Physical Hunger vs. Cravings on Retatrutide: A Personal Take

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BioDad

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I've been using retatrutide for 4 months now. My starting dose was 1mg/week, and I've worked my way up to 10mg/week over the last month. During the first couple of months, I dropped a good amount of weight, but I've also been hitting the weights hard to try to regain some muscle I had 20 years ago, so there's been some recomposition happening—though I can't say exactly how much I've gained or lost. That part isn't really the point.

What I have noticed, particularly over the past few weeks even at a higher dose, is a pretty strong hunger. Like, genuinely hungry. Ready to eat at every meal. I've seen people say a GLP-1 agonist "stopped working," which I interpret as either 1) weight loss has stalled (plateau), or 2) hunger is back. I haven't been tracking my weight since the scale isn't my focus, so I decided to address the second one.

Here's what clicked for me. There's homeostatic hunger (stomach emptying, normal hunger signals) and hedonic hunger (food cravings, regardless of whether you're hungry). I think for me, it's the first type, not the second.

As far as I understand, GLP-1 agonists don't truly "stop working"—there's no receptor downregulation or desensitization, or autoantibody formation significant enough to effectively reduce your dose or increase your medication needs. What does seem to occur is tachyphylaxis of gastric emptying delay, meaning the body adapts and re-regulates vagal and enteric nerves to the new hormonal signaling 'norm,' allowing faster gastric emptying than before when the medication was started or doses were increased. A stomach that empties faster will signal hunger to some degree.

This nervous system adaptation reminds me of how you first notice a strong smell, but then quickly get used to it—it becomes the new 'normal' for your olfactory system, and you stop smelling it even though the odor is still there. This happens throughout much of the nervous system.

Other possible reasons could be less fat leading to lower leptin and more hunger, more muscle raising metabolic rate and causing hunger, or increased activity (exercise) driving hunger.

But here's the key difference: even though I'm really hungry lately, I have zero interest in candy bars at the checkout, finishing a pint of ice cream, or even Celsius drinks anymore—all of which used to be issues for me.

Retatrutide is currently more effective for weight loss than anything else available, and I think part of that comes from not keeping you in an unnaturally suppressed state forever. Real, physiologic hunger, especially when it's not tied to cravings or bingeing, might actually mean you're in a healthier place than when the drug made eating feel impossible.

Just my two cents after looking into this. I'd love to hear what others think.
 
Effects seem to vary a lot from person to person, but strong suppression of hunger or food noise isn't something retatrutide is really recognized for. When it comes to GLP-1 binding affinity, it's relatively weak.

For those using reta mainly to lose weight, some choose to stack a second medication that targets that side of things. My own preference would be to first give a strict, all-day approach built on heavy hydration and a protein-dense way of eating a fair shot before adding anything else.
 
BioDad said:

I've been using retatrutide for 4 months now. My starting dose was 1mg/week, and I've worked my way up to 10mg/week over the last month. During the first couple of months, I dropped a good amount of weight, but I've also been hitting the weights hard to try to regain some muscle I had 20 years ago, so there's been some recomposition happening—though I can't say exactly how much I've gained or lost. That part isn't really the point.

What I have noticed, particularly over the past few weeks even at a higher dose, is a pretty strong hunger. Like, genuinely hungry. Ready to eat at every meal. I've seen people say a GLP-1 agonist "stopped working," which I interpret as either 1) weight loss has stalled (plateau), or 2) hunger is back. I haven't been tracking my weight since the scale isn't my focus, so I decided to address the second one.

Here's what clicked for me. There's homeostatic hunger (stomach emptying, normal hunger signals) and hedonic hunger (food cravings, regardless of whether you're hungry). I think for me, it's the first type, not the second.

As far as I understand, GLP-1 agonists don't truly "stop working"—there's no receptor downregulation or desensitization, or autoantibody formation significant enough to effectively reduce your dose or increase your medication needs. What does seem to occur is tachyphylaxis of gastric emptying delay, meaning the body adapts and re-regulates vagal and enteric nerves to the new hormonal signaling 'norm,' allowing faster gastric emptying than before when the medication was started or doses were increased. A stomach that empties faster will signal hunger to some degree.

