Science Friday - Is a shorter course of antibiotics OK? + Genetic risk of fibromyalgia

Episode Date: September 12, 2026

You’ve probably been warned that if you don’t finish that course of antibiotics, you could wind up battling antibiotic-resistant bacteria. But a growing body of research suggests that the opposite might be true. What does this mean for you and your next sinus infection? Flora talks with antimicrobial resistance expert Amy Mathers to find out.Plus, the driver of fibromyalgia, a condition that can cause debilitating chronic pain and brain fog, has been something of a mystery. Patients’ imaging and blood work often turn up normal, and many have felt dismissed by doctors.A recent large-scale study identified a group of genes associated with the disease, a breakthrough that may help doctors understand people’s risk of developing the condition and reveal something about the nature of this mysterious illness. Flora talks with Nasa Sinnott-Armstrong, one of the study’s lead authors.Guests:Dr. Amy Mathers is medical director of antimicrobial stewardship and an associate professor of medicine and pathology at the University of Virginia School of Medicine.Dr. Nasa Sinnott-Armstrong is an assistant professor of computational biology and public health at Fred Hutch Cancer Center in Washington state.Transcript will be available after the show airs on sciencefriday.com. Subscribe to this podcast. Follow our show on Instagram, TikTok, Facebook, and Bluesky @scifri and sign up for our newsletters. Got a science question that’s keeping you up at night? Call us: 877-472-4374 Hosted by Simplecast, an AdsWizz company. See pcm.adswizz.com for information about our collection and use of personal data for advertising.

Hey, it's Flora and you're listening to Science Friday. You've probably been warned that you'd better finish that course of antibiotics because if you don't, you could find yourself battling antibiotic-resistant bacteria. Well, guess what? Apparently there is more to this story. In fact, a growing body of research suggests that the exact opposite might be true. So what does this mean for you and your next sinus infection? Here to tell us more is Dr. Amy.

Mathers, Medical Director of Antimicrobial Stewardship and an Associate Professor of Medicine and Pathology at the University of Virginia. Amy, thanks for being here. Thank you, Flora. Thanks for having me. Okay. This seems like a big shift from what I have always heard. Yeah, so there was this dogma that finished the course or you will develop resistant bacteria. and it comes from long ago before we really understood how resistant bacteria worked, not finishing the course sometimes would cause relapse. However, what we now understand is that a lot of relapse infections that were assumed to be because of resistant bacteria were actually more complicated than that.

They may be a new infection or they may have been that the first infection didn't get completely cleared out. but it didn't necessarily mean that the bacteria was resistant. For example, strep that causes strep throat doesn't have any resistance to penicillin, and that's never been described. So it's not resistance that's driving it. It's something else if you have a relapse. You know, I thought the logic was that if you don't take the full course,

you might not fully wipe out the bacteria causing the infection. And then the ones that weren't eliminated are ones that are ones that are. are likely to have, to be resistant to that antibiotic, and then they could, you know, go forth and multiply. So what's wrong with that picture? You're on the right track for sure, because what happens is, is antibiotics actually target the infecting organism, but they also target a lot of other stuff and flora. And so the only bacteria that are lower- Flora, like microflora. Yeah, like microflora, like healthy bacteria that live in your gut that use up nutrients and probably don't carry resistance. And so when you expose all of those bacteria to an antibiotic, you may wipe all of those out,

leaving behind only the resistant organisms. And so the next time you have an infection, if you get a new infection, say in your bladder, in your sinus, it may develop resistance to antibiotics the next time you try to treat it. So you're not actually wrong. The issue is, is the longer you're exposed to them, the more you're getting rid of that healthy flora and selecting for resistant bacteria. So what a lot of people and a lot of clinical trials have been doing lately is seeing what the shortest course possible is to decrease the collateral damage while still treating the infecting organism effectively. So the upshot here is that a lot of course of antibiotics might actually make you more likely to develop antibiotic-resistant bacteria

inside of you. That is correct. The longer you're on the antibiotic, the more selective pressure you put on your microbiome, and therefore, the more likely you are to have resistant bacteria. Have we measured that? You know, how much bacteria you lose after seven days versus 14 days? So some of that research is emerging, and depending on the antibiotic and the situation, not all of that's been filled out completely, but there is a dose effect. And some scientists have

shown the longer you're on an antibiotic or the more broad spectrum, the antibiotic, that may have a different impact on your gut floor. So some antibiotics that might be more targeted won't cause as much selection for resistance as other antibiotics and the, the duration we know makes a difference. It also can select for other infections such as C. diff, which may be a microbe that you select for when you kill everything else off, C diff is left behind and can cause a gut infection because your normal flora is not there taking up the nutrients. C. diff has a chance to get a footh in and overgrow and then cause a bad colon infection. there's definite research saying that almost every day of antibiotic that you take

