August 18, 2025 • 35 mins
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Metabolic adaptation is a powerful physiological process that explains why weight loss is so challenging and why keeping it off can feel like your body is working against you.
• Your body burns fewer calories than expected after weight loss, creating an "energy gap"
• For every kilogram lost, metabolism slows by approximately 25 calories
• Weight loss affects hormones like leptin (satiety) and ghrelin (hunger) that control appetite
• Metabolic adaptation is a survival mechanism, not a personal failure or lack of willpower
• Research suggests metabolic adaptation is strongest during weight loss and the first few months after
• Evidence from "The Biggest Loser" contestants suggests extreme weight loss may cause longer-lasting metabolic changes
• Exercise (200-300 minutes weekly) helps counteract metabolic adaptation
• High-protein, high-fiber diets with low glycemic loads help manage increased hunger
• Even modest weight loss (5-10%) significantly improves health markers like blood pressure and blood sugar
• Medical interventions like GLP-1 medications and bariatric surgery can help address the hormonal drivers of weight regain
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Production and Content: Edward Delesky, MD & Nicole Aruffo, RN
Artwork: Olivia Pawlowski
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Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:09):
Hi, welcome to your checkup.
We are the Patient EducationPodcast, where we bring
conversations from the doctor'soffice to your ears.
On this podcast, we try tobring medicine closer to its
patients.
I'm Ed Dolesky, a familymedicine doctor in the
Philadelphia area, and I'mNicole.
Speaker 2 (00:24):
Rufo, I'm a nurse and we are family medicine doctor
in the Philadelphia area, andI'm Nicola.
Speaker 1 (00:25):
Rufo, I'm a nurse and we are so excited you were able
to join us here again today.
So I was thinking well, lastweek we didn't talk about Trent
and our experience at State andLiberty.
Speaker 2 (00:37):
We need to talk about Trent.
Speaker 1 (00:38):
We got to talk about Trent.
Tell us about Trent.
Speaker 2 (00:41):
Trentrent.
Well, we went to go get eddie'ssuit for our wedding at state
and liberty in rittenhouse.
Highly recommend it was so muchfun, even for me and like I
wasn't even getting anythingyeah but trent was.
How would you describe trent?
Speaker 1 (01:00):
how would I describe Trent?
Speaker 2 (01:01):
Yeah.
Speaker 1 (01:02):
He was an excited, stylish man who loved what he
did and took great pride inhelping people look their best.
He was a calming presence, butalso reassuring and discerning,
because he also knew whensomething didn't look good and
he wasn't afraid to tell you hewas doing his job.
(01:23):
He immediately told you whensomething was good and I
appreciated that.
Um, it was like you said, itwas really fun.
We were the first appointmentof the day to take about an hour
.
Um, he asked us this disarmingfirst question so what fabrics
are you thinking of?
And tweedweedledee andTweedledum over here didn't know
(01:46):
anything about fabrics andwe're just like uh, and he's
like uh, I want a black suit.
Make it black please.
And like I had no idea what todo, and so he just, I think he
just took, like I knew I wanteda vest, that was like the thing
I knew I wanted.
But then, like these suits aregreat, right in the ballpark of
(02:10):
other places I've gotten to getsuits too, and it looks way
better than anything else.
Speaker 2 (02:14):
Oh my gosh, it looks so good.
I can't wait.
I'm excited To get it.
Speaker 1 (02:18):
And I'm excited to go back.
I'm a state and liberty guy.
Well, it's an athletic fitstore.
It is For men with thatV-shaped body.
You know this is an audio showbut you can't see me.
But I'm going to state andliberty.
Speaker 2 (02:37):
It's got the athletic build.
Speaker 1 (02:39):
Some might say it's a place to shop for people with
an athletic build.
I like the store.
It was fun, though.
Did you have an athletic build?
I liked the store, it was fun,though.
Did you have any other takeaway?
They were so nice.
They were just really kind tous yeah.
Speaker 2 (02:50):
They really took care of us.
Yeah, and we're probably goingto go back and get some work
clothes.
Well, the thing is the secretbutton under the collar of their
dress shirts, which is thething that is the bane of your
existence with collared shirtsfor work, because the collar is
up or doesn't lay right, blah,blah, blah, blah, blah.
(03:12):
But they have this hiddenbutton like under the collar, so
that it everything just laysright and looks nice yeah, look
at now we need to buy like 17shirts for them.
Speaker 1 (03:23):
Oh yeah, well, it bothers me because when the even
if it's not so much a problemwhen you're wearing a tie, like
it all gets bunched up andtucked in with the tie, but when
you're not, and then you getwhat someone called the jersey
flare, where I guess you looklike you're like a club owner
sloppy.
And it looks a little sloppyand like the.
The collar flares out a littlebit there, looks a little sloppy
(03:44):
and like the the the collarkind of flares out a little bit.
There's like too much chestshowing that like second button
is like too far down, but thefirst button is like choking you
and it's like what do you do?
And then the collar is flaredout.
It's just a mess.
So the hidden button yeah, hugehidden button guy, didn't even
know it.
Now I am you didn't even knowyou were looking for it no, and
(04:09):
now I'm like I'm locked in and II can't wait do you think trent
will listen to our podcast?
I think if we told trent thatthere was a a rave review of his
services that he's the best andwe wish we could hang out with
him.
Speaker 2 (04:23):
I can't wait until your suit comes in so we can go
get it and see him again.
Speaker 1 (04:30):
That's.
I mentioned that.
They were like emailing us tooLike they were like letting us
know and giving us updates, and.
I was like this is so nice, itwas great.
Even that person who was on thephone call with us, who was
like in the beginning, was nice,a little shocked that I was
like only getting a suit formyself for a wedding and I was
like I don't think that's such abig deal, but that's neither
here nor there.
Any last thoughts about trent Idon't think so.
(04:52):
Yeah, so what we also watched,or kind of snooze through um
most recently, is this stormarea 51.
It seems like it's been out fora little while on netflix.
It's part of this train wreckseries, same thing as the poop
cruise.
This like film team.
I guess it's like productioncompany finds like unique
stories and then like interviewspeople and gotta say, the guy
(05:16):
who put this together, who gotall of this like notoriety, only
made 1700 from like sellingshirts and not very
entrepreneurial.
Speaker 2 (05:28):
No, not at all Missed opportunity Totally.
I mean, he also was only like20.
Speaker 1 (05:33):
Was he?
Yeah, hmm, cause a lot ofhoopla.
Did you know this live when itwas happening?
Speaker 2 (05:39):
Um, like very minimally Okay.
Speaker 1 (05:43):
Yeah, and then through this I learned well, I
still have to look it up alittle bit more about what fire
fest was?
Um, like very minimally, Okay,yeah, and then through this I
learned well, I still have tolook it up a little bit more
about what fire fest was.
Speaker 2 (05:50):
Oh yeah, there are a couple of documentaries about
that.
We can watch them.
Speaker 1 (05:53):
Yeah, I I'm into a documentary recently.
I'm liking learning about realthings that happened in the
world and having it spoon fed tome on the TV.
I'm liking that.
All right, we can watch somemore.
Yeah, we'll see.
Tell us about the rest of ourviewing experience.
Speaker 2 (06:10):
Oh, I think there was a new also, not to cut you off.
Speaker 1 (06:13):
That's okay.
Speaker 2 (06:13):
And then we can talk about that, because it'll be a
good segue.
Yeah, I think there's a newHurricane Katrina one.
Speaker 1 (06:21):
Oh, that did just pop up.
Yeah oh, that did just pop up.
Yeah, yeah, saw that.
Can add that to the list.
We can add that to the list.
Maybe we could talk about thatnext week.
