Do you think we’re going to see GLP-1-related eating disorders?

[futureapppsy2]

Not talking about the people who are obese and using GLP-1 agonists to get back to a normal weight but rather the folks who are normal or slightly overweight (BMIs of 27-ish or below) using them to drop into the underweight category. I was thinking about this because a YouTuber I follow on and off always looked somewhere between the high normal BMI range to the low-mid overweight range and is now looking like she’s in the low normal/underweight range after about 4-6 months of “weightlifting and eating healthy”, which no one really buys as being the full story. More broadly, there’s a solid market of people in the normal BMI range paying out of pocket for GLP-1 agonists, including a lot who admit having histories of restrictive disordered eating behaviors. It makes me wonder if we’ll start to see a rise in people using GLP-1s to fuel full-blown restrictive EDs. Thoughts? Clinical observations?

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[Sushirolls]

Bound to happen. But suspect will be miniscule numbers, in realm of case reports.

I think it will be a shift from the people who are chronically on phentermine. The ones who continue to lean into the med only strategy. I've got one right now who gets the phentermine from a 'weightloss' doc they've had for years. Goes on, goes off, goes on, goes off. Trying to point out the cycle and stopping...

 

[comp1]

Of course, people with restrictive eating disorders are going to restrict. On the plus side, the new drugs do seem relatively safer than things like high dose laxatives and stimulants. Might be a net positive even if GLP-1 agonists certainly do have risks?

 

[clozareal]

I've already been seeing it. I've had patients who have had significant insomnia, anxiety, fatigue (decreased exercise tolerance/endurance) on GLP-1 agonists. One of them had a BMI of <27 and was prescribed it by a lifestyle medicine physician.

This new cohort study just came out that I think should alarm all of us to the population risk for psychiatric adverse effects of using these medication.

The risk of depression, anxiety, and suicidal behavior in patients with obesity on glucagon like peptide-1 receptor agonist therapy - Scientific Reports

This large community-based cohort study investigates the impact of glucagon-like peptide-1 receptor agonists (GLP-1 RAs), specifically Liraglutide and Semaglutide, on the risk of developing psychiatric conditions such as depression, anxiety, and suicidal behaviors in patients with obesity...

www.nature.com

 

[clausewitz2]

I've already been seeing it. I've had patients who have had significant insomnia, anxiety, fatigue (decreased exercise tolerance/endurance) on GLP-1 agonists. One of them had a BMI of <27 and was prescribed it by a lifestyle medicine physician.

This new cohort study just came out that I think should alarm all of us to the population risk for psychiatric adverse effects of using these medication.

The risk of depression, anxiety, and suicidal behavior in patients with obesity on glucagon like peptide-1 receptor agonist therapy - Scientific Reports

This large community-based cohort study investigates the impact of glucagon-like peptide-1 receptor agonists (GLP-1 RAs), specifically Liraglutide and Semaglutide, on the risk of developing psychiatric conditions such as depression, anxiety, and suicidal behaviors in patients with obesity...

www.nature.com

Definitely a paper that shows some concerning data but frustratingly it is only incidence of psychiatric disorders in people not diagnosed with them rather than having anything to say about exacerbations in people already diagnosed with these disorders. As such, it is of limited direct utility for me as someone who generally treats people who already have psychiatric disorders. The sample sizes are so different in magnitude that plausibly also there is a pre-existing difference between the people who are willing/interested/able to pursue GLP-1 agonist treatment and those who are not. Also plausibly something about those patients that makes providers want to push harder for them to receive it. Especially given the time frame (before they became super common and well known), I do wonder if you are going to essentially have an enriched sample of people for whom things are not going well who are a bit more desperate to try potential solutions and are already in a fair amount of distress.

I really hope someone is collecting prospective data.

 

[Stagg737]

There was already a warning that came out about GLP-1 induced eating disorders. If I can find the posting/article I will, but remember seeing it and discussing it with our residents and med students during one of our journal clubs. The warning was specifically talking about induction of anorexic/restricting behaviors AFTER overweight patients had lost significant amounts of weight and I believe raised concerns that some patients may need to be discontinued d/t ED symptoms appearing.