puts you at higher risk for C-diff depending on whether or not you're at risk for that infection. Really? Every day. It's that granular. I mean, do we have a sense of what the Goldilocks zone is for different antibiotics and different infections? Yeah, so there's a lot of really great research coming out about it. And for example, there was a clinical trial last year that looked at seven days versus 14 days for even bloodstream infections and showed that seven days was adequate. So now physicians should be treating most bloodstream infections with seven days of antibiotics instead of 14. There's studies in pneumonia, urinary track infections. Having said that, it's not a panacea and not all conditions have been studied,

and there are some situations where shorter course was not necessarily equivalent. And so you really need to talk to your doctor about, do I need this antibiotic and do I need to take it for this long? And so making sure that your physicians up on the most current research of what has actually been studied for a shorter course so that you can kill off the infecting bacteria as soon as possible, and decrease unnecessary days of antibiotics. I mean, are doctors up to date on this?

Well, you know, there's a lot of people in antibiotic stewardship that are trying to make sure that everybody is up on the literature. And so I think within hospitals in the last decade, the duration of antibiotic prescribing has changed completely for hospitalized patients. So in our hospital for pneumonia, for example, most patients are getting five days. and if it's a more complicated pneumonia, seven days, instead of the old 14 days, which was a decade ago. Are there guidelines somewhere? I don't know how prescriptions work, like if the AMA has, you know, puts out guidelines around this, but like if doctors aren't reading the literature, would they know that those standards have changed? Yeah, so the Infectious Disease Society of America puts out guidelines around how long to treat. And so, for example, the urinary track infection guidelines have recently been updated to reflect the shorter courses and who needs a longer course and who needs a shorter course.

So hopefully physicians are getting that message and shortening the course. Yeah. There's a lot of nuance in psychology in the way that antibiotics get prescribed. And I think getting the message out that if you don't need an antibiotic at all, don't take it. and understanding some of the downsides of antibiotics, I think it's just really important getting the word out. What do you mean there's psychology involved? So we know from studies that when doctors score more tired,

they're more likely to prescribe antibiotics. When doctors are more tired, they are more likely to prescribe antibiotics. Because, well, when you go to your doctor, a lot of times people want something done. If you're feeling terrible, you went to the doctor to have something done. And so sometimes patient satisfaction scores can be linked to getting an antibiotic. And so having that long, nuanced discussion like you and I are having, may not be easy when a doctor's in a rush and a patient is feeling bad.

And so that time is well spent in that if you don't need an antifference, We now understand so many of the downsides of taking antibiotics we don't need, supporting both you as a patient, not getting an antibiotic you don't need, as well as, you know, not demanding an antibiotic that you don't need if a physician's trying to tell you, I think this is a virus. I think this will get better without antibiotics. Yeah. Yeah. So ask your doctor and also ask your doctor about duration. That's right. That's a message too. 100%. And so just say this seems 14 days seems like a really long time. Is this the typical duration for antibiotics at this point? That's great advice. Okay. Thank you, Amy. Thank you so much, Flora. Dr. Amy Mathers is the medical director of antimicrobial stewardship and an associate professor of medicine and pathology at the University of Virginia. Don't go away. We have to take a break. But when we come back, a new large-scale study about the genes associated with fibromyalgia,

What does this result tell us about this illness? Fibromyalgia is a condition that can cause debilitating chronic pain and brain fog. But what causes it has been something of a mystery. For patients, imaging and blood work often turn up normal, and as a result, patients have historically often felt dismissed by doctors. Now a new large-scale study has identified a group of genes that are associated with the disease, a breakthrough that may help doctors understand people's risk of developing it, but also may reveal something about the nature of this mysterious illness. Joining me now is one of the study's lead authors. Dr. NASA's Senate Armstrong is an assistant professor of computational biology and public health

at Fred Hutch Cancer Center. NASA, welcome to Science Friday. Thanks so much for having me. I mean, for people with fibromyalgia, this must be such a gratifying result to have something tangible. Yeah, I agree. I think it's been a really long time coming for us to understand better what are the biological processes that drive fibromyalgia risk, and this is just one step in that journey. I mean, did we already know that fibromyalgia had a genetic component or that it ran in families? There has been evidence in other studies that there were familial associations. For example, twins have higher risk of developing fibromyalgia if their other twin has fibromyalgia, but there hadn't been any specifically known genetic risk factors. And this study kind of