A very real thing for a lot ofpeople.
Speaker 2 (06:30):
Sorry if you were affected by hurricane katrina um
, okay, and then we watched thebiggest loser documentary oh yes
it was three episodes.
I don't know what I wasexpecting Me neither.
I feel like I don't knowBecause like they had a couple
(06:54):
contestants, like previouscontestants that were on, I
guess they were supposed tooffer like background
information and like behind thescenes stuff, but I don't really
feel like we got a lot of that.
Speaker 1 (07:05):
No, it was interesting to see like the
producers come out and talkabout their views, like they
were making television first andforemost, and I think, like
that's a yes, it was a veryinspiring show.
Yes, it was flawed, but like Ithink they own that, like they
were, like we were out to make aTV show.
Speaker 2 (07:24):
Yeah, I think the public outrage that the biggest
loser wasn't quote unquoteethical or healthy or safe.
Yeah, you don't make a realityTV show about losing weight and
it's not crazy losing weight andit's not like crazy.
Speaker 1 (07:48):
Well, I guess you know we were a big bob harper
stands and there was a flavor ofthe show that like yeah, I mean
cast him in a unfavorable light.
Um, I found the dr hyzengastuff really interesting, like
how he like really advocated forthe contestants like through
and through, and that was metwith, uh, countenance from the
trainers and the producers whowere really trying to steamroll
(08:09):
him, and it does like get into alittle bit of the power dynamic
between the two.
And I mean, growing up I alwaysthought, like the even before I
realized that I wanted to be adoctor, like I thought the dr
haizanga stuff on the show wasso fun and I was like, whoa, are
you kidding, that's so cool.
So I thought it was cool tohave him on the show, like the
documentary inspiration to beget certified in obesity
(08:31):
medicine not really um, but itwas cool to see.
I didn't realize that he waslike the team doctor for the
raiders oh, I, know me neitherno, I like charlie sheen
randomly.
Speaker 2 (08:42):
Yeah, I mean, I guess you don't get the role of a
doctor on any sort of realitytelevision show by like just
being like a random doctor.
Speaker 1 (08:53):
Yeah, that's a good point.
You know that's a good point.
Yeah, Julia Michaels was not inthe documentary.
Speaker 2 (08:58):
Yeah, a lot of people don't like her.
Speaker 1 (09:02):
I think she has some weird views on the world that
I've been seeing on threads.
Speaker 2 (09:07):
Yeah, I mean she's also like come out and basically
said the show would like themlike yelling during workouts and
like being all like extreme andstuff was like all an act that
the producers told them to doand stuff.
Speaker 1 (09:23):
Yeah.
Speaker 2 (09:24):
But she, yeah, yeah, that's all I'll say about that,
yeah but bob harper was ontraders.
Speaker 1 (09:31):
So like we love bob circulating in the the zeitgeist
in the last year or two, likeevery year, like bob harper's
got something else going on andgood for him.
I think I was left a littlecrestfallen.
Speaker 2 (09:45):
I was left wanting more.
I was I don't know what thatmore is, but it didn't give me
what I thought it was going to.
Speaker 1 (09:53):
No, I was.
I'm glad we watched it Me too.
Yeah, I'm glad we watched it.
I was hoping for more Fredo.
Speaker 2 (09:59):
Our King Fredo.
Speaker 1 (10:00):
Yeah, I was hoping for more of him.
I forget what season that'sfrom, but he was a dastardly
fellow that I wish there wasmore of on the TV, isn't he like
from New Jersey or New Yorkmaybe?
The area and you can just tellthis guy had a whole following
of like dudes on the show.
It was funny.
(10:23):
I wish they had more of him andI said like 400 contestants.
They're probably like couldhave pulled a few more people to
talk.
The one thing that was crazywas like that first they had
this um, spoiler alert, ifyou're gonna watch, okay, now
we're gonna go.
Um, the lady who was likerunning a running a mile
(10:44):
legitimately almost passed away.
She had rhabdomyolysis fromrunning the mile.
That's crazy.
Speaker 2 (10:50):
Is it rhabdomyolysis?
Speaker 1 (10:53):
You can just stop at rhabdo.
Speaker 2 (10:55):
Is that how you say it?
Speaker 1 (10:55):
Yeah, oh really, how do you think it should be said?
Speaker 2 (10:59):
Not like that.
Speaker 1 (11:01):
Rhabdomyolysis.
Speaker 2 (11:03):
Maybe Wait say it again Rhabdomyolysis.
I've never heard anyone say itlike that.
Speaker 1 (11:11):
Not just truncated to rhabdo.
Yeah, no, she nearly passedaway.
Speaker 2 (11:19):
Okay, but the interesting part, which is a
great segue into today's episode, is that they talked about I
guess, like the very small,limited study that they did,
which was still interesting ofessentially the people that lost
a bunch of weight and thengained it back.
Speaker 1 (11:39):
Yes.
Speaker 2 (11:40):
And so what was that about?
Speaker 1 (11:41):
Yeah, so that, um, I've been meaning to talk about
this for a while.
So, like, as you mentioned, I'mlike studying for the obesity
boards, so I was like lookinginto this stuff and have been
talking and thinking about thesesubjects more again.
And it's a subject, it's a, itis a physiological phenomenon
called metabolic adaptation oradaptive thermogenesis.
(12:06):
Before we really get into toomuch of it, I want to let you
know that the information fromthis episode comes from
published research in obesitymedicine, including guidelines
from the Obesity Society andAmerican Diabetes Association,
as well as recent scientificreviews in journals like JAMA,
the American Journal of ClinicalNutrition and Obesity.
And, while we keep thingsconversational, all the details
(12:30):
are drawn from peer-reviewedstudies and expert guidelines.
So the simple idea behindmetabolic adaptation is it gets
at the concept of why weightloss is so hard and why it is so
hard to keep off.
Specifically, it's not the onlything, but it comes up in a
(12:54):
situation like this have youreally ever worked so hard to
lose 10 or 20 pounds only tofeel like your body was fighting
you the whole way?
And then, when you do that,that it's pulling you back to
the weight that it was before,whether it's by appetite or just
making you feel like blah andyou can't do more.
It turns out that this isn'tabout a lack of discipline.
What it is, at least in part,is that your body has built in
(13:18):
defenses against weight lossbecause it is seen as a survival
disadvantage Okay and it'sknown as metabolic adaptation.
So the simple definition isthat your body burns fewer
calories than expected afterweight loss, and I'll give a
couple different examples hereto try to illustrate this point.
(13:40):
So let's say that someoneweighed 250 pounds.
Then let's suppose that theylose 25 pounds.
Now they weigh 225 pounds, butif you compare their baseline
metabolism to someone else whoweighs 225 pounds but didn't
(14:00):
just lose 25 pounds, theirmetabolism the person who lost
the weight is proposed to belower.
This has been researched, thishas been studied in different
facets.
It's been looked at inindividual small cohorts.
(14:21):
It was looked at in people inthe biggest loser study and we
can talk a little bit more aboutwhy that was so unique.
But it's the idea that there isan energy gap.
Another way to think about thisis that there is a study done by
this physician called Dr KevinHall, and another way to
(14:43):
illustrate it is that it wassuggested that every kilogram
lost slows the metabolism yourresting metabolism, by 25
calories and that it makes you95 calories hungrier every
kilogram you lose.
People often get to a pointwhen they're losing weight and
they say like, oh, I've beenlosing my weight, I've been
(15:05):
losing weight.
And then they get to a plateauand you suggest that maybe
someone has been in a caloriedeficit.
They've been eating lesscalories than they bring in.
Energy out is greater thanenergy in helping them to lose
weight.
