---
title: '''Sulfur burps'' and other GLP-1 things we''re learning'
source: 'https://youtube.com/watch?v=3mhocuACAKw'
video_id: '3mhocuACAKw'
date: 2026-06-28
duration_sec: 1725
---

# 'Sulfur burps' and other GLP-1 things we're learning

> Source: ['Sulfur burps' and other GLP-1 things we're learning](https://youtube.com/watch?v=3mhocuACAKw)

## Summary

Adam Ragusea discusses the fat acceptance movement, the 'health at every size' philosophy, and the new class of weight loss drugs (GLP-1 agonists). He explores the tension between fat acceptance advocates and medical traditionalists, and how emerging research on these drugs may vindicate the idea that weight is just one factor in metabolic health.

### Key Points

- **Fat acceptance movement origins** [00:00] — From the 1960s, a social movement to destigmatize fatness led to organizations like NAAFA promoting better accommodations and HAES (Health at Every Size).
- **Medical traditionalist counterargument** [01:49] — Traditionalists argue that obesity is clearly linked to worse health outcomes, and being healthy at every size is impossible.
- **Enlightened consensus on metabolic syndrome** [02:14] — Fatness is associated with diseases like cardiovascular disease and diabetes, but is not necessarily the cause; it's part of a complex web called metabolic syndrome.
- **Naming the new drugs** [03:10] — The drugs are often called GLP-1 drugs, but they also affect other hormones like GIP. 'Incretin mimetics' is more accurate but less common. They are the first truly effective weight loss drugs.
- **Fat acceptance suspicion** [04:47] — The fat acceptance crowd worries these drugs reinforce a thin ideal and are expensive, with side effects some cannot tolerate.
- **Vindication from drug research** [05:34] — Clinical trials show health improvements even in people who don't lose weight, supporting the view that weight is not the sole cause of metabolic disease.
- **Common side effects: the 'big four'** [07:51] — Nausea, vomiting, constipation, and diarrhea are the most common side effects. Sulfur burps also occur due to delayed gastric emptying.
- **Muscle loss concerns** [12:33] — Weight loss from these drugs results in about 25-35% lean mass loss, similar to crash dieting. Protein intake and resistance training can help preserve muscle.
- **Gallstones and long-term unknowns** [14:03] — Rapid weight loss increases risk of gallstones. Long-term safety beyond 5-10 years is still unknown.
- **No receptor desensitization** [17:59] — Unlike opioids, these drugs do not seem to cause tolerance. Data from the SURPASS-CVOT trial shows sustained weight loss over 4.5 years.
- **Prediction: obesity rates may plummet** [22:04] — New triple agonist retatrutide can achieve bariatric surgery-level weight loss (24-29% at 48-68 weeks). Adam predicts obesity as a pandemic may end in developed countries within a decade.

### Conclusion

The conversation highlights that these new drugs are not just about weight loss; they are reshaping our understanding of metabolic health. While side effects and long-term risks remain, the potential to dramatically reduce obesity rates and associated diseases is real, and the drugs may ultimately vindicate the body positivity movement's emphasis on treating health beyond weight.

## Transcript

Adam:
This video is sponsored by Squarespace. Hi,  
it's Adam Ragusea, and yes, my weight is yo-yoing 
as it has my whole life. From the 1960s, there  
grew a social movement to de stigmatize fatness. 
That is where we get the National Association to  
Advance Fat Acceptance, which most famously 
has pushed for better public accommodations,  
bigger seats for big bodied people. You also get 
the Association for Size Diversity and Health,  
which pushes this public health frame 
they call health at every size. What the  
health at every size people observed is that 
people who carry a lot of body fat tend to be  
discriminated against in the healthcare system.
There are many permutations of the same old joke  
and it goes something like this. What did the 
doctor say to the fat guy with the gaping head  
wound? Have you tried diet and exercise? It's 
actually a fair amount of research to back up  
this claim that doctors tend to look at a person 
and assume that all of their problems stem from  
their obesity. And what obese people have 
said in response is, number one, no, I have  
health problems that have nothing to do with my 
weight and you need to pay attention to those.  
Number two, even if my health problems are related 
to my weight, I still deserve treatment. Judging  
by the study outcomes, it is nearly impossible 
for people to lose a lot of weight and keep it  
off without serious medical help, so let's not 
wait for something to happen that is statistically  
almost impossible before you start treating me 
for my problems. Treat me now as I am. Anyway.
 
