Using a large database of (deidentified) medical records, the researchers compared the outcomes of people taking a GLP-1 for their type 2 diabetes to people taking other common diabetes drugs between 2017 and 2025. GLP-1 users were significantly less likely to be diagnosed with TB for up to a five-year span, they found.
Both of these studies are observational and retrospective, meaning they can only show a correlation between GLP-1 use and reduced (or at least less severe) infections, not prove a direct cause-and-effect relationship. At the same time, these are the only latest pieces of evidence pointing to a genuine germ-busting benefit from GLP-1 drugs.
I wonder if the likelihood that people taking a GLP-1 are probably better off financially, have a health care provider willing to spend on the drugs (and therefore probably a better medical system) or a combination of these and other traits are the real reason there are fewer infections.
They use a method called propensity score matching to try their best to match patients on both sides using a simple linear model with various features that try to ensure that only pairs of closely matched patient histories are compared.
Unfortunately this is rarely clean. Its also easy to make mistakes. Sometimes two arms are fundamentally incomparable. The quality and rigor of the comparison is often determined by a lot of extra checks and validations, and different journals demand different levels of rigor. I need to read it carefully to judge if this is good or not.
It looks like both do standard individual covariate checks for post-match balance, with SMDs. I'm surprised they haven't assessed balance for at least pairwise interactions, too -- we should be balancing out joint risk factors too, no?
I haven't worked on these designs, but I remember the methodologist that taught me this in grad school giving us a lecture about this.
EDIT: the BMJ article (laudably) provides access to the analyis code, although I won't have time to review it:
They already do acknowledge socioeconomic (and other confounding factors) in the analysis.
The primary analysis they perform is a ‘Propensity Score Match’ which is a technique used specifically to address for confounders in observational studies, and they do report balanced cohorts.
Still they write in their discussion “Although we adjus-
ted for several available proxies of socioeconomic and lifestyle status,
direct measures of income, insurance coverage, or out-of-pocket
payment were not available in the TriNetX database. Residual confounding related to unmeasured socioeconomic factors, therefore,
cannot be excluded“
Given the size of the dataset, the effect size, significance and sensitivity testing they did I think it’s very strong evidence for GLP1s causing this and it would be very very surprising to me to see the effect disappear even if they had perfect socioeconomic data.
With so many signs of improvement, even if some of them happens to be just flukes, from so many different areas, it feels like a penicillin moment. And i suppose penicillin also was initially mostly available to the ones with better socio-economy.
I’m sure you can just look up the studies, but note that GLP1s are widely prescribed to people without weight issues —— weight loss itself was originally an off-target effect. I have friends who run marathons who are on semaglutide.
This video by a medical doctor cites many studies showing that GLP-1 health benefits go beyond weight loss (see video description for link to papers): https://www.youtube.com/watch?v=yKPaVhpomks
The benefit is probably from the removal of fat, not a direct antibacterial/antiviral effect. Fat plays a complex immunoregulatory role in human physiology: it down-regulates some pathways, while up-regulating others (notoriously, the production of IL6 is carried out, in part, by adipocytes). The overall effect of fat on the immune system, however, is negative: it tends to increase the chances of rheumatological disorders, cancers, and many other diseases. Alternatively, the effect may be due to some sociological factor that their analysis failed to account for.
Nobody's denying this, but the interesting story about GLP-1s is that after you control for fat loss (for instance, by taking cohorts of patients that aren't losing weight) you still get evidence of these off-target effects.
I would imagine people going out of their way to take GLP-1 might also lose weight, be more active, and be also likely to eat better. Which I imagine would have a large effect on "germ busting"
That's true, and it's also one of those factoids that everybody already knows but certain people can't help themselves from bringing up every time it's even tenuously relevant.
The fact that it was the top comment only shows that people agreed or liked it, not that it was actually valuable, accurate, or useful. Popularity and value aren't the same thing, correlation is not causation, etc, etc...