But this theory suggests thatthe body slows the metabolism
(15:26):
where that calorie deficit maynot be a calorie deficit anymore
at all.
Did you know about this?
Speaker 2 (15:34):
Well, no, not until you told me about it.
Well, we mentioned it in ourone obesity episode, I think too
.
Or like weight loss orsomething Like the general idea
that you lose weight and thenyour body tries to gain it back,
essentially, it turns on you,yes, which is really frustrating
, but I also understand it loseweight and then your body tries
to like, gain it back,essentially, and it turns on you
, yes which is reallyfrustrating, but I also
understand it and there's acertain degree of now that we
(15:58):
kind of understand what this is,um, and illustrate this a
couple different ways.
Speaker 1 (16:03):
Uh, it's one thing to explain why it happens and
there are this is complex thingLike your body doesn't like
change.
It's called homeostasis andyour body likes things to stay
the same and there are soundsdramatic.
Yeah, there are like leversthat the body pulls and there
(16:26):
are hormones and like I'm goingto give them names.
I think a lot of people likethere are a lot of things online
when people just quote unquotehormones, but there are hormones
that have names and functions.
What are you grumbling aboutover?
Speaker 2 (16:39):
there.
That drives me crazy.
Speaker 1 (16:41):
It drives me crazy too.
But what I want to get at isthat there are specific hormones
that cause some of these thingsto happen.
So there are two that I want toname and define.
They're called leptin andghrelin.
Ghrelin is the easier one todefine.
It is a hunger hormone, and sowhen you lose weight or you're
(17:04):
ready to eat, ghrelin goes up,and that's kind of the simplest
way to do it and to think aboutit is that ghrelin is a hunger
hormone and when you're hungryit goes up.
Leptin is the other one.
Leptin is a hormone that helpsyou think that you are satiated.
So when it is up, it is makingyour body think that you are
(17:28):
energy neutral or energypositive, like you've had enough
to eat.
Your leptin is high and you'renot going to feel like you need
to go out and get food anymore.
And one place that leptin comesfrom is adipose tissue, which
is also fat tissue, so adiposetissue is hormonally active.
(17:49):
There are a lot of differenthormones being sent out by
adipose tissue and only one ofthem is leptin, and this is also
kind of the base of whereestrogen, testosterone, gets
converted essentially intoestrogen in fat tissue, which
kind of supposes sort of thereason of why different cancers,
(18:10):
like endometrial cancer, hasincreased risk for people who
live with obesity because ofthis underlying feature.
But let's say that when someoneloses weight, leptin decreases
and so when leptin is decreased,your body thinks it's in a
starvation mode and that drivesforward appetite, which makes
(18:34):
you hungrier and makes you wantto eat more.
So in that little section therewe defined two different
hormones, leptin and ghrelin,but there are so many more of
them.
There are also implications ofthyroid hormones sex hormones
involved in this.
There are also implications ofthyroid hormones sex hormones
involved in this, and these mayimplicate a slower metabolism
(19:00):
and dictate fat storagethroughout the body, whether fat
is stored internally asvisceral fat around the internal
organs, which is the moredangerous type, or elsewhere in
the body.
There are other features thathappen, other things that change
to help this the shrinking fatcells themselves.
When someone loses weight, thefat cells shrink and what
(19:20):
eventually happens and this is areally interesting point when I
was listening to these lecturesis that the mitochondria become
more efficient at burningcalories or essentially creating
energy and using it.
They become more efficient,which is actually maybe better
for you in the course of alifetime.
There was a whole lecture thatI watched about aging and aging
(19:45):
and the calorie deficit andcalorie restriction and because
they looked at people in Okinawaand they were like why do these
people live longer than peoplewho live on mainland Japan, like
right over there?
And one theory was that theyjust had so many, they had a
huge calorie restrictioncompared to the people who live
on Japan.
So then there was this wholelike aging lecture that I
(20:08):
watched that supposed that ifthe mitochondria became more
efficient or your body'scellular processes themselves
became more efficient and usedless calories throughout the day
to accomplish the same tasks,there would be less iterations
of the cells needed in the bodyas a whole and less aging.
(20:31):
Because, like, none of this islike a limitless thing.
Like you can, your cells canonly divide so many times before
it's like curtains, so CurtainsBefore it's curtains.
So the idea is that if they canmore efficiently do this, then
they would be able to go and doit longer.
(20:54):
So it's possible that metabolicadaptation might not be a bad
thing in the grand scheme ofthings.
It might just be something thatis frustrating for people who
are trying to lose weightbecause the body's being more
efficient at doing what it doesin living.
There's also suggestion thatthere's inflammation that drops
and that, like adipose tissue,is inflammatory in itself.
(21:16):
There's.
I mean, we looked at a lot ofliterature and research before
this to collate this episode andthe big take home point is that
there are some immune cellsthat are still involved.
There is some baselineinflammation that might still be
there that may make someonemore susceptible to weight
regain as well.
So that was like the meatiest,nerdiest part of the episode
(21:40):
that I could possibly give you.
Is there any like thought orfurther explanation you think I
could give?
Speaker 2 (21:47):
No, I think that was great.
Speaker 1 (21:48):
But yeah, and before we get too far away from those
hormones yeah, there's leptin,there's ghrelin.
Everyone knows what GLP-1 is.
Now, because of the medications, that's another one of these
hormones.
They're called incretins Notall of them, but like a GLP-1 or
a hormone, pyy orcholecystokinin.
(22:09):
These are hormones that arereleased after someone eats and
communicates to the brain to sayI'm full, you don't need to eat
anymore, please stop eating,because if you do, I'll be too
full and I'll feel uncomfy, andthat's how that happens.
So when someone's injecting aGLP-1, they're essentially
telling their brain GLP-1,they're essentially telling
(22:33):
their brain hey, relax, stopdoing this.
Like back in the day they triedto look at leptin.
And can you inject leptin intosomeone and increase those
levels and make people lesshungry?
It didn't bear out.
I think it wasn't safe.
Something happened, but theydid look at this.
Speaker 2 (22:48):
Darn Right Could use a good leptin shot.
But they're looking like youknow, go to a med spa, get a B12
shot and a leptin shot, get aleptin shot.
Speaker 1 (22:58):
But there's, I mean, I think, now in the pipeline.
They're probably looking atlike PYY, or they're looking at
I mean you have GLP, gip they'relooking at.
They may look at leptin again,who knows, but it's a
complicated process that they'relooking at to try to make safe
and effective options formedications for the management
of obesity.
So just know there are a lot ofthese hormones.
(23:21):
They do have names, they havefunctions.
Let me try to keep it as simpleas possible here without
overwhelming you.
Speaker 2 (23:27):
So how long does this metabolic adaptation last?
If someone loses weight, arethey fighting this forever?
Speaker 1 (23:36):
Maybe Probably not, though it's an area of active
investigation but what we couldglean was it's most active
during weight loss and withinthe first few months of weight
maintenance.
But there is a decent amount ofsuggestion in the literature
(23:57):
that the metabolic adaptationmay fade around 6 to 12 months
if the weight stays steady.
In episode 20, we talked aboutthe obesity set point theory and
there's some suggestion in thatschool of thought that if you
stick around at the weight forlong enough in a new environment
it might stick, and so thismetabolic adaptation piece may
(24:21):
attenuate or get smaller.
The thing we saw yesterday inthe show and they even brought
this up and I'm curious to hearyour thoughts on the show here
was in the Biggest Losercompetition and it and I'm
curious to hear your thoughts onthe show here was in the
Biggest Loser competition and itwas a very small study.
I think there were some 30people, 30 contestants from the
show, and they had somesuggestion that between the
start time and six years laterthat the metabolic adaptation
(24:45):
which is a reminder is like yourbasal metabolic rate if you're
sitting doing nothing and theamount of calories you burn
decreases lower than it shouldwith weight loss.