Over on the other side of this particular 
discourse, you had the medical traditionalists  
saying this is all hogwash, it's very well 
established that people who are carrying  
a lot of extra body fat have much worse health 
outcomes in almost every area you could imagine.  
It is not possible to be healthy at every size. 
Now, in the 21st century, I think that we've  
seen an enlightened consensus emerge where we 
acknowledge that fatness is associated with lots  
of bad things, but fatness is not necessarily the 
cause of those things. Cardiovascular disease, and  
diabetes, and kidney disease, and non-alcoholic 
fatty liver disease, and all these things exist  
in a dense web of causality that we now call 
the metabolic syndrome, and a person's fatness  
is at most an imperfect proxy for the total 
problem. People with these problems do tend  
to be fat, but they're not always fat, and the 
relationship between the fatness and the problem  
is murky. Anyway, I think the emergence of that 
enlightened consensus seemed to ease tensions a  
bit between the fat acceptance crowd and the fat 
rejection crowd, but now enter the new drugs.
 
Speaking of consensus, we cannot seem to form one 
about what to call these drugs. You can call them  
GLP-1 drugs, but that's not quite right. These 
drugs do imitate the natural GLP-1 peptide hormone  
that all our bodies produce to make us feel full 
when we've had plenty to eat. But some of these  
drugs also imitate different peptides like GIP, 
which works on a totally different receptor,  
and there are more things like that on 
the way, so calling them GLP-1 drugs is  
incomplete. It's like calling all of my cups 
glassware. They're not all made out of glass.
 
You could call these drugs incretin mimetics. 
The chemicals that our bodies make that  
regulate blood sugar and appetite are known 
as incretins. And a mimetic is something that  
imitates another thing, which is what these 
drugs do. They imitate your hunger hormones.  
But, incretin mimetic is even harder to say out 
loud than GLP-1 so I can understand why that name  
hasn't caught on among the general public.
I suppose you might just start calling these  
weight loss drugs because they are the only safe 
weight loss drugs ever proven to have dramatic  
and long-lasting effects. These are the only 
weight loss drugs that actually work according  
to any reasonable, real world standard of what it 
means for something to work. So let's just call  
them the weight loss drugs, they're the weight 
loss drugs. The fat acceptance crowd naturally  
views these drugs with some amount of suspicion. 
The medical industrial complex has made a lot  
of money selling false hope to generations of 
fat people. And even if the hope is not false,  
which seems to be the case this time, the body 
acceptance crowd is still worried that these drugs  
will reinforce a toxic, thin ideal in society. 
Now, there will be even more pressure to conform  
to that ideal since, hey man, all you need to 
do to stop being fat is to take a medicine,  
which is still extremely expensive and 
not all people's bodies can tolerate it.
 
I am, as you can tell, very sympathetic to the 
fat acceptance arguments. But, I do think that  
the ongoing research on these drugs points to 
something that the body positivity community  
should view as something of a vindication. The 
latest evidence is on your side, my friends,  
because these drugs work even if you aren't 
fat, or even if they don't change your level  
of fatness. In clinical trials, in people who 
either did not lose weight or did not need  
to lose weight, we are still seeing dramatic 
improvements in cardiovascular health, kidney  
health, brain health, addiction, substance abuse 
disorders. Science is still untangling all the  
whys and the hows, but it sure seems like these 
drugs are proving the enlightened consensus about  
weight to be essentially correct. If a drug treats 
some elements of the metabolic syndrome without  
impacting weight, if you get healthier on these 
drugs, even if you keep your calories exactly  
the same, that would indicate that weight is only 
one node on this whole dense web of causality.
 
