these drugs are scary, and we shouldn’t take them.’ And that ‘this one is easy to take in and it’s very safe, so we should start there.’ That tells me almost immediately that that clinician didn’t do diligence to discuss the disease process first. And I really think this is a discussion that cannot be rushed. It can’t be done in 10 minutes. It needs to be something where the clinician, who has this knowledge as part of their education and training, is able to convey that in a meaningful way to the patient and the family and the rest of the village that attended.

 

Geoff Allix  13:19

One of the risks you’re talking about that often comes up is PML. I’m not going to try and pronounce it…

 

Dr. Aaron Boster  13:29

Progressive multifocal leukoencephalopathy. It is the ultimate scrabble word, isn’t it? And so you know, there’s a medication called natalizumab (Tysabri), which is one of the most effective medicines on the market. And there’s a constellation of situations while on Tysabri that can result in a very serious brain infection. And that serious brain infection, as you just pointed out, is called PML or progressive multifocal leukoencephalopathy. The reality is that we’ve now seen rare cases of PML amongst several of the MS drugs. You bring up a most excellent point, the risk of developing PML on Tysabri – depending on whether or not you’ve been exposed to the virus – in the first year, it could be as low as a 100th of a percent, or a 1,000th of a percent. Now, a 100th of a percent, Geoff, is you take an American dollar and you split it into 100 pennies, and then you take one American penny and you split it into 100 pieces. And that’s a 100th of a percent. I bring that up to you, not because PML is no big deal, PML is a very big deal. It can even be fatal. However, the likelihood of developing PML is infinitesimally small, and it’s the obligation of the clinician to put that risk in context. I oftentimes point out that the likelihood of being struck by lightning is much higher than the risk of PML. In the likelihood, where I live in in central Ohio here in the United States, the likelihood of being in a fatal car accident is orders of magnitude higher than the risk of PML. So to use this as an example, if I’m talking to a family about a therapeutic, and we discuss PML, it’s not my right, it’s not my privilege to tell them they’re okay with that risk. It’s also not my right to tell them they’re not okay with that risk. I view it, instead, as my obligation to educate them on what PML is, what is the realistic expectation or risk profile, and then to listen to what they think and feel. And if you tell me ‘look, man, that’s a risk that doesn’t scare me’, we’re gonna consider that therapy. And if you say, ‘look, that terrifies me, I’m uncomfortable.’ Even if the risk is very, very small, I have to honour that. So, in my opinion, as it relates to PML as this example, we sometimes throw the baby out with the bathwater. Think about it this way, Geoff: there’s 100 percent likelihood that the person we’re talking to has MS. And if we’re considering a high efficacy drug, such as Tysabri, there’s a very high likelihood there’s a reason we’re talking about this high efficacy drug. We don’t need statistics to make that comment. We have to weigh the risk of undertreated significant MS against a 100th or 1,000th of a percent risk of an infection. Moreover, we also have to discuss how we mitigate risk. So it’s our strong belief that by checking JC virus antibody titers, which is a blood test, and by obtaining MRIs with frequency, we can identify PML, God forbid if it occurs early, even before it presents with symptoms. And stopping the medicine in this example, improves the outcome substantially. So, obviously, this isn’t a quick, easy discussion. It’s not simple, because the immune system and the nervous system are not simple. But where I see most clinicians, if you will, make an error is rushing that conversation and not properly educating the patient and family about the disease itself. And what happens if we allow it to go under treated and not taking the time to put the risk/benefit of the drug in context.

 

Geoff Allix  17:41

Would you encourage most people then to start on a medium efficacy drug, the pills?

 

Dr. Aaron Boster  17:50

Yes, unequivocally, I would. You know, I have developed three rather inflammatory questions that I oftentimes ask patients, and I tell them ahead of time, look, these are inflammatory, but it’s intended to help them think about the disease long term.  I’ll just share them with you briefly: the first question is, presuming that your daughter is young, is it okay to wheel her down the aisle on her wedding night? Or is it your goal to walk her down the aisle? Because we’re dealing with a disease that risks taking that away from you. And I need the person I’m talking to not to focus on side effects today, but about neurological function 20 years from now. The second question that I oftentimes ask is, if God forbid, we were having a discussion about breast cancer, as opposed to MS, would you mind if I use the 10th best drug to treat you? And you know, there’s an obvious answer there. The third question, I tend to ask the significant other or the spouse, and presuming that my patient is a wife, there with her husband, I might say to the husband, ‘sir, I showed you her MRI, I showed you the areas of brain damage that she’s already suffered, what percentage more brain damage are you comfortable with allowing her to accrue over the next couple of years?’ Now, obviously, Geoff, these are inflammatory and it’s not my intention to be impolite. But I need the family to be thinking long term. And if you answer those questions in your heart, I think it preps us for why I want to start with, at minimum, a medium efficacy drug. I’ll also point out, at least here in the United States, that the lower efficacy drugs are the same cost point as the medium and high efficacy drugs. So it’s not like there’s a cost savings by starting someone on a low efficacy shot.