That that persisted over thecourse of six years, which was
unexpected, and that kind ofstill bears out in the
literature with a big questionmark.
(25:05):
And they even talked about thison the documentary.
They were like did we like hurtthese people, did we ruin their
metabolisms by doing this?
And I still think the answer isI don't know.
And I don't think they knoweither, because I think it has
to do with how you measure thisstuff too and it's reliable.
But I think the theory behindit is that they were I mean,
(25:29):
they said it on the show theywere burning like 6,000 calories
a day.
Speaker 2 (25:34):
Yeah, that was insane .
Speaker 1 (25:35):
And maybe eating 800.
And so what the body was maybedoing was lowering the resting
metabolic rate to accommodatethe total energy expenditure,
which is resting metabolic rateplus active energy expenditure.
These people were doing 6,000calories of active energy
(25:56):
expenditure.
The body's like please relaxfor a second, bro, and so it
just kind of turns a coupleknobs down, which as a
compensatory mechanism makessense to me.
But then that it they suggestthat it lasts for six years is a
(26:17):
little confusing and I wassurprised.
Speaker 2 (26:22):
Yeah, I mean also not everyone loses weight as
extremely as they did on thebiggest loser, but six years
still feels like a long time.
I think it is an extreme bodyto still be like ah yeah.
Speaker 1 (26:37):
I think it was an extreme use case the medical
term.
Ah yeah, and I don't think Imean I don't think many people
listening to this show will havea very similar experience to
them and perhaps it's not themost relatable case to think of,
but maybe it illustrates thepoint to some degree that in
extreme cases this is whatmetabolic adaptation is, whether
(27:00):
this actually bears itself outor not.
It does seem that they lookedat in the study that it didn't
necessarily correlate with theamount of weight someone lost
but with the amount of exercisethat they did, and that the
people who exercised more mayhave had a more significant
change to their baselinemetabolism, to that theory, like
(27:21):
that supposition I made beforeabout trying to compensate for
the energy deficit.
All right, well, that was a funlittle detour back to the
biggest loser.
Speaker 2 (27:32):
So if someone is listening and struggling with,
or thinks they are, what canhelp to counteract the metabolic
adaptation?
Speaker 1 (27:59):
bring it up in conversation when someone's like
struggling to lose weightupfront anyway and maybe they
really have a great grasp of howmany calories are going in and
going out, or if they hit aweight loss plateau.
I think it invites aconversation about recalculating
a calorie deficit based off of,like where you were to where
you aren't I don't know thislike if this 25 calories per
(28:21):
kilogram is something that likeworks for everyone all the time,
but at least helps toillustrate that, like, if you
lose two pounds, your metabolismslows down a little bit.
If you lose 10 pounds, it slowsdown a little bit more and
maybe you have to rethink.
If you need to keep losingweight, you need to rethink
where your calorie deficit is.
I also think it invites aconversation that you're not
(28:45):
crazy and if you're doingeverything that you can to lose
weight, that, like this is justit's your body, it's not you,
it's not your fault.
This is a really decent theoryand science that this happens to
people and it is not anindictment on your character or
(29:10):
who you are like.
This is very clearly somethingthat happens to people, not
something that people do, whichI think is like huge.
I think weight loss itself likea five to 10% total body.
Weight loss can improve thingslike way more than just
(29:31):
aesthetics when it comes toweight.
Like that kind of weight lossimproves diabetes.
It improves cholesterol figures.
Blood pressure Greater than 10or 15% can put diabetes into
remission, and so, like when wetalk about this, that's where
we're coming from, like theseunderlying things, these
metabolic abnormalities andcardiovascular abnormalities
(29:54):
that can be fixed with somelifestyle changes that are so
important.
And what else can you do aboutit?
We talk a lot about 150 minutesof exercise per week, of a
moderate intensitycardiovascular exercise.
We talk about that in episode10 in the power of exercise.
The suggestion of some of theliterature I was reading is that
(30:17):
bumping that up can helpmaintain muscle and burn the
calories in excess, and somoving that to 200 to 300
minutes per week of whereas dietand calorie deficits in weight
loss are paramount, and so thescale for lack of a better word
(30:48):
flips when it comes to weightmaintenance.
So increasing that number maybe something to think about,
maybe something to think about,and then staying attuned to
basic foundational nutritionalcomponents like high protein,
high fiber diets, low glycemicloads, to help kind of
neutralize or at least curb yourappetite so you're not feeling
(31:10):
like oh, I ate this bag of likesour cream and onion chips all
at once and I still feel hungry,but now I'm like a thousand
calories down from where Ishould be.
Speaker 2 (31:21):
This sounds very specific and personal and
familiar.
Speaker 1 (31:26):
It is very specific, personal and familiar.
Hi, I'm Ed and.
I love sour cream and onionchips more than I should.
What's more is that thebreakthrough in the science has
been so important, especiallywhen it comes to pharmaceuticals
.
I mentioned them earlier in theshow, but medications like
GLP-1s, which go by the names ofOzempic Wagovi, and the
(31:49):
terzepatide component ones,zepbound and Moonjaro, help.
They help with the appetite.
So much of obesity is appetitedysregulation, and that's where
these medicines step in, and sothey themselves may blunt the
hormonal signals that help driveweight regain.
So that's an important thing.
(32:13):
There are also other options,like bariatric surgery is still
reasonable and on the table, anda fascinating thing is that
after bariatric surgery thereare significant changes to gut
hormone signaling and anatomythat change the way people burn
calories and the way that theyprocess food, and it changes all
(32:34):
of that hormone profile that wetalked about before, and we're
talking about people withdurable weight loss of 25 to 30%
after a year after a bariatricsurgery.
That's a whole differentconversation that we've never
introduced before, so I'm awareof that.
So I hope this was helpful.
It's a little bit of a windingroad to discuss metabolic
(32:55):
adaptation.
It's a little bit of a vague,tough concept to explain.
I hope I did it justice today.
What do you think?
Speaker 2 (33:03):
I think it was great.
Speaker 1 (33:04):
Thank you.
One core message that I reallywant to get is that if you've
struggled, this is biology.
It's not your behavior.
It's not a failure of willpower.
This is something that happensto you.
So relax a little bit and takethat burden off your shoulders.
If you're listening to this,doing whatever, it's not your
(33:26):
fault.
We all can do better and it'sokay.
Just take the step forward andget that exercise in and make
some better food choices.
That's all we ask.
All right, so thank you forcoming back to another episode
of your Checkup.
Hopefully you were able tolearn something for yourself, a
loved one or a neighbor.
(33:47):
Check out our website.
You can find us on threads.
We're very active there.
You can send us an emailyourcheckuppod at gmailcom.
You can also send us some fanmail if you wish.
We are very interested ineverything you have to say.
When you reach out to us, it'slike rocket fuel.
We love that sort ofinteraction.
Speaker 2 (34:10):
Yeah, we got a really nice message from someone the
other day.
Speaker 1 (34:12):
We did.
It was really really nice andwe really appreciated that.
Speaker 2 (34:17):
Someone who we didn't know.
Speaker 1 (34:19):
Right.
We had never met this personbefore.
It was so encouraging.
Speaker 2 (34:23):
Usually it's like my mom, it is usually.
Speaker 1 (34:25):
So that was awesome and we look forward to having
you back for our next episode.
But, most importantly, untilnext time, stay healthy, my
friends.
I'm Ed Dolesky.
I'm Nicola Rufo.
Thank you, goodbye, bye.
This information may provide abrief overview of diagnosis,
treatment and medications.
It's not exhaustive and is atool to help you understand
(34:48):
potential options about yourhealth.