This nervous system adaptation reminds me of how you first notice a strong smell, but then quickly get used to it—it becomes the new 'normal' for your olfactory system, and you stop smelling it even though the odor is still there. This happens throughout much of the nervous system.

Other possible reasons could be less fat leading to lower leptin and more hunger, more muscle raising metabolic rate and causing hunger, or increased activity (exercise) driving hunger.

But here's the key difference: even though I'm really hungry lately, I have zero interest in candy bars at the checkout, finishing a pint of ice cream, or even Celsius drinks anymore—all of which used to be issues for me.

Retatrutide is currently more effective for weight loss than anything else available, and I think part of that comes from not keeping you in an unnaturally suppressed state forever. Real, physiologic hunger, especially when it's not tied to cravings or bingeing, might actually mean you're in a healthier place than when the drug made eating feel impossible.

Just my two cents after looking into this. I'd love to hear what others think.
Click to expand...

When someone stays on a GLP1 for an extended period, this tends to happen often. Appetite reduction fades away, yet body weight largely stays down.
 
Habibibi said:

BioDad said:

I've been using retatrutide for 4 months now. My starting dose was 1mg/week, and I've worked my way up to 10mg/week over the last month. During the first couple of months, I dropped a good amount of weight, but I've also been hitting the weights hard to try to regain some muscle I had 20 years ago, so there's been some recomposition happening—though I can't say exactly how much I've gained or lost. That part isn't really the point.

What I have noticed, particularly over the past few weeks even at a higher dose, is a pretty strong hunger. Like, genuinely hungry. Ready to eat at every meal. I've seen people say a GLP-1 agonist "stopped working," which I interpret as either 1) weight loss has stalled (plateau), or 2) hunger is back. I haven't been tracking my weight since the scale isn't my focus, so I decided to address the second one.

Here's what clicked for me. There's homeostatic hunger (stomach emptying, normal hunger signals) and hedonic hunger (food cravings, regardless of whether you're hungry). I think for me, it's the first type, not the second.

As far as I understand, GLP-1 agonists don't truly "stop working"—there's no receptor downregulation or desensitization, or autoantibody formation significant enough to effectively reduce your dose or increase your medication needs. What does seem to occur is tachyphylaxis of gastric emptying delay, meaning the body adapts and re-regulates vagal and enteric nerves to the new hormonal signaling 'norm,' allowing faster gastric emptying than before when the medication was started or doses were increased. A stomach that empties faster will signal hunger to some degree.

This nervous system adaptation reminds me of how you first notice a strong smell, but then quickly get used to it—it becomes the new 'normal' for your olfactory system, and you stop smelling it even though the odor is still there. This happens throughout much of the nervous system.

Other possible reasons could be less fat leading to lower leptin and more hunger, more muscle raising metabolic rate and causing hunger, or increased activity (exercise) driving hunger.

But here's the key difference: even though I'm really hungry lately, I have zero interest in candy bars at the checkout, finishing a pint of ice cream, or even Celsius drinks anymore—all of which used to be issues for me.

Retatrutide is currently more effective for weight loss than anything else available, and I think part of that comes from not keeping you in an unnaturally suppressed state forever. Real, physiologic hunger, especially when it's not tied to cravings or bingeing, might actually mean you're in a healthier place than when the drug made eating feel impossible.

Just my two cents after looking into this. I'd love to hear what others think.
Click to expand...

When someone stays on a GLP1 for an extended period, this tends to happen often. Appetite reduction fades away, yet body weight largely stays down.
Click to expand...
From what the trials showed, that's the conclusion I reached. If hunger could overpower the drug, the weight reduction probably wouldn't have been so substantial. Thanks!
 
indolent said:

Effects seem to vary a lot from person to person, but strong suppression of hunger or food noise isn't something retatrutide is really recognized for. When it comes to GLP-1 binding affinity, it's relatively weak.