I think that body acceptance advocates should 
view these developments as vindication. It's not  
just about fatness. It might not even be primarily 
about fatness. It's about our brains. The common  
denominator here is the hormones that influence 
how we relate to food, both physiologically and  
psychologically. We are evolved to live a 
life where food is only available some of  
the time. And so to be healthy, our bodies seem 
to need some downtime when we are not eating,  
or when we are not getting the hormonal signal 
to eat. The signal itself may have a role in how  
these very complicated biological systems 
actually operate. We ought not view these  
drugs as a miracle cure, and we certainly 
ought not drop our guard around big pharma.
 
I am curious about the side effects that we're 
starting to see now that vast numbers of people  
are taking these drugs. I'm curious about how 
effective they will be in the very long term  
after decades of use. And I am curious about why 
they seem to work for so many different things.
 
A great expert on the internet to follow for 
this stuff is David White. David is a nurse  
practitioner. That is a nurse whose level of 
education entitles them to prescribe medications  
in the US system. He doesn't need to go through 
a doctor to give you medicine. And nothing that  
David says on my channel should be construed as 
medical advice, yada, yada, yada. He's just a real  
smart guy who deals with these drugs every day in 
his practice, and he spends a lot of time at night  
reading and posting about the latest research. 
His blog is called The Incretin Space. That and  
his social links are in the description.
So, here's the first of what I hope will  
be some ongoing conversations with Nurse David 
about weight loss drugs. First thing to ask is,  
what kind of side effects are we seeing?
David:
 
I mean, the biggest one, and the trial data 
bears this out as well, is usually nausea. I  
just informally call it the big four. So whenever 
you see a top line result or a published result,  
they'll almost always have nausea, 
vomiting, constipation, and diarrhea.
 
Adam:
Guess what? There's an over-the-counter  
medication that I've heard can treat all four 
of those things, and it even has a song.
 
David:
Yeah, yes. Yeah. And the fifth that I would  
add is usually some form of heartburn. You'll 
hear patients, and I don't even have to mention  
my patients. You can look on Reddit, or really any 
social media circle, people will call it sulfur  
burps, which is just the drugs delay your gastric 
emptying, they delay your stomach from moving  
forward, and so you get a little fermentation.
Adam:
 
Yeah.
David:
 
But even that, same thing, there are ways of 
managing that like pineapple or to go to the  
cooking side of things, pineapple, papaya.
Adam:
 
The enzymes.
David:
 
Yeah, the enzymes will help. And people look 
at you funny, but I'm like, "I'm telling you  
it'll work." But yeah, that's one thing with 
the side effects. I tell patients all of it's  
manageable.
Adam:
 
Yeah.
David:
 
A lot of it too in the trials is their goal 
is let's get you up to the highest dose,  
let's lose the most amount of weight as fast as we 
can. But if you are slow in titrating these drugs,  
they're really actually quite tolerable. 
And even when you look at the side effects,  
the actual absolute rate of side effects, even 
with the nausea, you're talking a 20% absolute  
rate. And over time, because most of the drug 
companies will publish the side effects over time,  
you'll watch it just slowly drops away as 
the body gets used to the new normal and.
 
Adam:
The new normal, right.  
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Squarespace. Anyway, we were talking 
with David White about side effects  
associated with the new weight loss drugs.
What about the more serious stuff like  
muscle wasting, which I've understood to 
essentially just be the normal amount of  
muscle loss that you would expect with 
any kind of rapid weight loss, right?
 