 

[Nontrad_FL_LGBT]

Not talking about the people who are obese and using GLP-1 agonists to get back to a normal weight but rather the folks who are normal or slightly overweight (BMIs of 27-ish or below) using them to drop into the underweight category. I was thinking about this because a YouTuber I follow on and off always looked somewhere between the high normal BMI range to the low-mid overweight range and is now looking like she’s in the low normal/underweight range after about 4-6 months of “weightlifting and eating healthy”, which no one really buys as being the full story. More broadly, there’s a solid market of people in the normal BMI range paying out of pocket for GLP-1 agonists, including a lot who admit having histories of restrictive disordered eating behaviors. It makes me wonder if we’ll start to see a rise in people using GLP-1s to fuel full-blown restrictive EDs. Thoughts? Clinical observations?

I saw a case of this as a MA at an obesity med clinic two years ago. Doc denied them, hx AN with 26ish BMI.

 

[clausewitz2]

There was already a warning that came out about GLP-1 induced eating disorders. If I can find the posting/article I will, but remember seeing it and discussing it with our residents and med students during one of our journal clubs. The warning was specifically talking about induction of anorexic/restricting behaviors AFTER overweight patients had lost significant amounts of weight and I believe raised concerns that some patients may need to be discontinued d/t ED symptoms appearing.

It would be strange if this was not a problem, given we have ample evidence that bariatric surgery or indeed any rapid and substantial weight loss can induce restricting ED behavior in people who had not previously ever struggled with it. It seems like there is just a switch in some people's hypothalamus that gets stuck in the on position if they are in calorie deficit long enough.

 

[futureapppsy2]

It would be strange if this was not a problem, given we have ample evidence that bariatric surgery or indeed any rapid and substantial weight loss can induce restricting ED behavior in people who had not previously ever struggled with it. It seems like there is just a switch in some people's hypothalamus that gets stuck in the on position if they are in calorie deficit long enough.

There's some interesting data showing that both unintentional and intentional weight loss/restriction triggers AN in children and adolescents--for some people weight loss and/or calorie restriction just sets off that neurological trigger and they spiral into AN (and often end up binging with and without purging during recovery attempts).

 

[ridethecliche]

There's some interesting data showing that both unintentional and intentional weight loss/restriction triggers AN in children and adolescents--for some people weight loss and/or calorie restriction just sets off that neurological trigger and they spiral into AN (and often end up binging with and without purging) during recovery attempts.

This doesn't surprise me at all. In fact, one of the triggers we talked about when I was in eating disorder clinic during child training was getting busy and not prioritizing eating and how that triggered symptoms to return. So basically when you have an eating disorder and start dropping weight for whatever reason... you brain is vulnerable AF to falling right back into old patterns.

 

[Ceke2002]

There's some interesting data showing that both unintentional and intentional weight loss/restriction triggers AN in children and adolescents--for some people weight loss and/or calorie restriction just sets off that neurological trigger and they spiral into AN (and often end up binging with and without purging during recovery attempts).

ANGI (the genetics study I was involved in as a participant) did have some interesting findings related to metabolic stuff in AN.

From their public blog post: The results from ANGI | Angi

Perhaps the most revolutionary findings of this study are not in the gene discovery per se, but rather in the pattern of genetic correlations that we observed with other traits and disorders. Genetic correlations (meaning some of the same genes are operative) reveal associations between traits. Our results indicate that:

• The genetic basis of anorexia nervosa overlaps with other psychiatric disorders such as obsessive-compulsive disorder, depression, anxiety, and schizophrenia.
• Genetic factors associated with anorexia nervosa also influence physical activity, which could help explain the tendency for people with anorexia nervosa to be highly active.
• Intriguingly, the genetic basis of anorexia nervosa overlaps with metabolic (including glycemic), lipid (fats), and anthropometric (body measurement) traits, and the study shows that this is not due to genetic effects that influence BMI.

In fact, this pattern of correlations led us to conclude that anorexia nervosa may best be conceptualized as a ‘metabo-psychiatric disorder’ and that it will be important to consider both metabolic and psychological risk factors when exploring new avenues for treating this potentially lethal illness...

...Perhaps a dysregulated metabolism is why individuals with anorexia nervosa can lose so much weight in the first place, when weight loss is so difficult for the majority of the people in the world. We have speculated that starvation and weight loss feel different to people who are genetically at risk for anorexia nervosa. Whereas to most people those are deeply unpleasant experiences, for many people with anorexia, they claim that starvation and low weight are associated with being less anxious and actually feeling better physically. In fact, may patients say that they begin to feel worse when they gain weight. Perhaps a greater focus on understanding the metabolic aspects of the illness will allow us to develop more effective interventions that are acceptable to patients and have enduring effects.