For those using reta mainly to lose weight, some choose to stack a second medication that targets that side of things. My own preference would be to first give a strict, all-day approach built on heavy hydration and a protein-dense way of eating a fair shot before adding anything else.
Click to expand...
Appreciate it, indolent. This isn't a gripe on my end. Honestly, I'm fine with feeling regular hunger signals — what I don't want is the urge to eat past fullness or to reach for less nutritious choices. In my view, it works best as a properly used instrument that lets someone experience eating sensible portions of the right foods, with the goal being that eventually the drug plays a smaller role, or maybe gets dropped entirely. That said, just like you pointed out, these compounds and how each person reacts to them vary enormously from one individual to the next.

Thanks!
 
Plenty of people arriving at GLP1s treat weight loss as a problem of calories rather than one of hormones, and they overdo it. The moment you frame things as calories in - calories out, your attention goes entirely to the intake side, and you stop accounting for the fact that the expenditure side swings wildly depending on any number of factors. From there the thinking becomes 'if I simply ate less, I would drop more weight', which is not wrong technically but is rarely a productive strategy, and in this space in particular it sends people chasing appetite suppression they think they feel, whatever their actual results say.

When you are on a single or dual agonist, watching appetite can still tell you something useful about dosing, but the moment a glucagon agonist joins, that mindset needs to go. Even someone who 'does not care' about the number on the scale and is chasing general health should keep tracking weight loss as a hard measure of progress. A lot of people keep losing on retatrutide while eating more than they believe they should, and more than they would on any other GLP drug, because perception in that area lies.
 
BioDad said:

I've been using retatrutide for 4 months now. My starting dose was 1mg/week, and I've worked my way up to 10mg/week over the last month. During the first couple of months, I dropped a good amount of weight, but I've also been hitting the weights hard to try to regain some muscle I had 20 years ago, so there's been some recomposition happening—though I can't say exactly how much I've gained or lost. That part isn't really the point.

What I have noticed, particularly over the past few weeks even at a higher dose, is a pretty strong hunger. Like, genuinely hungry. Ready to eat at every meal. I've seen people say a GLP-1 agonist "stopped working," which I interpret as either 1) weight loss has stalled (plateau), or 2) hunger is back. I haven't been tracking my weight since the scale isn't my focus, so I decided to address the second one.

Here's what clicked for me. There's homeostatic hunger (stomach emptying, normal hunger signals) and hedonic hunger (food cravings, regardless of whether you're hungry). I think for me, it's the first type, not the second.

As far as I understand, GLP-1 agonists don't truly "stop working"—there's no receptor downregulation or desensitization, or autoantibody formation significant enough to effectively reduce your dose or increase your medication needs. What does seem to occur is tachyphylaxis of gastric emptying delay, meaning the body adapts and re-regulates vagal and enteric nerves to the new hormonal signaling 'norm,' allowing faster gastric emptying than before when the medication was started or doses were increased. A stomach that empties faster will signal hunger to some degree.

This nervous system adaptation reminds me of how you first notice a strong smell, but then quickly get used to it—it becomes the new 'normal' for your olfactory system, and you stop smelling it even though the odor is still there. This happens throughout much of the nervous system.

Other possible reasons could be less fat leading to lower leptin and more hunger, more muscle raising metabolic rate and causing hunger, or increased activity (exercise) driving hunger.

But here's the key difference: even though I'm really hungry lately, I have zero interest in candy bars at the checkout, finishing a pint of ice cream, or even Celsius drinks anymore—all of which used to be issues for me.

Retatrutide is currently more effective for weight loss than anything else available, and I think part of that comes from not keeping you in an unnaturally suppressed state forever. Real, physiologic hunger, especially when it's not tied to cravings or bingeing, might actually mean you're in a healthier place than when the drug made eating feel impossible.

Just my two cents after looking into this. I'd love to hear what others think.
Click to expand...

I get where you're coming from, so I'll share what happened in my case. My Tirz journey began around 5.5 months back, and roughly a month in I made the switch to Reta. During those first 3-3.5 months, weight loss was my sole focus. The appetite suppression was fantastic. Then, about 1.5 months ago, I added testosterone and started hitting the gym consistently. Almost immediately, I was hit with intense hunger, even while on 6 mg of Reta. Mentally I could push it aside without much trouble, so it wasn't a huge burden. In the past couple of weeks, though, that feeling has clearly faded.