It doesn't cover all detailsabout conditions, treatments or
medications for a specificperson.
This is not medical advice oran attempt to substitute medical
advice.
You should contact a healthcareprovider for personalized
guidance based on your uniquecircumstances.
We explicitly disclaim anyliability relating to the
information given or its use.
This content doesn't endorseany treatments or medications
(35:10):
for a specific patient.
Always talk to your healthcareprovider for complete
information tailored to you.
In short, I'm not your doctor,I am not your nurse, and make
sure you go get your own checkupwith your own personal doctor.
Hi, welcome to your checkup.
We are the Patient EducationPodcast, where we bring
conversations from the doctor'soffice to your ears.
On this podcast, we try tobring medicine closer to its
patients.
I'm Ed Dolesky, a familymedicine doctor in the
Philadelphia area, and I'mNicole.
Speaker 2 (00:24):
Rufo, I'm a nurse and we are family medicine doctor
in the Philadelphia area, andI'm Nicola.
Speaker 1 (00:25):
Rufo, I'm a nurse and we are so excited you were able
to join us here again today.
So I was thinking well, lastweek we didn't talk about Trent
and our experience at State andLiberty.
Speaker 2 (00:37):
We need to talk about Trent.
Speaker 1 (00:38):
We got to talk about Trent.
Tell us about Trent.
Speaker 2 (00:41):
Trentrent.
Well, we went to go get eddie'ssuit for our wedding at state
and liberty in rittenhouse.
Highly recommend it was so muchfun, even for me and like I
wasn't even getting anythingyeah but trent was.
How would you describe trent?
Speaker 1 (01:00):
how would I describe Trent?
Speaker 2 (01:01):
Yeah.
Speaker 1 (01:02):
He was an excited, stylish man who loved what he
did and took great pride inhelping people look their best.
He was a calming presence, butalso reassuring and discerning,
because he also knew whensomething didn't look good and
he wasn't afraid to tell you hewas doing his job.
(01:23):
He immediately told you whensomething was good and I
appreciated that.
Um, it was like you said, itwas really fun.
We were the first appointmentof the day to take about an hour
.
Um, he asked us this disarmingfirst question so what fabrics
are you thinking of?
And tweedweedledee andTweedledum over here didn't know
(01:46):
anything about fabrics andwe're just like uh, and he's
like uh, I want a black suit.
Make it black please.
And like I had no idea what todo, and so he just, I think he
just took, like I knew I wanteda vest, that was like the thing
I knew I wanted.
But then, like these suits aregreat, right in the ballpark of
(02:10):
other places I've gotten to getsuits too, and it looks way
better than anything else.
Speaker 2 (02:14):
Oh my gosh, it looks so good.
I can't wait.
I'm excited To get it.
Speaker 1 (02:18):
And I'm excited to go back.
I'm a state and liberty guy.
Well, it's an athletic fitstore.
It is For men with thatV-shaped body.
You know this is an audio showbut you can't see me.
But I'm going to state andliberty.
Speaker 2 (02:37):
It's got the athletic build.
Speaker 1 (02:39):
Some might say it's a place to shop for people with
an athletic build.
I like the store.
It was fun, though.
Did you have an athletic build?
I liked the store, it was fun,though.
Did you have any other takeaway?
They were so nice.
They were just really kind tous yeah.
Speaker 2 (02:50):
They really took care of us.
Yeah, and we're probably goingto go back and get some work
clothes.
Well, the thing is the secretbutton under the collar of their
dress shirts, which is thething that is the bane of your
existence with collared shirtsfor work, because the collar is
up or doesn't lay right, blah,blah, blah, blah, blah.
(03:12):
But they have this hiddenbutton like under the collar, so
that it everything just laysright and looks nice yeah, look
at now we need to buy like 17shirts for them.
Speaker 1 (03:23):
Oh yeah, well, it bothers me because when the even
if it's not so much a problemwhen you're wearing a tie, like
it all gets bunched up andtucked in with the tie, but when
you're not, and then you getwhat someone called the jersey
flare, where I guess you looklike you're like a club owner
sloppy.
And it looks a little sloppyand like the.
The collar flares out a littlebit there, looks a little sloppy
(03:44):
and like the the the collarkind of flares out a little bit.
There's like too much chestshowing that like second button
is like too far down, but thefirst button is like choking you
and it's like what do you do?
And then the collar is flaredout.
It's just a mess.
So the hidden button yeah, hugehidden button guy, didn't even
know it.
Now I am you didn't even knowyou were looking for it no, and
(04:09):
now I'm like I'm locked in and II can't wait do you think trent
will listen to our podcast?
I think if we told trent thatthere was a a rave review of his
services that he's the best andwe wish we could hang out with
him.
Speaker 2 (04:23):
I can't wait until your suit comes in so we can go
get it and see him again.
Speaker 1 (04:30):
That's.
I mentioned that.
They were like emailing us tooLike they were like letting us
know and giving us updates, and.
I was like this is so nice, itwas great.
Even that person who was on thephone call with us, who was
like in the beginning, was nice,a little shocked that I was
like only getting a suit formyself for a wedding and I was
like I don't think that's such abig deal, but that's neither
here nor there.
Any last thoughts about trent Idon't think so.
(04:52):
Yeah, so what we also watched,or kind of snooze through um
most recently, is this stormarea 51.
It seems like it's been out fora little while on netflix.
It's part of this train wreckseries, same thing as the poop
cruise.
This like film team.
I guess it's like productioncompany finds like unique
stories and then like interviewspeople and gotta say, the guy
(05:16):
who put this together, who gotall of this like notoriety, only
made 1700 from like sellingshirts and not very
entrepreneurial.
Speaker 2 (05:28):
No, not at all Missed opportunity Totally.
I mean, he also was only like20.
Speaker 1 (05:33):
Was he?
Yeah, hmm, cause a lot ofhoopla.
Did you know this live when itwas happening?
Speaker 2 (05:39):
Um, like very minimally Okay.
Speaker 1 (05:43):
Yeah, and then through this I learned well, I
still have to look it up alittle bit more about what fire
fest was?
Um, like very minimally, Okay,yeah, and then through this I
learned well, I still have tolook it up a little bit more
about what fire fest was.
Speaker 2 (05:50):
Oh yeah, there are a couple of documentaries about
that.
We can watch them.
Speaker 1 (05:53):
Yeah, I I'm into a documentary recently.
I'm liking learning about realthings that happened in the
world and having it spoon fed tome on the TV.
I'm liking that.
All right, we can watch somemore.
Yeah, we'll see.
Tell us about the rest of ourviewing experience.
Speaker 2 (06:10):
Oh, I think there was a new also, not to cut you off.
Speaker 1 (06:13):
That's okay.
Speaker 2 (06:13):
And then we can talk about that, because it'll be a
good segue.
Yeah, I think there's a newHurricane Katrina one.
Speaker 1 (06:21):
Oh, that did just pop up.
Yeah oh, that did just pop up.
Yeah, yeah, saw that.
Can add that to the list.
We can add that to the list.
Maybe we could talk about thatnext week.
A very real thing for a lot ofpeople.
Speaker 2 (06:30):
Sorry if you were affected by hurricane katrina um
, okay, and then we watched thebiggest loser documentary oh yes
it was three episodes.
I don't know what I wasexpecting Me neither.
I feel like I don't knowBecause like they had a couple
(06:54):
contestants, like previouscontestants that were on, I
guess they were supposed tooffer like background
information and like behind thescenes stuff, but I don't really
feel like we got a lot of that.
Speaker 1 (07:05):
No, it was interesting to see like the
producers come out and talkabout their views, like they
were making television first andforemost, and I think, like
that's a yes, it was a veryinspiring show.