We don’t know what the metabolic factors are yet, but our results strongly encourage research that addresses that question. Our results may also explain the importance of adequate renourishment when we treat anorexia nervosa.

 

[Crayola227]

ANGI (the genetics study I was involved in as a participant) did have some interesting findings related to metabolic stuff in AN.

From their public blog post: The results from ANGI | Angi

Perhaps the most revolutionary findings of this study are not in the gene discovery per se, but rather in the pattern of genetic correlations that we observed with other traits and disorders. Genetic correlations (meaning some of the same genes are operative) reveal associations between traits. Our results indicate that:

• The genetic basis of anorexia nervosa overlaps with other psychiatric disorders such as obsessive-compulsive disorder, depression, anxiety, and schizophrenia.
• Genetic factors associated with anorexia nervosa also influence physical activity, which could help explain the tendency for people with anorexia nervosa to be highly active.
• Intriguingly, the genetic basis of anorexia nervosa overlaps with metabolic (including glycemic), lipid (fats), and anthropometric (body measurement) traits, and the study shows that this is not due to genetic effects that influence BMI.

In fact, this pattern of correlations led us to conclude that anorexia nervosa may best be conceptualized as a ‘metabo-psychiatric disorder’ and that it will be important to consider both metabolic and psychological risk factors when exploring new avenues for treating this potentially lethal illness...

...Perhaps a dysregulated metabolism is why individuals with anorexia nervosa can lose so much weight in the first place, when weight loss is so difficult for the majority of the people in the world. We have speculated that starvation and weight loss feel different to people who are genetically at risk for anorexia nervosa. Whereas to most people those are deeply unpleasant experiences, for many people with anorexia, they claim that starvation and low weight are associated with being less anxious and actually feeling better physically. In fact, may patients say that they begin to feel worse when they gain weight. Perhaps a greater focus on understanding the metabolic aspects of the illness will allow us to develop more effective interventions that are acceptable to patients and have enduring effects.

We don’t know what the metabolic factors are yet, but our results strongly encourage research that addresses that question. Our results may also explain the importance of adequate renourishment when we treat anorexia nervosa.

Very interesting, thank you for sharing.

The last paragraph at least anecdotally seems to fit my 3 relatives with ED issues.

 

[Ceke2002]

Very interesting, thank you for sharing.

The last paragraph at least anecdotally seems to fit my 3 relatives with ED issues.

Anecdotally it fits for me as well. Part of my recovery process was working on learning and developing hunger recognition cues. I am a lot better with that than I was, but I don't think it will ever be something that I'll score a 10/10 on. I don't necessarily register the sensation of hunger in the same way as other people do, haven't done so since childhood. Hunger/starvation to me can be a really pleasant, grounding, calming experience, and it's something I do still monitor in the background to mitigate any risk of inadvertently flipping that ED switch inside my head. The metabolic findings and their implications for the study was something I was really interested to see.

 

[Mad Jack]

Going to? I've already seen it

 

[futureapppsy2]

ANGI (the genetics study I was involved in as a participant) did have some interesting findings related to metabolic stuff in AN.

From their public blog post: The results from ANGI | Angi

Perhaps the most revolutionary findings of this study are not in the gene discovery per se, but rather in the pattern of genetic correlations that we observed with other traits and disorders. Genetic correlations (meaning some of the same genes are operative) reveal associations between traits. Our results indicate that:

• The genetic basis of anorexia nervosa overlaps with other psychiatric disorders such as obsessive-compulsive disorder, depression, anxiety, and schizophrenia.
• Genetic factors associated with anorexia nervosa also influence physical activity, which could help explain the tendency for people with anorexia nervosa to be highly active.
• Intriguingly, the genetic basis of anorexia nervosa overlaps with metabolic (including glycemic), lipid (fats), and anthropometric (body measurement) traits, and the study shows that this is not due to genetic effects that influence BMI.

In fact, this pattern of correlations led us to conclude that anorexia nervosa may best be conceptualized as a ‘metabo-psychiatric disorder’ and that it will be important to consider both metabolic and psychological risk factors when exploring new avenues for treating this potentially lethal illness...