I'm aware that hard training can drive hunger in a big way. What I'm most thankful for is how simple it was for me to resist the cravings. Over the first 4 months on Tirz/Reta, I dropped 60 lbs, and across the last 1.5-2 months I've been recomping very effectively. The scale hasn't really moved downward, but my arms have grown, my waist has shrunk, and my muscle definition is far better than it was only a couple of months back, all without adding a single pound on the scale.
 
There’s a different kind of hunger that I believe exists. It might not affect everyone, but for me—and likely for plenty of others dealing with binge eating disorder or food addiction, which is often seen alongside obesity—it’s a huge factor.

Some of this comes down to biology: when you drop weight, hunger climbs. Your body isn’t thrilled about running on fewer calories for an extended period, and it lets you know. I suspect this explains a lot of the complaints about GLP medications “not working” for appetite anymore. If your weight isn’t going up, the medication is still doing its job—you’ve just settled into a different, stable set point.

In my case, the reason I regained weight after past losses comes from this lower-weight state. After I eat even a tiny amount of highly rewarding, calorie-dense food—ice cream, milk chocolate, chips—an hour or several hours later, I get hit with an extreme, almost impossible-to-fight rebound hunger. Research on this is limited, but it does exist. The more weight I lose, the stronger this reaction gets, at least for me.

So far, the only thing that has worked—besides Tirzepatide plus a small amount of reta, which clearly lowers appetite and cravings—is avoiding those foods entirely. I treat them like addictive substances I’m vulnerable to. I haven’t deliberately tested whether GLP medications can block this rebound by triggering it, because that could be risky; in the past, that pattern is exactly what led to regaining weight. Luckily, small amounts of dark chocolate don’t seem to set it off, so I allow myself that one small treat. Other than that, it’s been 3 years of eating only low-calorie-density foods—basically very low fat, lean protein, fruit, and vegetables—with zero slips. Whether I can keep this up long term is still uncertain, but it’s been a bit over 2 years since I lost about 50% of my body weight. I think the GLP medications make the odds much better.
 
mraajr said:

BioDad said:

I've been using retatrutide for 4 months now. My starting dose was 1mg/week, and I've worked my way up to 10mg/week over the last month. During the first couple of months, I dropped a good amount of weight, but I've also been hitting the weights hard to try to regain some muscle I had 20 years ago, so there's been some recomposition happening—though I can't say exactly how much I've gained or lost. That part isn't really the point.

What I have noticed, particularly over the past few weeks even at a higher dose, is a pretty strong hunger. Like, genuinely hungry. Ready to eat at every meal. I've seen people say a GLP-1 agonist "stopped working," which I interpret as either 1) weight loss has stalled (plateau), or 2) hunger is back. I haven't been tracking my weight since the scale isn't my focus, so I decided to address the second one.

Here's what clicked for me. There's homeostatic hunger (stomach emptying, normal hunger signals) and hedonic hunger (food cravings, regardless of whether you're hungry). I think for me, it's the first type, not the second.

As far as I understand, GLP-1 agonists don't truly "stop working"—there's no receptor downregulation or desensitization, or autoantibody formation significant enough to effectively reduce your dose or increase your medication needs. What does seem to occur is tachyphylaxis of gastric emptying delay, meaning the body adapts and re-regulates vagal and enteric nerves to the new hormonal signaling 'norm,' allowing faster gastric emptying than before when the medication was started or doses were increased. A stomach that empties faster will signal hunger to some degree.

This nervous system adaptation reminds me of how you first notice a strong smell, but then quickly get used to it—it becomes the new 'normal' for your olfactory system, and you stop smelling it even though the odor is still there. This happens throughout much of the nervous system.

Other possible reasons could be less fat leading to lower leptin and more hunger, more muscle raising metabolic rate and causing hunger, or increased activity (exercise) driving hunger.

But here's the key difference: even though I'm really hungry lately, I have zero interest in candy bars at the checkout, finishing a pint of ice cream, or even Celsius drinks anymore—all of which used to be issues for me.

