00:00
Hey everyone, it's Mikki here. You're listening to Mini-Mikkipedia on a Monday and today I want to chat about the intersection of GLP-1 medications and ADHD. Now this cropped up with a client of mine actually and they were asking me whether there were any considerations for them as an adult with a diagnosis for ADHD and whether GLP might be particularly helpful. So

00:27
I'm going to dive into what I know about this topic. And by all means, I'm not an expert, would love to hear from someone who is. But I thought it was a conversation worth sharing with you or information worth sharing with you because of the, obviously the emerging of GLP-1 medications, they're coming down in cost, more people are having access to them. And of course, absolute sort of explosion of ADHD diagnoses in adults. I think it's just something worth

00:56
chatting about. Before I crack on into it though, I'd like to remind you or tell you actually that I have a Mastering Your Weight Maintenance webinar happening this Sunday, 21st of June, 2pm New Zealand time. Put it on your calendar. I've got a link in the show notes for you to go and sign up. This is for anyone who has feared eating at maintenance calories after coming off

01:23
weight loss. So basically anyone who is currently in weight loss, anyone who is contemplating going into fat loss or someone who, if you've just finished your fat loss phase and you're like, what on earth do I do now? This is a webinar for you. I talked to so many people who are terrified of weight gain post weight loss because they do not understand the physiology. They don't know what types of foods to eat, how to figure out what's the gold standard way of figuring out how much to eat.

01:52
What should my exercise look like? What are the guardrails that I need to have in place on a daily, weekly and monthly basis in order to ensure that I don't gain weight? All of the good things. So it is one of my most comprehensive webinars on this topics to date. And I'm so passionate about weight loss and weight loss maintenance. I hope that you join me. So we will put a link in the show notes or head to my website, mickeybulliedin.com. There is a banner across the top there for you to sign up.

02:21
And if you can't make it live or it isn't favorable for your time zone, it is being recorded and sent out after the fact. All right, back to the topic at hand. So let me first say is, is there's no direct evidence that these medications do anything for attention and focus. So that isn't actually the focus of what I want to chat about today. But what I was curious to understand is whether or not there is something about the GLP-1 medications

02:50
that change or influence eating behaviors and impulse control in people who have been diagnosed with ADHD as an adult. And of course, for some people in this scenario, this is they're now making sense of a lifetime of food struggles and reward seeking behavior that no one ever sort of connected with this diagnosis. And I would say as well that it isn't just for people who may

03:16
be excessively overweight or carry a lot of excess body fat who may be interested in this topic. Of course, GLP-1s are for people who have a BMI of 30 and above or 27.5 with another sort health comorbidity. I know the use case is expanding for other sort of scenarios, but I do want to sort of explore the idea of it in this sort of impulse control area.

03:45
So let's start with ADHD. So people often think about it primarily as an attention and focus problem, which of course it is, but underneath the attention difficulties, people often describe a dopamine problem. Specifically, the research describes as hypo dopaminergic, so low dopamine, in the prefrontal cortex, meaning that the brain's regulatory and executive system is chronically under-activated. There isn't enough dopamine

04:13
tone to sustain attention, regulate impulses, or manage the gap between intention and action in the way a neurotypical brain does. When a brain doesn't experience adequate reward from ordinary life, from tasks, routine, from the slower burning satisfactions of reward working towards something, it goes looking for reward elsewhere. Fast, immediate, high intensity, anything that moves the dopamine needle quickly. And that's neurobiology.

04:43
So the mesolimbic dopamine system, that's the circuit running from one area of the brain through into the prefrontal cortex, is the brain's reward highway. In ADHD, that system is underactive, and an underactive reward system creates a state of chronic reward insufficiency that drives seeking behavior. The brain is essentially doing whatever it takes to get dopamine because it isn't getting it from normal sources.

05:12
And this is why ADHD in adults looks the way it does. The inability to do boring tasks is a sign that the dopamine reward signal for completing that task is too weak to compete with anything more stimulating. And the hedonic behaviors, eating, drinking, spending, scrolling, risk taking, these aren't separate issues sitting alongside the ADHD. They are

05:39
part and parcel of the diagnosis playing out in the reward domain. Now let's sort of think about ADHD and obesity. So the research on ADHD and weight is pretty striking when you look at it. So adults with ADHD have a 70 % higher risk of obesity. ADHD is overrepresented in people seeking treatment for obesity, regardless of where the binge eating is present. And in bariatric surgery populations,

06:07
ADHD rates are substantially higher than in general population and the outcomes from behavioral weight loss programs are consistently poorer in adults with ADHD, even when motivation appears intact. And there's also a relationship between ADHD symptom severity and what researchers call food addiction. And I chatted to Jen Unwin about food addiction last year. And this is a pattern of eating behavior that mirrors the compulsive loss of control characteristics of substance addiction.