Most observational studies do in fact account for the first thing a random HN poster can come up with 5 seconds after reading the title. So there is very little value in such a comment.
This was published in Nature, I'm pretty sure the reviewers understand and account for that. HN and reasonably educated people always think this is some huge gotcha, second only to "CORRELATION != CAUSATION!!!!"
Nature isn't an arbiter of truth, it's a publisher of papers. It's also meant to be read critically by people who see a paper like this and and think "interesting, but this is just an observational study, I'd like to see more research, maybe something with more controls before I believe this".
Say what you want about the "correlation doesn't imply causation", but many people do not understand why that is. As a shorthand for "hey, you don't know the statistics behind this, so don't take the pretty picture at face value", it's pretty good.
Question for people using GLP-1s: Do you plan to stay on them indefinitely? Are you concerned about gaining back the weight if you ever stop taking them?
I've had success with weight loss through diet and exercise (exclusive and inclusive at different points) but had trouble keeping it off. GLP-1s are attractive for sure but I cannot make up my mind on if it's worth the risks (both known and unknown). I know everything has risks, including lots of risks about being overweight and maybe keeping the weight off is an easier problem for a healthier version of myself after using a GLP-1. I don't know.
I hike 5 miles a day, I ate super-healthy (no ultra-processed foods, cook at home every day etc), only drink water, coffee & tea. Actually rarely eat stuff which has added sugar on the package, and avoid foods that have > 5 ingredients (more means it's too processed for me). I bake my own bread (sourdough, salt, flour, water, maybe home-grown japalenos).
And yet, I kept on gaining weight...
My problem is don't get the signal that I'm full fast enough. I have tried _everything_. Drink 2 glasses of water, fibers, eat slower, smaller plates, dietician, track calories.
They work in isolation, but I always end up hungry. Compare it to alcohol. The desire to drink. The solution there is easy. No more alcohol, and that works for most people.
With food? Can't completely abstain...
Went on GLP-1, worked great. Because of hip surgery had to stop for a while, and the weight just came back, because naturally, you revert to your old eating habits, as you chase the signal of satiation.
Now back on them and I'll be on it until the day I die. I pay $450 a month for now because insurance doesn't think I am fat enough now (I'm not). They expect me to go back to my overweight weight..., and even then, acceptance is not guaranteed.
In terms of risks: If I don't take it I'll wear out my knees sooner (hips were related to genetics, not weight). If I don't take it I need 1h more / sleep every night, I have sleep apnea, higher blood pressure, higher cholesterol (doesn't mater how healthy EVOO is, if you eat a huge salad you'll eat a lot of oil).
It's not a risk of GLP-1 against nothing. It's GLP-1 risks vs heart-disease/etc.
That's a known fact. That's why the first thing doctors say to overweight people is to lose weight for pretty much any disease. Some get hurt and blame the doctors, which doesn't help them.
Could be due to better control of blood sugar. E.g. lower blood sugar increases inflammation, decrease immune response and provides bacteria a readily available source of food.
I self pay for one from lilly-direct for about $200/mo. Insurance doesn't cover any part of it yet. It required a prescription from my doc and it comes in the mail.
Are you sure that it is not 30mg total per vial, with $100 being the price for 10 vials? Because this stuff comes in powder form, not in liquid form, so mg/mL is an odd unit of measurement. Perhaps I misunderstand your comment.
It's 30mg per vial. In addition to that being the going rate for 300mg total...the calculations and final price for 20 weeks match up to 300mg total, not 300mg per vial.
> GLP-1 receptor agonist medications typically cost between $149 and $350 per month for cash-pay oral pills, and $900 to $1,400+ per month for list-price injectables without insurance.
I don't know that anyone really pays list price for injectables, because the vendors do discount programs. Without insurance coverage, tirzepetide via Amazon Pharmacy is something like $450/mo.