Retatrutide is currently more effective for weight loss than anything else available, and I think part of that comes from not keeping you in an unnaturally suppressed state forever. Real, physiologic hunger, especially when it's not tied to cravings or bingeing, might actually mean you're in a healthier place than when the drug made eating feel impossible.

Just my two cents after looking into this. I'd love to hear what others think.
Click to expand...

I get where you're coming from, so I'll share what happened in my case. My Tirz journey began around 5.5 months back, and roughly a month in I made the switch to Reta. During those first 3-3.5 months, weight loss was my sole focus. The appetite suppression was fantastic. Then, about 1.5 months ago, I added testosterone and started hitting the gym consistently. Almost immediately, I was hit with intense hunger, even while on 6 mg of Reta. Mentally I could push it aside without much trouble, so it wasn't a huge burden. In the past couple of weeks, though, that feeling has clearly faded.

I'm aware that hard training can drive hunger in a big way. What I'm most thankful for is how simple it was for me to resist the cravings. Over the first 4 months on Tirz/Reta, I dropped 60 lbs, and across the last 1.5-2 months I've been recomping very effectively. The scale hasn't really moved downward, but my arms have grown, my waist has shrunk, and my muscle definition is far better than it was only a couple of months back, all without adding a single pound on the scale.
Click to expand...
That's great to hear,

lessthanhalf said:

There’s a different kind of hunger that I believe exists. It might not affect everyone, but for me—and likely for plenty of others dealing with binge eating disorder or food addiction, which is often seen alongside obesity—it’s a huge factor.

Some of this comes down to biology: when you drop weight, hunger climbs. Your body isn’t thrilled about running on fewer calories for an extended period, and it lets you know. I suspect this explains a lot of the complaints about GLP medications “not working” for appetite anymore. If your weight isn’t going up, the medication is still doing its job—you’ve just settled into a different, stable set point.

In my case, the reason I regained weight after past losses comes from this lower-weight state. After I eat even a tiny amount of highly rewarding, calorie-dense food—ice cream, milk chocolate, chips—an hour or several hours later, I get hit with an extreme, almost impossible-to-fight rebound hunger. Research on this is limited, but it does exist. The more weight I lose, the stronger this reaction gets, at least for me.

So far, the only thing that has worked—besides Tirzepatide plus a small amount of reta, which clearly lowers appetite and cravings—is avoiding those foods entirely. I treat them like addictive substances I’m vulnerable to. I haven’t deliberately tested whether GLP medications can block this rebound by triggering it, because that could be risky; in the past, that pattern is exactly what led to regaining weight. Luckily, small amounts of dark chocolate don’t seem to set it off, so I allow myself that one small treat. Other than that, it’s been 3 years of eating only low-calorie-density foods—basically very low fat, lean protein, fruit, and vegetables—with zero slips. Whether I can keep this up long term is still uncertain, but it’s been a bit over 2 years since I lost about 50% of my body weight. I think the GLP medications make the odds much better.
Click to expand...
This is wonderful, and I truly value you opening up about this experience and viewpoint.
 
lessthanhalf said:

There’s a different kind of hunger that I believe exists. It might not affect everyone, but for me—and likely for plenty of others dealing with binge eating disorder or food addiction, which is often seen alongside obesity—it’s a huge factor.

Some of this comes down to biology: when you drop weight, hunger climbs. Your body isn’t thrilled about running on fewer calories for an extended period, and it lets you know. I suspect this explains a lot of the complaints about GLP medications “not working” for appetite anymore. If your weight isn’t going up, the medication is still doing its job—you’ve just settled into a different, stable set point.

In my case, the reason I regained weight after past losses comes from this lower-weight state. After I eat even a tiny amount of highly rewarding, calorie-dense food—ice cream, milk chocolate, chips—an hour or several hours later, I get hit with an extreme, almost impossible-to-fight rebound hunger. Research on this is limited, but it does exist. The more weight I lose, the stronger this reaction gets, at least for me.