 

Geoff Allix  19:47

If we have the option of the high efficacy medication, there’s three main medications available at the moment. What’s the distinction between those? So between Tysabri (natalizumab), Ocrevus (ocrelizumab), and Lemtrada (alemtuzumab).

 

Dr. Aaron Boster  20:01

So I think for starters, they’re all top shelf. You know, if you’re choosing amongst those three, I think that you are in a really great position because all three drugs are rather outstanding in their ability to impact MS. I sometimes say it’s kind of like arguing over Ferrari, Lamborghini and Bugatti. You know, you’re probably not going to end up with with a cruddy car. Now, when you look at the three drugs, they’re very different. Lemtrada (alemtuzumab) is an induction therapy, it’s resetting the immune response and you take five consecutive days of infusions, wait a year, three days of infusions, and then you may not ever be dosed again. In fact, going on eight years, half of patients have never been retreated with Lemtrada. Tysabri is a continuous therapy every 28 days, or sometimes as far out as every 42 days, you’re receiving an infusion, and that infusion functions like the Great Wall of China. It makes a barrier and the blood brain barrier, it makes it almost impenetrable, so that the naughty autoreactive cells in the bloodstream can’t cross into the brain. And ocrelizumab is an immunosuppressant in that it depletes B cells, but it does it in a very, very selective way. And it’s a therapy where you’re knocking out adult B cells only, and you take therapy continuously every six months. So, the routes of administration are the same, they’re IV, but the way it’s given, and the way that it works are very, very different. Also, all three have very different side effect profiles. But I want to come back to the point that, if we’re having a discussion, gaming out which of the three infusions is the best fit for you, I am happy, because I know that no matter which one we pick, we’re going to start kicking this disease in the teeth and we’re going to start by really using the top tier medicines to try to suppress disease activity early on, when we can have the most impact. And that’s one point I just want to bring up again, if I may, the time of the highest pathology is during the first five to 10 years of the disease. That is also simultaneously the time when the human being feels the best. Because they’re the youngest age chronologically, they have the most neuroplasticity or ability to rewire, and they rebound the fastest from attacks. The damage done early on, they recover from functionally very often, but it leaves brain damage, which will then set a trajectory for disease progression years and years later, they just don’t realize it. Also, at the time of the diagnosis, and in the first couple years, that’s when the human with MS has the least knowledge, you know, they haven’t had the disease very long. And so we can fall into a trap, where they feel okay, they don’t realize what’s coming down the pipe. If they’re told, ‘hey, this drug is really easy, and it’s safe’, they might gravitate towards it without realizing what they’re signing up for.

 

Geoff Allix  23:24

So I started with Tecfidera, and then moved on to Lemtrada. So I’m aware of how Lemtrada is, if you’d like, deployed. So I had infusions one year, and then I had further infusions a year later, and then I don’t have to have any other – hopefully – don’t have to have any other infusions. So, I can’t stop taking it, can I? If I have side effects, then there’s nothing I can do about that?

 

Dr. Aaron Boster  23:51

Well, I would disagree with you slightly. And let me explain, if I may: so I have high cholesterol and I take a pill every day, and I will do that forever. My cholesterol medicine is a continuous therapy. And in MS therapeutics, all the medicines I’ve listed, save two, are continuous therapies. So, if you’re taking a shot, you just keep taking them. If you’re taking Tysabri or if you’re taking Gilenya, that’s a medicine that you take on a regular basis because of how it’s working in the body and trying to interrupt the inappropriate immune response. But cladribine (Mavenclad) and also Lemtrada are discontinuous therapies. They’re not continuous in that you take them forever, you take them for a set period of time, and they really are a form of what I refer to as induction therapy. Friends, sometimes instead referred to it as an immune reboot or a reset. So what Lemtrada in specific is doing is, to me, fascinating. It’s going in and identifying adult B and T cells. And we believe that the adult B and T cells, which are members of your immune system, have made an error in judgment, and they’ve learned the wrong thing. They’ve learned that parts of your brain are a foreign invader, so to speak, and they attack it when they see it as if they were attacking a virus or you know, a bacteria. And so what Lemtrada does, is it identifies those adult B and T cells and murders them, it kills them. And then something in my opinion, rather remarkable happens. It influences the way that the young guns grow up, the pluripotent stem cells that have yet to develop, it alters the way that they grow up, and it replaces the immune response with a much more tolerating milieu, with an immune response that’s less autoreactive. So going back to what you were saying, when you take Lemtrada, it makes a change or a reboot in your immune response, which is intended to be durable. Meaning it’s intended to have long lasting effects, not because the medicine is still on board, but because it’s changed the way your immune system now works. And you don’t need to redose it necessarily because of that. So, when you look out eight years, for example, we now have eight year long term follow up data for people in clinical trials that took Lemtrada, around half of them went out the full eight years and never took another course of Lemtrada, they never had another therapy. And during that whole time, they had no attacks, they had no new spots on the MRI. And I think this speaks to the durable effect. Now when you talk about side effects, or safety, Geoff, with Lemtrada, there’s really four categories, which I’ll review with you very briefly. But they’re all temporally linked, and they’re mostly front loaded. So, you can see things like creating autoimmunity, you can see a slight risk of certain specific infections, there’s a very, very low risk of cancer, and I mean less than a third of a percent. And of course, you can have infusion reactions. And these risks are front loaded in the first couple of years. And we don’t see ongoing risks. And that has more to do with the way the Lemtrada has altered your immune system, and less to do with sassy effects from constantly taking the drug.