06:37
measured using tools like the Yale Food Addiction Scale. Impulsivity in particular, especially what's called negative urgency, which is acting impulsively when emotionally distressed, it consistently predicts higher food addiction scores in people with ADHD. And this has been formalized in research under the concept of reward deficiency syndrome, which is exactly what it sounds like. It's a framework for understanding how insufficient dopamine reward signaling

07:06
creates a cluster of seemingly different problems. ADHD, binge eating, alcohol misuse, substance use disorders, compulsive behaviors. These are understood as different endophenotypes, different expressions of the same underlying reward deficit. The common root is this hypodopaminergic state. The individual disorders are different ways that deficiency manifests, depending on the person's environment,

07:35
genetics and life circumstances. What may be helpful with this framework from a clinical perspective is that it stops us treating these as separate problems requiring separate explanations and interventions. If someone walks in with ADHD, obesity, a history of disordered eating, and they're drinking more than they'd like, that is like one coherent story. These aren't separate issues. So I do think probably from a practical perspective, this changes how you might approach it.

08:04
Interestingly, from a pharmacological perspective, binge eating disorder in ADHD share enough neurobiology that lysidexamphetamine, Vivansi, I think that's how I say that, it's the only FDA approved medication for binge eating disorder that is a stimulant, and it's a stimulant. It's the same class of drug used to treat ADHD. So, you know, that is probably not a coincidence. Drugs that potentiate

08:33
dopaminergic nor adrenergic transmission work across both conditions because the underlying deficit is shared. So let's talk about these GLP-1 medications and specifically about their central nervous system effects because, you know, this is super interesting, right? So GLP-1, which I often use that to describe almost all the medications and it is an accurate A. So GLP-1 specifically is GlucaCon like peptide one.

09:03
and it's an incretin hormone. So most people know it as the hormone that signals insulin release after eating, slows gastric emptying, and reduces appetite. But the GLP-1 receptors are not limited to the gut and pancreas. They are expressed in the brain and specifically in regions that have nothing to do with metabolic regulation in that traditional sense. They're in the nucleus accumbens, which is the primary reward center. They're in the prefrontal cortex, which handles the executive function and

09:33
impulse control, and they're in the habanula, which is an area involved in regulating mood and encoding negative outcomes. So when GLP-1 receptor agonists like semaglutide, liraglutide, and others are administered, they activate receptors in these regions and modulate dopamine, serotonin, glutaminergic, and gabaergic neurotransmission across the reward circuit. So this isn't

10:02
peripheral appetite suppression filtering through the behavior, this is direct central nervous system action on the reward system. And so of course, this is why the effects people report go well beyond simply not feeling hungry. People on these medications consistently describe what gets called the quieting of food noise. That's not news to you. That constant background mental preoccupation with food. What to eat next. Thinking about eating when they've just eaten.

10:30
They describe being physically present around food, at a dinner party, in a kitchen, walking past a bakery, and just not being particularly compelled by it, which is so different from what they experienced before these medications. They also describe eating in better alignment with genuine hunger, rather than responding to emotions, stress, boredom, or environmental clues. And a significant number report that other reward-seeking behaviors also change, less desire for alcohol.

11:00
reduced pull towards other compulsive or impulsive habits, shopping, scrolling, those kind of things. And if you look at functional MRI evidence, you can see it directly. Studies using brain imaging in people on GLP-1 receptor agonists show reduced activation in the ventral striatum. And this is the reward hub. Studies using brain imaging in people on GLP-1 receptor agonists show that reduced activation in the ventral striatum

11:29
in response to food cues in high calorie images. And that ventral striatum is the reward hub. So the brain is literally responding differently to reward signals. So the cue reactivity that drives much of compulsive eating behavior in this population is being modulated at that neural level. So let's look specifically at evidence for compulsive eating. So this may be directly relevant to the ADHD overlap.

11:55
So a 2025 systematic review and meta-analysis looking at GLP-1 receptor agonists in binge eating disorder, pulling five studies with 182 participants. So not a big, a massive data, but it found significant reductions in binge eating scale scores alongside weight loss. It's also worth saying that there is heterogeneity in the study. it is more difficult to compare them.