So far, the only thing that has worked—besides Tirzepatide plus a small amount of reta, which clearly lowers appetite and cravings—is avoiding those foods entirely. I treat them like addictive substances I’m vulnerable to. I haven’t deliberately tested whether GLP medications can block this rebound by triggering it, because that could be risky; in the past, that pattern is exactly what led to regaining weight. Luckily, small amounts of dark chocolate don’t seem to set it off, so I allow myself that one small treat. Other than that, it’s been 3 years of eating only low-calorie-density foods—basically very low fat, lean protein, fruit, and vegetables—with zero slips. Whether I can keep this up long term is still uncertain, but it’s been a bit over 2 years since I lost about 50% of my body weight. I think the GLP medications make the odds much better.
Click to expand...
This strikes me as a fairly perceptive reply, because the addictive dimension that so frequently rides along with obesity tends to get overlooked. Saying to someone with obesity "just put the fork down" lands about the same way as telling an alcoholic to simply quit drinking — which, as I mentioned earlier, may be accurate yet is close to useless when actually applied. What gets ignored is that a great deal of today's food is deliberately built to maximize hedonic pleasure, and for plenty of people those addiction pathways are the real mechanism keeping the obesity in place.

Anyone who has done genuine keto before (not the same thing at all as picking up boxed "keto" desserts) will immediately recognize the phenomenon you're describing: after you manage to get through that transition without GLPs on board, food noise usually drops sharply, and stretching 12 hours between meals instead of 4 hours becomes pretty unremarkable, provided your surroundings make that the easier option. It's almost as though the body dials the volume of the usual addiction signaling far down, to a level you can reliably tune out. Unfortunately, work-from-home arrangements generally aren't set up in a way that helps you ignore it — but that's a side note.

I'm with you that dark chocolate (especially 85% or above) is a strong illustration of something you can consume in a smaller quantity without setting off that specific addiction pathway. The keto and paleo communities might be worth a look, since both tend to emphasize eating food that is less "engineered" and closer to what occurs in nature. That isn't to claim engineering is inherently harmful — only that most food processing exists to make starch or glucose absorb quickly (high-glycemic) after consumption, alongside other routes to maximizing pleasure. Often it's that particular pleasure we're unconsciously chasing, and it's the hamster wheel we end up stuck on. None of us has to become a monk, but seeing this cycle clearly is the first move toward getting off it.
 
lessthanhalf said:

There’s a different kind of hunger that I believe exists. It might not affect everyone, but for me—and likely for plenty of others dealing with binge eating disorder or food addiction, which is often seen alongside obesity—it’s a huge factor.

Some of this comes down to biology: when you drop weight, hunger climbs. Your body isn’t thrilled about running on fewer calories for an extended period, and it lets you know. I suspect this explains a lot of the complaints about GLP medications “not working” for appetite anymore. If your weight isn’t going up, the medication is still doing its job—you’ve just settled into a different, stable set point.

In my case, the reason I regained weight after past losses comes from this lower-weight state. After I eat even a tiny amount of highly rewarding, calorie-dense food—ice cream, milk chocolate, chips—an hour or several hours later, I get hit with an extreme, almost impossible-to-fight rebound hunger. Research on this is limited, but it does exist. The more weight I lose, the stronger this reaction gets, at least for me.

So far, the only thing that has worked—besides Tirzepatide plus a small amount of reta, which clearly lowers appetite and cravings—is avoiding those foods entirely. I treat them like addictive substances I’m vulnerable to. I haven’t deliberately tested whether GLP medications can block this rebound by triggering it, because that could be risky; in the past, that pattern is exactly what led to regaining weight. Luckily, small amounts of dark chocolate don’t seem to set it off, so I allow myself that one small treat. Other than that, it’s been 3 years of eating only low-calorie-density foods—basically very low fat, lean protein, fruit, and vegetables—with zero slips. Whether I can keep this up long term is still uncertain, but it’s been a bit over 2 years since I lost about 50% of my body weight. I think the GLP medications make the odds much better.
Click to expand...
What you put into words matches exactly what I had been thinking.

This is something I go through as well. When I first began reta, every craving I had went quiet. Roughly 10 weeks in now, and a number of those cravings have clearly returned. Considerable weight has come off, yet I catch myself fixating on high calorie ''binge'' foods.

Like you, the only way I can keep from overeating is to keep them entirely out of reach. My pantry is a pretty bleak sight these days, but I would rather have that than lose my peace of mind.
 
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