 

Geoff Allix  27:34

And so if someone were looking at Ocrevus as an alternative, or a choice, there they’re having an infusion every six months, right? So if they stopped, would side effects stop? Would that work? Could they could they stop those side effects? So with Lemtrada, obviously, if it had an autoimmune thyroid reaction, you can’t not take it because it’s actually changed the way your immune system works. If you were taking Ocrevus, is that something where you could actually go back to where you were before, if you didn’t have the six month infusion?

 

Dr. Aaron Boster  28:11

Absolutely. So just to speak for a brief second about Lemtrada thyroid that you brought up, there’s a high risk of autoimmune thyroid, that can be caused as a result of Lemtrada. It’s not, necessarily, a permanent change. We’ve seen plenty of thyroids that sort of mellow out, and it’s treatable. And I just wanted to stress that, that the side effect profile from Lemtrata. They’re all treatable. But to answer your question, Ocrevus is a continuous medicine and as you point out, you need to take it every six months. So if you stopped taking it, you would stop seeing the benefit of Ocrevus. And if there were side effects, you would presumably not see the side effects. These medicines are tricky, Geoff, because they’re very, very, custom tailored, biologic agents. What Ocrevus is doing, essentially, is it’s identifying adult B cells, not the B and T cells, as with Lemtrada, but just the B cells, and it’s knocking them out. And we don’t feel like it’s altering the immune response. It’s just interrupting the immune response by knocking out one of the cell lines. And so it takes six months to grow back your B cells, which is why the drug is redosed every six months. Now, in specific with Ocrevus, the side effect profile, or at least in my experience, is pretty lovely. You can have infusion reactions with any of the infusions I’ve listed, most commonly with Lemtrada, but also to a much lesser extent with Ocrevus and there’s a risk of infection with Ocrevus. It’s a very small risk actually, but it’s present. And to your point, if you stop the medication that concern would be alleviated.

 

Geoff Allix  29:58

And do the most effective medications always have the most side effects or the most extreme side effects?

 

Dr. Aaron Boster  30:04

I don’t think that’s always true. If we think about Ocrevus, for example, the side effect profile of Ocrevus includes about a 30% chance of infusion reactions, with the very first infusion only, then that drops down to an 8% chance. And these infusion reactions, which are things like red rash, itchy throat, headache, are very well tolerated. You know, we’ve infused well over 1,000 humans with the drug at our centre and it’s a pretty easy infusion to get people through. The risk of infection is quite low, I can count on my hands, you know, the fingers in my hands, where we’ve had a problem with infections, very, very low risk. And the reason that we check laboratories and medications is to monitor how the medication is being processed by the body. Ocrevus in specific is catabolized. It’s not metabolized. So catabolism is where the drug dissolves in the bloodstream. And so there isn’t a need to monitor liver or kidney, for example. So I’d submit to you that in this specific example of Ocrevus, the side effect profile was rather lovely, maybe amongst the very best of all the different medications. And so here’s an example of what I consider to be a top shelf efficacy drug, with a side effect profile that is probably better in many respects to the self injections, or a lot of the pills. So I don’t think that we can make a sweeping statement that you’re required to exchange tolerability for efficacy, you know, I’ll use the Lemtrada that you received as another example, there is most certainly a lot of side effects and tolerability concerns early on. The infusion reactions of Lemtrada can be quite intense. But if you look at someone who’s received Lemtrada five years ago, or four years ago, or even three years ago, in my experience in clinic, these folks are not experiencing any tolerability effects. You know, the drug has left their body quite some time ago. So here’s a situation where they reap benefits, we hope, from a highly effective therapy, but they’re not having ongoing intolerable side effects. So, I think that we can’t make that blanket statement.