started off the process of trying to look at that more. So how many genes did you identify and how much is the risk increased if you have these variants? Yeah. So overall, in our huge study, we found a total of 26 different genetic variants that increased or decreased risk of fibromyalgia. And overall, these explain a pretty small fraction of risk. If you look at all of the genetic variants that we're able to identify in the study, it's a total of about 10% increased or decreased risk. So this isn't saying that genetics means that you will or will not have fibromyalgia, but rather it helps us understand better the process of the disease and the consequences of that on your health. I mean, 10% feels low still. Does that mean that we're

still looking for other gene variants or that the environment plays a big role? What does that tell you? I think both are true. I think that probably there are other genetic variants that increase risk of fibromyalgia. And I think that probably some of the factors that we haven't identified aren't genetics at all. That there's a lot of factors that we already know about related to individual environmental exposures. And those differences matter a lot, too. I mean, did the variants that you found, And do they tell us anything about the nature of fibromyalgia, something we didn't know before? Yeah, I think the biggest thing that we identified in this study is that a lot of the genetics of fibromyalgia is attributable to the nervous system. So there are factors in the genes that act

in the nervous system that are close to these genetic variants. And what that means is that probably some of the biology of fibromyalgia is biology of the nervous system. And that can take many different forms, but I think that that's probably the biggest thing that we learned. And then the other big thing that is kind of part of the story is that the factors that we identified for the genetics of fibromyalgia don't seem to be sex-specific. So individuals, regardless of sex, have the same risk from a genetic perspective that we understand for developing fibromyalgia. You know, I know that there have been hypotheses that there's an immune system link to fibromyalgia. does this finding rule that out?

It does not rule out that possibility. There's definitely still the possibility of an immune link, and a lot of different immune factors could be relevant, both to the environment or to genetic factors that we haven't identified as closely as the ones that were presented in this study. I know that one of the genes you've found is also associated with Huntington's disease.

How do you interpret that? What do you make of that? I think that the gene being associated with Huntington's is something that can help us learn about biological processes, but it doesn't tell us that individuals with fibromyalgia have an increased risk of developing Huntington's disease. All it means is that some of the stuff that we've learned about how Huntington's works can now help us hopefully learn more about how fibromyalgia does as well. You know, I know that fibromyalgia often requires some kind of trigger to come on, like a physical trauma or severe stress or an infection. Does anything about your findings help explain why that is? I think that our study suggests that fibromyalgia does have a component related to nociplastic pain or how people experience pain. And that nocapastic component could be related to all of these different types of triggers.

But our study, because it was looking mostly at genetic factors and not across all of the different possible ways that people might develop or that they could have risk contributed for fibromyalgia, because we weren't looking at all of those at the same time, we can't say necessarily which ones might be more specific to the genetics versus to other parts of the development of the disease. Are there any implications for screening now? I think in the immediate term, it could teach us how we want to do screening, but there's not a specific, like, you wouldn't want to take a genetic test to determine if you had fibromyalgia. What this study does is it more helps us understand ways that people might benefit from different types of treatments or the ways in which additional research could be done to better understand how and when fibromyalgia develops. Let's talk about that. How could this lead to better treatments? So I think one of the big opportunities that this study reveals is that there's actually a lot of known genes that are being presented as part of the findings that we had in this work. So one of the big ones that we're really excited about is looking more into GPR 52.

That's a gene that's associated with some of this Huntington's disease biology that we previously described and some of the other findings within the study. and there's already an investigational drug being used to treat Huntington's that acts through the GPR 52 gene. So what that means is that maybe some of what we're learning about fibromyalgia could be applied in the context of this GPR 52 variant. And we might be able to use drugs that target GPR 52 to help with fibromyalgia. I don't know if that's necessarily going to work, but I do think that hopefully we'll get to a point where we'd be able to understand better if it might. So where do you go from here? Well, I think definitely some of that work in GPR-52 and some of our other target genes to say, like, are these going to improve care?

Are there ways in which we could develop new drugs against some of the targets here? How can we think about the role of noosoplastic pain in the development of fibromyalgia or how people experience pain? I think all of those are important directions to look at. And I think the other big direction that we should go in is trying to identify whether or not these risk factors, are relevant for everybody with fibromyalgia, or maybe there's different subsets of people where some of these risk factors are more or less important. And I think those are both important directions to go in.

Dr. NASA, Senate Armstrong, is an assistant professor of computational biology and public health at Fred Hutch Cancer Center. NASA, thanks for being here. Thanks so much for having me. It was great talking about this. This episode was produced by Shoshana Bucksbaum. If you're already listening to the podcast,

check out our social media accounts or our newsletters, Science Friday.com slash newsletters. I'm Florida Lichten. We'll catch you next time.