David:
If you talk to people in obesity  
medicine research, they will reference something 
like a three to one ratio or 75/25. And by that,  
they mean you should... If you were to just crash 
diet, we would expect you to lose about 75% fat  
mass and about 25% lean mass.
Adam:
 
Yeah.
David:
 
And when you look at these drugs, it's 
usually anywhere from about 25 to about 35%  
lean mass loss and the rest is fat mass loss. 
But even with lean mass, that depends on your  
definition of lean mass. It depends on, are you 
using a DEXA scan? Are you using an MRI? I have  
the conversation with patients like, "If you are 
going to eat anything, at least get your protein  
in and at least do resistance training." Those are 
the two things that I ask, because those are the  
things that will at least preserve your functional 
strength, preserve what you already have.
 
Adam:
I mean, this is territory that has been explored  
by bodybuilders and people like that.
David:
 
Yes.
Adam:
 
They know that when you diet down, you're going 
to lose some muscle, but if you keep lifting  
the weights and if you keep getting protein, 
you're going to be able to keep most of it.
 
David:
Yes, yeah. Correct, exactly.
 
Adam:
Any other big side effects  
that are concerning you so far?
David:
 
There's a slightly increased risk of gallstones 
and inflamed gallbladder, but even that too is  
also more related to the weight loss and not 
the drug without getting into the physiology,  
but you lose weight rapidly and sometimes your 
gallbladder's not happy about that. And even that,  
patients can get their gallbladder out and then 
just continue on with treatment like nothing ever  
happened.
Adam:
 
And then there's the big unknown that not 
even all of the clinical trials can tell us,  
which is what happens to people when 
they've been on these drugs for decades.
 
David:
Yes. Yeah. I mean, there's a subset. I mean,  
there is probably a reasonable subset of diabetics 
that have been on them for an extended period of  
time just.
Adam:
 
At this point.
David:
 
Yeah. I mean, liraglutide or Victoza, that was FDA 
approved in 2012. I'd have to double check my.
 
Adam:
Oh, 2010 in the US. He got real close.
 
David:
But that's been around, I mean, that's  
generic now. That's how long it's been around. So 
even Ozempic, semaglutide, that was FDA approved  
in 2017, so we're going on 10 years for that even. 
There are definitely people that have been on them  
for a while. But even the clinical trials, the 
longest clinical trials are about five years,  
and obviously we just continue to see a benefit as 
time passes. I say this understanding I don't have  
any evidence to back this up.
Adam:
 
Very scientific.
David:
 
But also, I mean, it doesn't make... Just 
on the mechanism, how the drug works.
 
Adam:
You're making a mechanistic  
argument. There you go. Go ahead.
David:
 
Yeah. On a mechanistic argument, there shouldn't 
be... It's like if I can use another well-known  
drug class, with statins, we know the longer 
you're on them, the lower your risk of  
cardiovascular diseases.
Adam:
 
Sure yeah.
David:
And so I have a feeling it's going to be the same 
thing. If you're on a drug that caused you to lose  
20% of your body weight and you stay on it for 
20 years, you probably will live longer. You'll  
probably have less comorbid conditions. You'll 
probably have less healthcare utilization. I mean,  
and actually there's already starting 
to be... Do you know what QALYs are?
 
Adam:
Yeah. Go ahead.
 
David:
Yeah. Or you can define it in the video, but.
 
Adam:
Oh, okay. QALY stands for  
quality adjusted life year. We don't just want to 
be alive, we want to be healthy while we're alive,  
and QALY is a crude way of measuring that. It's 
like how many healthy years this medicine gets  
you. That's a QALY. Anyway.
David:
 
The QALY data is already starting to line up that 
if patients are on these for X amount of time,  
they do start paying for themselves, even with the 
current costs. And insurance companies obviously,  
and actuaries everywhere, that's 
what they're looking for, right?
 