 

Geoff Allix  32:30

And so there’s one other therapy that we haven’t discussed, which is HSCT. Yes, haematopoietic stem cell transplantation? So HSCT, where does that fit? Because it is starting to become available. And I was sort of told it is, you know, above Lemtrada, that’s really the only higher level if you like, but then you’re going to quite extreme side effects. So how does that fit?

 

Dr. Aaron Boster  33:07

Absolutely, I would love to talk about that. So a stem cell transplantation is a hard reboot of the immune system. You know, a moment ago, we talked about Lemtrada, and I told you, it’s a reboot, and I oftentimes will refer to it as a soft reboot. You know, a stem cell transplant is a hard reboot. And if I use a computer analogy, if you had a computer with a virus or something that was going wrong, and you rebooted all the software, you know, you wipe the motherboard and then reloaded software. That, to me, is like Lemtrada. A stem cell transplant is when you open up the case of the computer, you remove the motherboard and you replace it with a different motherboard. And that’s kind of what you’re doing with a stem cell transplant. Now, stem cell transplantation is something that is being very actively studied in MS. And it’s my opinion that in 2019, it’s not yet primetime. I do believe that stem cell transplantation will, in the relatively near future, take its place amongst the MS armamentarium. But today, I’m reluctant to recommend stem cell transplantation outside of a controlled clinical trial. I participated in the MS clinical trial called the HALT trial, where we did some stem cell transplantation. And it’s it’s a very, very promising therapy. But as you allude, it’s also a very intense therapy with a tremendous amount of risk.

 

Geoff Allix  34:37

So you would advise going for the most efficacious therapy available but stem cell therapy is maybe one for the future.

 

Dr. Aaron Boster  34:46

It’s my opinion that stem cell transplantation could be considered by someone but in the context of a controlled clinical trial. And the reason I harp on that point, is there’s a is a plague within the United States of charlatans doing fake stem cell transplants. And there’s actually an entire stem cell transplant tourism business, which the FDA, our you know, our American FDA is cracking down on.

 

Geoff Allix  35:15

Yeah, I mean, I hear it tends to be people going to Russia or Mexico.

 

Dr. Aaron Boster  35:19

And the problem I have with that are multiple. One of them is the safety involved, because what you’re doing with a stem cell transplant is pretty serious stuff. You’re harvesting stem cells and putting them on ice. And then you’re murdering the human being, you’re giving them lethal doses of chemo and sometimes radiation to remove their immune system forever. So now they have no immune system. And they would most certainly succumb to almost any infection. But before that were to happen, they give them back the stem cells in an attempt to repopulate their stem cells. And there’s a period during that repopulation, where they’re at significant risk of infection, it’s a pretty serious thing to do. And so, you know, when when someone goes to some foreign land, whether that be India or Russia or Chicago, we don’t always know what they’re getting. So I’m very concerned, I’ve had patients go to Mexico and have what they were told was a stem cell transplant in a hotel room, not in a hospital. And so I think that the safety is a major, major factor. The second concern is, there isn’t a consensus on which type of stem cell transplant is the most appropriate. When you get into the weeds, there’s various ways of doing stem cell transplantation, various conditioning regimens of various severity, and the jury is still out as far as what’s the best type of stem cell transplantation. And so you’re right, if someone that I cared about was diagnosed with multiple sclerosis, I would most certainly encourage them to consider the most effective medicine that they’re comfortable with. And if they bring up a discussion of stem cell transplantation, I’m probably going to lean towards using the very high efficacy monoclonal antibodies first, unless they want to consider participation in a clinical trial.

 

Geoff Allix  37:15

Okay, thank you very much for that. And I’d like to thank you for joining us, and we’ve had some excellent advice about medication choices.

 

Dr. Aaron Boster  37:22

Well, thank you, it’s a pleasure talking to you. Thanks for having me.

 

Geoff Allix  37:28

With that, I would like to thank you all for listening to this episode of Living Well with MS. Remember that there is a wealth of information at overcomingms.org including show notes, and an archive of all Living Well with MS episodes. Once again, that’s overcomingms.org. There you can also find OMS friendly recipes and exercise tips. Connect with other OMSers in your local area through our OMS circles programme, and learn about the latest research going on in the MS world generally and related to OMS specifically. I encourage you to register on the site and stay informed about the latest news and updates. I also encourage you to subscribe to this podcast, so you never miss an episode. And please feel free to share it with others who might find it of value. Let us know what you think about the podcast by leaving a review. And if you have ideas for future episodes, we’d love to hear from you. So please contact us via our website overcomingms.org. Thanks again for listening, and for joining me on this journey to Overcoming MS and Living Well with Multiple Sclerosis. I’m Geoff Allix And I’ll see you next time.