Yes, it was flawed, but like Ithink they own that, like they
were, like we were out to make aTV show.
Speaker 2 (07:24):
Yeah, I think the public outrage that the biggest
loser wasn't quote unquoteethical or healthy or safe.
Yeah, you don't make a realityTV show about losing weight and
it's not crazy losing weight andit's not like crazy.
Speaker 1 (07:48):
Well, I guess you know we were a big bob harper
stands and there was a flavor ofthe show that like yeah, I mean
cast him in a unfavorable light.
Um, I found the dr hyzengastuff really interesting, like
how he like really advocated forthe contestants like through
and through, and that was metwith, uh, countenance from the
trainers and the producers whowere really trying to steamroll
(08:09):
him, and it does like get into alittle bit of the power dynamic
between the two.
And I mean, growing up I alwaysthought, like the even before I
realized that I wanted to be adoctor, like I thought the dr
haizanga stuff on the show wasso fun and I was like, whoa, are
you kidding, that's so cool.
So I thought it was cool tohave him on the show, like the
documentary inspiration to beget certified in obesity
(08:31):
medicine not really um, but itwas cool to see.
I didn't realize that he waslike the team doctor for the
raiders oh, I, know me neitherno, I like charlie sheen
randomly.
Speaker 2 (08:42):
Yeah, I mean, I guess you don't get the role of a
doctor on any sort of realitytelevision show by like just
being like a random doctor.
Speaker 1 (08:53):
Yeah, that's a good point.
You know that's a good point.
Yeah, Julia Michaels was not inthe documentary.
Speaker 2 (08:58):
Yeah, a lot of people don't like her.
Speaker 1 (09:02):
I think she has some weird views on the world that
I've been seeing on threads.
Speaker 2 (09:07):
Yeah, I mean she's also like come out and basically
said the show would like themlike yelling during workouts and
like being all like extreme andstuff was like all an act that
the producers told them to doand stuff.
Speaker 1 (09:23):
Yeah.
Speaker 2 (09:24):
But she, yeah, yeah, that's all I'll say about that,
yeah but bob harper was ontraders.
Speaker 1 (09:31):
So like we love bob circulating in the the zeitgeist
in the last year or two, likeevery year, like bob harper's
got something else going on andgood for him.
I think I was left a littlecrestfallen.
Speaker 2 (09:45):
I was left wanting more.
I was I don't know what thatmore is, but it didn't give me
what I thought it was going to.
Speaker 1 (09:53):
No, I was.
I'm glad we watched it Me too.
Yeah, I'm glad we watched it.
I was hoping for more Fredo.
Speaker 2 (09:59):
Our King Fredo.
Speaker 1 (10:00):
Yeah, I was hoping for more of him.
I forget what season that'sfrom, but he was a dastardly
fellow that I wish there wasmore of on the TV, isn't he like
from New Jersey or New Yorkmaybe?
The area and you can just tellthis guy had a whole following
of like dudes on the show.
It was funny.
(10:23):
I wish they had more of him andI said like 400 contestants.
They're probably like couldhave pulled a few more people to
talk.
The one thing that was crazywas like that first they had
this um, spoiler alert, ifyou're gonna watch, okay, now
we're gonna go.
Um, the lady who was likerunning a running a mile
(10:44):
legitimately almost passed away.
She had rhabdomyolysis fromrunning the mile.
That's crazy.
Speaker 2 (10:50):
Is it rhabdomyolysis?
Speaker 1 (10:53):
You can just stop at rhabdo.
Speaker 2 (10:55):
Is that how you say it?
Speaker 1 (10:55):
Yeah, oh really, how do you think it should be said?
Speaker 2 (10:59):
Not like that.
Speaker 1 (11:01):
Rhabdomyolysis.
Speaker 2 (11:03):
Maybe Wait say it again Rhabdomyolysis.
I've never heard anyone say itlike that.
Speaker 1 (11:11):
Not just truncated to rhabdo.
Yeah, no, she nearly passedaway.
Speaker 2 (11:19):
Okay, but the interesting part, which is a
great segue into today's episode, is that they talked about I
guess, like the very small,limited study that they did,
which was still interesting ofessentially the people that lost
a bunch of weight and thengained it back.
Speaker 1 (11:39):
Yes.
Speaker 2 (11:40):
And so what was that about?
Speaker 1 (11:41):
Yeah, so that, um, I've been meaning to talk about
this for a while.
So, like, as you mentioned, I'mlike studying for the obesity
boards, so I was like lookinginto this stuff and have been
talking and thinking about thesesubjects more again.
And it's a subject, it's a, itis a physiological phenomenon
called metabolic adaptation oradaptive thermogenesis.
(12:06):
Before we really get into toomuch of it, I want to let you
know that the information fromthis episode comes from
published research in obesitymedicine, including guidelines
from the Obesity Society andAmerican Diabetes Association,
as well as recent scientificreviews in journals like JAMA,
the American Journal of ClinicalNutrition and Obesity.
And, while we keep thingsconversational, all the details
(12:30):
are drawn from peer-reviewedstudies and expert guidelines.
So the simple idea behindmetabolic adaptation is it gets
at the concept of why weightloss is so hard and why it is so
hard to keep off.
Specifically, it's not the onlything, but it comes up in a
(12:54):
situation like this have youreally ever worked so hard to
lose 10 or 20 pounds only tofeel like your body was fighting
you the whole way?
And then, when you do that,that it's pulling you back to
the weight that it was before,whether it's by appetite or just
making you feel like blah andyou can't do more.
It turns out that this isn'tabout a lack of discipline.
What it is, at least in part,is that your body has built in
(13:18):
defenses against weight lossbecause it is seen as a survival
disadvantage Okay and it'sknown as metabolic adaptation.
So the simple definition isthat your body burns fewer
calories than expected afterweight loss, and I'll give a
couple different examples hereto try to illustrate this point.
(13:40):
So let's say that someoneweighed 250 pounds.
Then let's suppose that theylose 25 pounds.
Now they weigh 225 pounds, butif you compare their baseline
metabolism to someone else whoweighs 225 pounds but didn't
(14:00):
just lose 25 pounds, theirmetabolism the person who lost
the weight is proposed to belower.
This has been researched, thishas been studied in different
facets.
It's been looked at inindividual small cohorts.
(14:21):
It was looked at in people inthe biggest loser study and we
can talk a little bit more aboutwhy that was so unique.
But it's the idea that there isan energy gap.
Another way to think about thisis that there is a study done by
this physician called Dr KevinHall, and another way to
(14:43):
illustrate it is that it wassuggested that every kilogram
lost slows the metabolism yourresting metabolism, by 25
calories and that it makes you95 calories hungrier every
kilogram you lose.
People often get to a pointwhen they're losing weight and
they say like, oh, I've beenlosing my weight, I've been
(15:05):
losing weight.
And then they get to a plateauand you suggest that maybe
someone has been in a caloriedeficit.
They've been eating lesscalories than they bring in.
Energy out is greater thanenergy in helping them to lose
weight.
But this theory suggests thatthe body slows the metabolism
(15:26):
where that calorie deficit maynot be a calorie deficit anymore
at all.
Did you know about this?
Speaker 2 (15:34):
Well, no, not until you told me about it.
Well, we mentioned it in ourone obesity episode, I think too
.
Or like weight loss orsomething Like the general idea
that you lose weight and thenyour body tries to gain it back,
essentially, it turns on you,yes, which is really frustrating
, but I also understand it loseweight and then your body tries
to like, gain it back,essentially, and it turns on you
, yes which is reallyfrustrating, but I also
understand it and there's acertain degree of now that we
(15:58):
kind of understand what this is,um, and illustrate this a
couple different ways.