Yeah this is what I pay for Zepbound through LillyDirect. I also eat less food and drink less alcohol than I used to. So the net loss is probably smaller, maybe $200/mo
I think you're right I confused wegovy prices with generics. Thank you for clarifying. I'm new to it and will find out about pricing very soon - my provider dropped covering the medication (the day I submitted for pre-approval) -because it worked so well it became popular :P
I pay $450 a month out of pocket and that is with a coupon, it used to be $1200 a month. It's worth it to me, it's life-changing. My bp went down from dangerous levels to normal.
I was at a hepatology meeting focussed on fatty liver a couple of years ago, where a well regarded head of hepatology at a major national quarternary referral centre, joked that we should be putting this in the water supply...
i can kinda get how a glp-1 can be a miracle drug for weight: if we assume that simple molecular fixes to problems will eventually be found by evolution, then when we change our environment rapidly (e.g., with cheap bountiful calories) then this presents an opportunity for a miracle drug, since evolution will take some time to find the fix.
but for something like reducing disease infection, i find it a lot harder to understand why we don't create this naturally unless there is some equal-but-opposite cost that we'd incur, or if there is not actually as big of a benefit as we believe (or if this is all just colinear with the weight loss stuff).
note: i have no background in any of this and have no idea what i'm talking about
I'm not a doctor or biologist, but remember that bacteria is a far simpler organism with a much shorter individual lifespan than a human. Depending on the species and their environment, they might divide every 12 minutes or every 24 hours. A new human generation will be more 15 to 35 years. Their reproduction is also simpler. Genes are inherited or mutated mostly at the time of reproduction. Selection is mostly therefore over the course of generations.
These things together mean their microevolution is on a different timescale than ours.
Your maintenance calories would rise as you gained weight. I don't think you're getting 20kg out of a fixed +100. I'm suspicious of a lot of your claims, but this really jumped out.
Last sentence doesn't make sense if this is what OP meant. "Once your maintenance drops, running a tiny surplus of just 100 ..." You don't need to drop your maintenance calories, with or without GLPs, to gain weight as you eat at a surplus.
"GLP medications blunt your appetite so you eat less, but you still end up feeling completely drained because your body lacks fuel."
How many people report that? Not that many, AFAIK.
"GLP drugs cannot distinguish between nutrient-dense meals and the junk food binges you are trying to avoid."
This again goes against what people report - aversion to junk food so strong that McDonalds et al. consider this a potential threat to their business model.
> Using a large database of (deidentified) medical records, the researchers compared the outcomes of people taking a GLP-1 for their type 2 diabetes to people taking other common diabetes drugs between 2017 and 2025. GLP-1 users were significantly less likely to be diagnosed with TB for up to a five-year span, they found.
This is incredibly manipulative. So, we're going to ignore all other factors that may have played into this and just assume it was due directly to GLP-1 use?
You read reporting about a study, made assumptions that it was bad, and posted your opinion without actually reading the study to see whether the scientists involved were smart enough to try to rule out other factors.
I read a news report on the study that was linked, yes. But my issue isn't with the researchers/their process, it's with how this is presented in the headline vs. what the actual reason was backing the claim.
There's nothing to "do better" about; you just don't like my opinion (and that's perfectly fine).
Yes, p-hacking happens, incentives in academia are increasingly misaligned etc, but I assume that there are competent people and systems to avoid such obvious issues? It's science 101 to avoid spurious correlations. Sure there might be some tricky ones, but if the's obvious one that came to your mind, very good chance it's been accounted for.
Both of these studies are observational and retrospective, meaning they can only show a correlation between GLP-1 use and reduced (or at least less severe) infections, not prove a direct cause-and-effect relationship. At the same time, these are the only latest pieces of evidence pointing to a genuine germ-busting benefit from GLP-1 drugs.
I wonder if the likelihood that people taking a GLP-1 are probably better off financially, have a health care provider willing to spend on the drugs (and therefore probably a better medical system) or a combination of these and other traits are the real reason there are fewer infections.
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