Adam:
If you'll permit me  
to make a mechanistic argument, and also I suppose 
one drawn from anecdotal experience, when you have  
a receptor in your body and you pummel it.
David:
 
Yeah.
Adam:
 
With stimulus a little bit more than it would 
normally get, you're going to start to notice some  
weird things happening among them. It's just going 
to take more and more stimulation in order to make  
that receptor feel anything.
David:
 
Yeah.
Adam:
 
Are we not seeing that with these drugs? We're not 
seeing people just get used to it and the whole  
system just equilibrates to it?
David:
 
There was a cardiovascular outcomes trial called 
SURPASS-CVOT, C-V-O-T, that Eli Lilly published  
last year, and it was almost five year long 
trial of tirzepatide in diabetics and looking  
at cardiovascular outcomes. And they included 
a graph and it showed the patient's weight.
 
Adam:
Yeah.
 
David:
And A1C control over that  
was about four and a half year period and there's 
almost no... They lose that weight. The A1C comes  
down, and if you look at the error bars and the 
confidence intervals, they're so tight. This is  
15,000 patient trial and no one is... I don't want 
to say no one, but the vast majority of people not  
regaining weight, not requiring a higher dose, 
their diabetes is under control. This is maybe  
above my pay grade in terms of understanding, but 
from what I can gather and from what I've talked,  
for some reason, there's just not that 
receptor desensitization that you would see  
with cannabinoids or opioids or various other. 
And it may be related to the fact that I mean,  
GLP-1 as a receptor is so integral to just 
our day-to-day physiological function.
 
Adam:
Sure.
 
David:
And it's one of those things that  
it took pharmacology to realize, oh, hey, this 
thing actually does way more than anyone...  
Simplistic understanding is, sure, it suppresses 
your appetite, it helps with insulin secretion,  
but I mean, it is-
Adam:
 
Tip of the iceberg.
David:
 
Yeah, half inch view. I mean, I'm working on 
a blog post right now on the anti-inflammatory  
infects, and I've been writing for a month and 
a half now because I'm just trying to translate  
it down to regular, in English, but also it's 
so... It's just like every time I read one paper,  
I'm like, "Oh, wait, there's another 
thing, do I need to add this now?"
 
I actually found an evolutionary development paper 
about where this came from, and you can track the  
development of the GLP-1 class, or I guess I shape 
more appropriately what's called pre-pro glucagon.  
So you get GLP-1, which everyone knows about. You 
get GLP-2, which is another intestinal hormone,  
and you also get glucagon, and then you get a 
couple other random bits that don't do much. And  
that family of those three hormones are so deeply 
conserved, evolutionarily speaking. So there's a  
really great paper that talks about some of the 
benefits of these drugs outside of the weight  
loss, and it had the actual amino acid sequences 
of glucagon. And I mean, you can go way back, way  
off from the primate family tree, and you could 
get whale glucagon and it would work in a human.
 
Even some of the bony fish glucagon is still 
similar enough that you could give it to a  
human and get an effect. So clearly evolution was 
like, "We need this, this class of hormones." And  
I think that's my speculation as to why you don't 
see desensitization, because it's like, this is  
actually mission-critical to keeping you alive.
Adam:
 
Well, I suppose all of that is a lot of reason 
to be excited, but also reason to proceed with  
caution.
David:
 
Yes.
Adam:
 
If we're dealing with such a 
powerful primordial force.
 
David:
Yeah.
 
Adam:
I, about three years ago, publicly predicted that  
obesity as we know it would be over as a pandemic 
in highly developed countries within 10 years.  
I've got seven more years for that admittedly 
bold prediction to come true. I wonder how  
on schedule you reckon we are. I actually 
feel kind of good about it so far because  
it is preceding the way I imagined, where you're 
starting to not see fat rich people anymore.
 
David:
Not to be crass, but that's your signal, right?
 
Adam:
Yeah. That's where it begins.
 
David:
But there was a big  
hullabaloo about how the rate of obesity in the 
US has flattened out in the last couple years. And  
it's like, is that the drugs? Is that the first 
signal that, oh, enough people are on these that  
we're starting to see a downward deflection in the 
obesity rate? You might be a little aggressive,  
but at the same time, I mean, some of the 
stuff that's in develop... So retatrutide,  
which is a triple agonist that will have phase 
three data, weight loss data here in about,  
I mean, it's mid-April when we're recording this, 
and the data's due to be published the first week  
of June, so not too long for that. And that drug 
is going to show bariatric surgery outcomes.
 