Speaker 1 (16:03):
Uh, it's one thing to explain why it happens and
there are this is complex thingLike your body doesn't like
change.
It's called homeostasis andyour body likes things to stay
the same and there are soundsdramatic.
Yeah, there are like leversthat the body pulls and there
(16:26):
are hormones and like I'm goingto give them names.
I think a lot of people likethere are a lot of things online
when people just quote unquotehormones, but there are hormones
that have names and functions.
What are you grumbling aboutover?
Speaker 2 (16:39):
there.
That drives me crazy.
Speaker 1 (16:41):
It drives me crazy too.
But what I want to get at isthat there are specific hormones
that cause some of these thingsto happen.
So there are two that I want toname and define.
They're called leptin andghrelin.
Ghrelin is the easier one todefine.
It is a hunger hormone, and sowhen you lose weight or you're
(17:04):
ready to eat, ghrelin goes up,and that's kind of the simplest
way to do it and to think aboutit is that ghrelin is a hunger
hormone and when you're hungryit goes up.
Leptin is the other one.
Leptin is a hormone that helpsyou think that you are satiated.
So when it is up, it is makingyour body think that you are
(17:28):
energy neutral or energypositive, like you've had enough
to eat.
Your leptin is high and you'renot going to feel like you need
to go out and get food anymore.
And one place that leptin comesfrom is adipose tissue, which
is also fat tissue, so adiposetissue is hormonally active.
(17:49):
There are a lot of differenthormones being sent out by
adipose tissue and only one ofthem is leptin, and this is also
kind of the base of whereestrogen, testosterone, gets
converted essentially intoestrogen in fat tissue, which
kind of supposes sort of thereason of why different cancers,
(18:10):
like endometrial cancer, hasincreased risk for people who
live with obesity because ofthis underlying feature.
But let's say that when someoneloses weight, leptin decreases
and so when leptin is decreased,your body thinks it's in a
starvation mode and that drivesforward appetite, which makes
(18:34):
you hungrier and makes you wantto eat more.
So in that little section therewe defined two different
hormones, leptin and ghrelin,but there are so many more of
them.
There are also implications ofthyroid hormones sex hormones
involved in this.
There are also implications ofthyroid hormones sex hormones
involved in this, and these mayimplicate a slower metabolism
(19:00):
and dictate fat storagethroughout the body, whether fat
is stored internally asvisceral fat around the internal
organs, which is the moredangerous type, or elsewhere in
the body.
There are other features thathappen, other things that change
to help this the shrinking fatcells themselves.
When someone loses weight, thefat cells shrink and what
(19:20):
eventually happens and this is areally interesting point when I
was listening to these lecturesis that the mitochondria become
more efficient at burningcalories or essentially creating
energy and using it.
They become more efficient,which is actually maybe better
for you in the course of alifetime.
There was a whole lecture thatI watched about aging and aging
(19:45):
and the calorie deficit andcalorie restriction and because
they looked at people in Okinawaand they were like why do these
people live longer than peoplewho live on mainland Japan, like
right over there?
And one theory was that theyjust had so many, they had a
huge calorie restrictioncompared to the people who live
on Japan.
So then there was this wholelike aging lecture that I
(20:08):
watched that supposed that ifthe mitochondria became more
efficient or your body'scellular processes themselves
became more efficient and usedless calories throughout the day
to accomplish the same tasks,there would be less iterations
of the cells needed in the bodyas a whole and less aging.
(20:31):
Because, like, none of this islike a limitless thing.
Like you can, your cells canonly divide so many times before
it's like curtains, so CurtainsBefore it's curtains.
So the idea is that if they canmore efficiently do this, then
they would be able to go and doit longer.
(20:54):
So it's possible that metabolicadaptation might not be a bad
thing in the grand scheme ofthings.
It might just be something thatis frustrating for people who
are trying to lose weightbecause the body's being more
efficient at doing what it doesin living.
There's also suggestion thatthere's inflammation that drops
and that, like adipose tissue,is inflammatory in itself.
(21:16):
There's.
I mean, we looked at a lot ofliterature and research before
this to collate this episode andthe big take home point is that
there are some immune cellsthat are still involved.
There is some baselineinflammation that might still be
there that may make someonemore susceptible to weight
regain as well.
So that was like the meatiest,nerdiest part of the episode
(21:40):
that I could possibly give you.
Is there any like thought orfurther explanation you think I
could give?
Speaker 2 (21:47):
No, I think that was great.
Speaker 1 (21:48):
But yeah, and before we get too far away from those
hormones yeah, there's leptin,there's ghrelin.
Everyone knows what GLP-1 is.
Now, because of the medications, that's another one of these
hormones.
They're called incretins Notall of them, but like a GLP-1 or
a hormone, pyy orcholecystokinin.
(22:09):
These are hormones that arereleased after someone eats and
communicates to the brain to sayI'm full, you don't need to eat
anymore, please stop eating,because if you do, I'll be too
full and I'll feel uncomfy, andthat's how that happens.
So when someone's injecting aGLP-1, they're essentially
telling their brain GLP-1,they're essentially telling
(22:33):
their brain hey, relax, stopdoing this.
Like back in the day they triedto look at leptin.
And can you inject leptin intosomeone and increase those
levels and make people lesshungry?
It didn't bear out.
I think it wasn't safe.
Something happened, but theydid look at this.
Speaker 2 (22:48):
Darn Right Could use a good leptin shot.
But they're looking like youknow, go to a med spa, get a B12
shot and a leptin shot, get aleptin shot.
Speaker 1 (22:58):
But there's, I mean, I think, now in the pipeline.
They're probably looking atlike PYY, or they're looking at
I mean you have GLP, gip they'relooking at.
They may look at leptin again,who knows, but it's a
complicated process that they'relooking at to try to make safe
and effective options formedications for the management
of obesity.
So just know there are a lot ofthese hormones.
(23:21):
They do have names, they havefunctions.
Let me try to keep it as simpleas possible here without
overwhelming you.
Speaker 2 (23:27):
So how long does this metabolic adaptation last?
If someone loses weight, arethey fighting this forever?
Speaker 1 (23:36):
Maybe Probably not, though it's an area of active
investigation but what we couldglean was it's most active
during weight loss and withinthe first few months of weight
maintenance.
But there is a decent amount ofsuggestion in the literature
(23:57):
that the metabolic adaptationmay fade around 6 to 12 months
if the weight stays steady.
In episode 20, we talked aboutthe obesity set point theory and
there's some suggestion in thatschool of thought that if you
stick around at the weight forlong enough in a new environment
it might stick, and so thismetabolic adaptation piece may
(24:21):
attenuate or get smaller.
The thing we saw yesterday inthe show and they even brought
this up and I'm curious to hearyour thoughts on the show here
was in the Biggest Losercompetition and it and I'm
curious to hear your thoughts onthe show here was in the
Biggest Loser competition and itwas a very small study.
I think there were some 30people, 30 contestants from the
show, and they had somesuggestion that between the
start time and six years laterthat the metabolic adaptation
(24:45):
which is a reminder is like yourbasal metabolic rate if you're
sitting doing nothing and theamount of calories you burn
decreases lower than it shouldwith weight loss.
That that persisted over thecourse of six years, which was
unexpected, and that kind ofstill bears out in the
literature with a big questionmark.
(25:05):
And they even talked about thison the documentary.
They were like did we like hurtthese people, did we ruin their
metabolisms by doing this?
And I still think the answer isI don't know.
And I don't think they knoweither, because I think it has
to do with how you measure thisstuff too and it's reliable.
But I think the theory behindit is that they were I mean,
(25:29):
they said it on the show theywere burning like 6,000 calories
a day.