...Perhaps a dysregulated metabolism is why individuals with anorexia nervosa can lose so much weight in the first place, when weight loss is so difficult for the majority of the people in the world. We have speculated that starvation and weight loss feel different to people who are genetically at risk for anorexia nervosa. Whereas to most people those are deeply unpleasant experiences, for many people with anorexia, they claim that starvation and low weight are associated with being less anxious and actually feeling better physically. In fact, may patients say that they begin to feel worse when they gain weight. Perhaps a greater focus on understanding the metabolic aspects of the illness will allow us to develop more effective interventions that are acceptable to patients and have enduring effects.

We don’t know what the metabolic factors are yet, but our results strongly encourage research that addresses that question. Our results may also explain the importance of adequate renourishment when we treat anorexia nervosa.

This lines up really well with Shaun Gusinger's theory of the evolutionary nature of AN: https://www.adaptedtofamine.com/wp-content/uploads/2015/01/guisinger-an-pr-2003.pdf (it's an article in a top tier journal--the link is to the full-text on her site).

 

[futureapppsy2]

Going to? I've already seen it

What type of stuff have you seen in clinic?

 

[Mad Jack]

What type of stuff have you seen in clinic?

Was on inpatient consults, but I don't want to discuss it too much because it might be identifiable. Gist is, no eating disorder, started on Ozempic, lost piles of weight, now has chronic gastric pain/nausea and an eating disorder that is complicated by symptoms reminiscent of gastroparesis.

Oh wait, I just reread the OP. This was not one of the cases they were looking for, more a typical obese to excessively thin middle-aged woman that went too far with Ozempic. I'm sure we will see some barely overweight patients that start using the stuff and having the same effect soon

 

[Atreides]

Interestingly enough, I’ve seen one case of the opposite. Wegovy effectively curing binge eating disorder. Patient gained most of her weight back after discontinuing but the binge eating disorder has not returned yet (been a year and a half off Wegovy at this point).

 

[Ceke2002]

This lines up really well with Shaun Gusinger's theory of the evolutionary nature of AN: https://www.adaptedtofamine.com/wp-content/uploads/2015/01/guisinger-an-pr-2003.pdf (it's an article in a top tier journal--the link is to the full-text on her site).

Thanks for the link, I'm very interested in reading that. Here's the link to the full results of the ANGI study, if you haven't already seen it (requires login from an institution or payment to read the full article). Genome-wide association study identifies eight risk loci and implicates metabo-psychiatric origins for anorexia nervosa - Nature Genetics

 

[PsyDr]

1) This is a long standing issue. Notably, the 1993 Law and Order episode "Black Tie" was centered around a plot where wealthy people were abusing DMII drugs for weight loss. (Late night reruns are an awesome thing).

"Law & Order" Black Tie (TV Episode 1993) ⭐ 7.6 | Crime, Drama, Mystery

1h | TV-14

www.imdb.com

2) People are already "home brewing" GLP-1 medications using internet acquired peptides, leading the FDA to issue public cautions about the practice.

Can You Mix Peptides Yourself for Weight Loss?

People are buying semaglutide and tirzepatide online to mix their own Ozempic, Wegovy and Mounjaro, but it’s risky.

www.everydayhealth.com

 

[mistafab]

ANGI (the genetics study I was involved in as a participant) did have some interesting findings related to metabolic stuff in AN.

From their public blog post: The results from ANGI | Angi

Perhaps the most revolutionary findings of this study are not in the gene discovery per se, but rather in the pattern of genetic correlations that we observed with other traits and disorders. Genetic correlations (meaning some of the same genes are operative) reveal associations between traits. Our results indicate that:

• The genetic basis of anorexia nervosa overlaps with other psychiatric disorders such as obsessive-compulsive disorder, depression, anxiety, and schizophrenia.
• Genetic factors associated with anorexia nervosa also influence physical activity, which could help explain the tendency for people with anorexia nervosa to be highly active.
• Intriguingly, the genetic basis of anorexia nervosa overlaps with metabolic (including glycemic), lipid (fats), and anthropometric (body measurement) traits, and the study shows that this is not due to genetic effects that influence BMI.

In fact, this pattern of correlations led us to conclude that anorexia nervosa may best be conceptualized as a ‘metabo-psychiatric disorder’ and that it will be important to consider both metabolic and psychological risk factors when exploring new avenues for treating this potentially lethal illness...