Adam:
Outcomes comparable to  
bariatric surgery, you mean?
David:
 
Yeah.
Adam:
 
And by triple agonist, you mean it's 
acting on three different receptors?
 
David:
Yes, yeah. So it acts on GLP-1,  
it acts on GIP, and then it acts on glucagon so 
acts on three things at once. The initial phase  
two data showed 24% weight loss at 48 weeks. There 
was a shorter phase three trial that showed 29%  
weight loss at 68 weeks with patients still losing 
weight at 68 weeks. And the trial that will have  
data published in June will have an 80-week and 
104-week data arm. So yeah, my expectation is,  
I mean, 29%, you're one point away from 30%, 
and 25% is the start of bariatric surgery  
loss. 30% to 35% is usually what most bariatric 
surgeons will say is the goal. So yeah, we could  
have a drug that has that level of efficacy.
And if that becomes broadly accessible, then yeah,  
it's pretty reasonable to expect obesity 
rates to plummet. And then even ignoring that,  
there are so many other drugs in development that 
it seems like the floor is about 15% to 20% weight  
loss, which again, like that's going to drive a 
significant number of people into just overweight  
and not obese anymore. So yeah, I mean, by 2035, 
I think it's reasonable to see significantly less  
obesity.
Adam:
 
What are you most excited about looking ahead?
David:
 
I mean, so the drug that I just mentioned, 
retatrutide, very excited for that. Just on  
the mechanism alone, I mentioned it, it acts on 
glucagon. If you ask most people in the medical  
field, they're like, "Oh, that's the drug we 
give to raise people's blood sugar." And except  
that in this case, when you are depressing the 
lever for it for an extended period of time,  
the opposite happens so it increases insulin 
sensitivity. It actually helps lower blood sugar  
as counterintuitive as that sounds, but it also 
is... So I like to explain this as glucagon is  
like a starvation signal to your body and you 
can, again, go back to maybe before clinical  
trials were as ethical as they are now where 
we did starvation studies on live human beings,  
but glucagon is the signal that comes through when 
people don't eat for a prolonged period of time,  
their insulin levels drop, and it forces 
your body to start burning fat.
 
Adam:
Right.
 
David:
And so another way to put this,  
so GLP-1 basically reduces your intake through 
appetite suppression and then glucagon's adding,  
basically telling your body, "Hey, grab the 
firewood out back and throw that on as well."
 
Adam:
Yeah. It's saying, "This is not a temporary  
decline in available calories. This is winter, 
we're in this for the long haul, we need to adjust  
our whole system to this new reality."
David:
 
Yeah. So you get less intake and then you are 
burning more. And so that's obviously a recipe  
for weight loss. And then side benefit, because 
you're burning lipids, that includes cholesterol  
so you will see pretty profound, again, going 
back to some of the earlier data on that drug,  
they saw almost 25% drop in LDL cholesterol, the 
bad cholesterol. That's what you would see with  
taking a statin medication. So I look at it as, 
imagine if you could take a drug that makes you  
lose weight and it drops your cholesterol like 
a statin. Again, on the economic argument-
 
Adam:
Yeah.
 
David:
... that's very compelling to me as  
a clinician like, "Oh, hey, you can take this one 
drug once a week and that fixes what ails you."
 
Adam:
Yeah. Awesome, so now  
you've met Nurse David and he's going to be our 
guy watching the incretin space for a while here.  
Check his blog and his socials in the description. 
There's clinical trials underway using these drugs  
to treat major depressive disorder, bipolar, 
schizophrenia, alcohol and opiate addiction.  
Like the man said, these drugs work on your 
brain more than they work anywhere else. Make  
good choices with your brain and your body, 
and we'll talk about this stuff again soon.