Speaker 2 (25:34):
Yeah, that was insane .
Speaker 1 (25:35):
And maybe eating 800.
And so what the body was maybedoing was lowering the resting
metabolic rate to accommodatethe total energy expenditure,
which is resting metabolic rateplus active energy expenditure.
These people were doing 6,000calories of active energy
(25:56):
expenditure.
The body's like please relaxfor a second, bro, and so it
just kind of turns a coupleknobs down, which as a
compensatory mechanism makessense to me.
But then that it they suggestthat it lasts for six years is a
(26:17):
little confusing and I wassurprised.
Speaker 2 (26:22):
Yeah, I mean also not everyone loses weight as
extremely as they did on thebiggest loser, but six years
still feels like a long time.
I think it is an extreme bodyto still be like ah yeah.
Speaker 1 (26:37):
I think it was an extreme use case the medical
term.
Ah yeah, and I don't think Imean I don't think many people
listening to this show will havea very similar experience to
them and perhaps it's not themost relatable case to think of,
but maybe it illustrates thepoint to some degree that in
extreme cases this is whatmetabolic adaptation is, whether
(27:00):
this actually bears itself outor not.
It does seem that they lookedat in the study that it didn't
necessarily correlate with theamount of weight someone lost
but with the amount of exercisethat they did, and that the
people who exercised more mayhave had a more significant
change to their baselinemetabolism, to that theory, like
(27:21):
that supposition I made beforeabout trying to compensate for
the energy deficit.
All right, well, that was a funlittle detour back to the
biggest loser.
Speaker 2 (27:32):
So if someone is listening and struggling with,
or thinks they are, what canhelp to counteract the metabolic
adaptation?
Speaker 1 (27:59):
bring it up in conversation when someone's like
struggling to lose weightupfront anyway and maybe they
really have a great grasp of howmany calories are going in and
going out, or if they hit aweight loss plateau.
I think it invites aconversation about recalculating
a calorie deficit based off of,like where you were to where
you aren't I don't know thislike if this 25 calories per
(28:21):
kilogram is something that likeworks for everyone all the time,
but at least helps toillustrate that, like, if you
lose two pounds, your metabolismslows down a little bit.
If you lose 10 pounds, it slowsdown a little bit more and
maybe you have to rethink.
If you need to keep losingweight, you need to rethink
where your calorie deficit is.
I also think it invites aconversation that you're not
(28:45):
crazy and if you're doingeverything that you can to lose
weight, that, like this is justit's your body, it's not you,
it's not your fault.
This is a really decent theoryand science that this happens to
people and it is not anindictment on your character or
(29:10):
who you are like.
This is very clearly somethingthat happens to people, not
something that people do, whichI think is like huge.
I think weight loss itself likea five to 10% total body.
Weight loss can improve thingslike way more than just
(29:31):
aesthetics when it comes toweight.
Like that kind of weight lossimproves diabetes.
It improves cholesterol figures.
Blood pressure Greater than 10or 15% can put diabetes into
remission, and so, like when wetalk about this, that's where
we're coming from, like theseunderlying things, these
metabolic abnormalities andcardiovascular abnormalities
(29:54):
that can be fixed with somelifestyle changes that are so
important.
And what else can you do aboutit?
We talk a lot about 150 minutesof exercise per week, of a
moderate intensitycardiovascular exercise.
We talk about that in episode10 in the power of exercise.
The suggestion of some of theliterature I was reading is that
(30:17):
bumping that up can helpmaintain muscle and burn the
calories in excess, and somoving that to 200 to 300
minutes per week of whereas dietand calorie deficits in weight
loss are paramount, and so thescale for lack of a better word
(30:48):
flips when it comes to weightmaintenance.
So increasing that number maybe something to think about,
maybe something to think about,and then staying attuned to
basic foundational nutritionalcomponents like high protein,
high fiber diets, low glycemicloads, to help kind of
neutralize or at least curb yourappetite so you're not feeling
(31:10):
like oh, I ate this bag of likesour cream and onion chips all
at once and I still feel hungry,but now I'm like a thousand
calories down from where Ishould be.
Speaker 2 (31:21):
This sounds very specific and personal and
familiar.
Speaker 1 (31:26):
It is very specific, personal and familiar.
Hi, I'm Ed and.
I love sour cream and onionchips more than I should.
What's more is that thebreakthrough in the science has
been so important, especiallywhen it comes to pharmaceuticals
.
I mentioned them earlier in theshow, but medications like
GLP-1s, which go by the names ofOzempic Wagovi, and the
(31:49):
terzepatide component ones,zepbound and Moonjaro, help.
They help with the appetite.
So much of obesity is appetitedysregulation, and that's where
these medicines step in, and sothey themselves may blunt the
hormonal signals that help driveweight regain.
So that's an important thing.
(32:13):
There are also other options,like bariatric surgery is still
reasonable and on the table, anda fascinating thing is that
after bariatric surgery thereare significant changes to gut
hormone signaling and anatomythat change the way people burn
calories and the way that theyprocess food, and it changes all
(32:34):
of that hormone profile that wetalked about before, and we're
talking about people withdurable weight loss of 25 to 30%
after a year after a bariatricsurgery.
That's a whole differentconversation that we've never
introduced before, so I'm awareof that.
So I hope this was helpful.
It's a little bit of a windingroad to discuss metabolic
(32:55):
adaptation.
It's a little bit of a vague,tough concept to explain.
I hope I did it justice today.
What do you think?
Speaker 2 (33:03):
I think it was great.
Speaker 1 (33:04):
Thank you.
One core message that I reallywant to get is that if you've
struggled, this is biology.
It's not your behavior.
It's not a failure of willpower.
This is something that happensto you.
So relax a little bit and takethat burden off your shoulders.
If you're listening to this,doing whatever, it's not your
(33:26):
fault.
We all can do better and it'sokay.
Just take the step forward andget that exercise in and make
some better food choices.
That's all we ask.
All right, so thank you forcoming back to another episode
of your Checkup.
Hopefully you were able tolearn something for yourself, a
loved one or a neighbor.
(33:47):
Check out our website.
You can find us on threads.
We're very active there.
You can send us an emailyourcheckuppod at gmailcom.
You can also send us some fanmail if you wish.
We are very interested ineverything you have to say.
When you reach out to us, it'slike rocket fuel.
We love that sort ofinteraction.
Speaker 2 (34:10):
Yeah, we got a really nice message from someone the
other day.
Speaker 1 (34:12):
We did.
It was really really nice andwe really appreciated that.
Speaker 2 (34:17):
Someone who we didn't know.
Speaker 1 (34:19):
Right.
We had never met this personbefore.
It was so encouraging.
Speaker 2 (34:23):
Usually it's like my mom, it is usually.
Speaker 1 (34:25):
So that was awesome and we look forward to having
you back for our next episode.
But, most importantly, untilnext time, stay healthy, my
friends.
I'm Ed Dolesky.
I'm Nicola Rufo.
Thank you, goodbye, bye.
This information may provide abrief overview of diagnosis,
treatment and medications.
It's not exhaustive and is atool to help you understand
(34:48):
potential options about yourhealth.
It doesn't cover all detailsabout conditions, treatments or
medications for a specificperson.
This is not medical advice oran attempt to substitute medical
advice.
You should contact a healthcareprovider for personalized
guidance based on your uniquecircumstances.
We explicitly disclaim anyliability relating to the
information given or its use.
This content doesn't endorseany treatments or medications
(35:10):
for a specific patient.
Always talk to your healthcareprovider for complete
information tailored to you.
In short, I'm not your doctor,I am not your nurse, and make
sure you go get your own checkupwith your own personal doctor.
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