...Perhaps a dysregulated metabolism is why individuals with anorexia nervosa can lose so much weight in the first place, when weight loss is so difficult for the majority of the people in the world. We have speculated that starvation and weight loss feel different to people who are genetically at risk for anorexia nervosa. Whereas to most people those are deeply unpleasant experiences, for many people with anorexia, they claim that starvation and low weight are associated with being less anxious and actually feeling better physically. In fact, may patients say that they begin to feel worse when they gain weight. Perhaps a greater focus on understanding the metabolic aspects of the illness will allow us to develop more effective interventions that are acceptable to patients and have enduring effects.

We don’t know what the metabolic factors are yet, but our results strongly encourage research that addresses that question. Our results may also explain the importance of adequate renourishment when we treat anorexia nervosa.

It is very interesting stuff. I had waded into the pools of the pure nerd stuff on this topic a few years ago. One conclusion I came up with was that presynaptic serotonin 1d/1b autoreceptors may be especially sensitive in these folks due to genetic differences, as well as the 2a receptor. Thus they become very sensitive to ebbs and flow of serotonin when exposed to the building blocks of it. You can check in the brain and see large differences (increases) after meals containing Large Neutral Amino Acids (LNAAs). What I had an epiphany about while working at an ED specialty center, is that it is NO COINCIDENCE that AN patients tend to all gravitate towards vegetarian and vegan restrictive diets. Most the times we consider this as a way to mask their restriction. However it occurred to me that these diets tend to restrict dietary protein (meats, cheeses), which in turn, lowers exposure to LNAAs dumping serotonin into their brains, and that the intake leads to sensations of discomfort and anxiety that folks with different receptors just dont have.

This was a specific epiphany I remembered having years ago because it was so caffeine-filled and nerdy that when I gave a talk about it I'm sure people thought I was on drugs. Yet it makes so much sense that we just dont see swathes of AN folks turning to all dairy or carnivore diets which are just as restrictive. They find these LNAAs very anxiogenic, and it promotes avoidance pathways via classical/operant conditioning.

 

[futureapppsy2]

Was on inpatient consults, but I don't want to discuss it too much because it might be identifiable. Gist is, no eating disorder, started on Ozempic, lost piles of weight, now has chronic gastric pain/nausea and an eating disorder that is complicated by symptoms reminiscent of gastroparesis.

Oh wait, I just reread the OP. This was not one of the cases they were looking for, more a typical obese to excessively thin middle-aged woman that went too far with Ozempic. I'm sure we will see some barely overweight patients that start using the stuff and having the same effect soon

Interested in both phenomena, really!

 

[Merovinge]

Yes, broadly speaking increased access to relatively safe options unlocks latent demand for products that either have or are perceived to have desirable effects. Adderall usage went up when you could ask a random NP online in 5 minutes for 30mg IR TID. Restrictive EDs will increase when people can use a shot (and even more when it is a pill) to produce the desired effect.

We do see this regularly at my practice which has an eating disorder specialization. More typically it is patient's who have pre-existing ED that then get on the medication, but there will be plenty more who have tip toed along the lines of having an ED and are inadvertly pushing themselves over by starting a GLP1 without medical indication.

 

[tr]

Not talking about the people who are obese and using GLP-1 agonists to get back to a normal weight but rather the folks who are normal or slightly overweight (BMIs of 27-ish or below) using them to drop into the underweight category. I was thinking about this because a YouTuber I follow on and off always looked somewhere between the high normal BMI range to the low-mid overweight range and is now looking like she’s in the low normal/underweight range after about 4-6 months of “weightlifting and eating healthy”, which no one really buys as being the full story. More broadly, there’s a solid market of people in the normal BMI range paying out of pocket for GLP-1 agonists, including a lot who admit having histories of restrictive disordered eating behaviors. It makes me wonder if we’ll start to see a rise in people using GLP-1s to fuel full-blown restrictive EDs. Thoughts? Clinical observations?

I don't know, it doesn't seem like most restricters need that much help to not feel hungry/ignore the feeling. It seems more like they have already destroyed their native hunger cues and need help restoring them if anything, but aren't really motivated to do that because they are invested in maintaining a low body weight.

Binge eating is far more prevalent than AN and GLP1s really get at the 'food noise ' problem that plagues these patients. I feel GLP1s are treating far more EDs than they are abetting.