12:22
but the direction is consistent across the studies. A pilot randomized controlled trial of laryngoglutide in binge eating disorder found that both objective binge eating episodes and weight decreased in the treatment group compared to placebo. The sample again was small and there were some methodological issues which does complicate the interpretation. But again, the direction of the data is similar. Beyond that eating domain, there is

12:51
emerging evidence from the addiction literature that's mechanistically very relevant. Cimaglutide has been shown in preclinical studies to reduce alcohol intake through those mechanisms I mentioned earlier, nucleus, accumbens, dependent mechanisms. So it attenuates that alcohol-induced dopamine release. So it shifts it down and it reduces that motivational drive to consume. A clinical trial of

13:17
Exanitide in alcohol use disorder showed that while it didn't reduce heavy drinking days overall, it significantly reduced brain Q reactivity in reward regions on functional MRI scans, and meaningfully reduced drinking in the subgroup of participants with obesity. There are case reports of dramatic reductions in cocaine craving and measured impulsivity. One case showed impulsivity scores dropping by nearly 60 % over three months on simagglutide.

13:46
Then there's something called the Mendelian randomized data. This is a method that uses genetic variants as proxies to get closer to being able to make causal inferences rather than just correlational. A 2025 study found that genetically proxied GLP-1 receptor agonism was associated with a substantially reduced risk of bulimia nervosa with an odds ratio of 0.34. Now, bulimia nervosa is that clinical diagnosis around purging.

14:16
That is a large effect. It is also associated with reduced risk of post-traumatic stress disorder and bipolar disorder. Critically, for ADHD specifically, the same analysis found no significant causal sign, which is an important piece of the picture that we will actually come back to. So the GLP-1 receptor agonists reduce dopamine signaling and reward circuits. That is the mechanism by which they reduce compulsive eating,

14:44
Q-reactivity and craving. Reduced reward salience, that's the thing that's driving the hedonic behavior, is the therapeutic target. But as I've said, and as you've picked up, ADHD is a condition of dopamine insufficiency. The reward system is already underactive. So the question you have to ask is, what happens when you take a medication that works by dampening dopamine reward signaling and apply it to a brain

15:10
whose fundamental problem is that it doesn't generate enough dopamine reward to begin with. Theoretically, the answer depends on which part of the dopamine problem you're dealing with. There are at least two distinct dopamine profiles that can coexist with ADHD. One is the hyperdopaminergic in the ventral striatum. I haven't talked about that, but that is in fact a hyperreactive reward response where cue-triggered dopamine surges are exaggerated.

15:37
driving impulsive seeking and compulsive consumption. The GLP-1 mechanism is likely quite helpful here because you are calming an overactive cue response system. The other, the one that I've already mentioned, it's a more pervasive hypodopaminergic system. It's a brain that genuinely is under rewarded at baseline and eating or drinking or whatever the behavior is, is serving as a self-medication for that low reward state.

16:06
In this case, reducing dopamine reward signaling further might quiet the eating behavior while making the underlying state worse. You remove the coping behavior without addressing, or potentially exacerbating, what is driving it. And the distinction has been formally flagged in research literature. One analysis put it plainly, GLP-1 agonists may represent a double-edged sword. Therapeutic in the hyper...

16:33
Dopaminergic states, the high dopamine states, potentially detrimental in those hypodopaminergic ones. The dopamine dampening mechanism that looks like a feature in addiction treatment may look like a bug in a dopamine deficient brain. In practice, I just think this means the clinical picture varies a lot. Some adults with ADHD on GLP-1 medications will notice that the food noise goes quiet, they feel more even keeled, eating is more regulated.

17:03
and life generally gets easier. Others might notice flatness, reduced motivation, low mood, or a kind of anhedonic quality, nothing feeling particularly satisfying or compelling. Both responses are mechanistically coherent actually. And the difference probably tells you something about the individual's underlying dopamine profile. And just so you know, this isn't an argument for or against using GLP-1 medications, but it's just,

17:32
It's to draw attention to, I guess, what happens when you do take it and having a framework for understanding it if you're someone who's considering it. So with that in mind, if you are diagnosed ADHD and you're on a GOP1 medication, just a few things worth considering. Firstly, watch your mood and motivation carefully, particularly in the early months. And this is because you're introducing a dopamine modulating agent.

17:59
into a neurological situation where dopamine is already a key variable. Some people feel more regulated and focused. Others notice a flatness or a reduction in the things they used to feel rewarding. So if you are noticing the latter, I think that that is definitely worth flagging with your uh medical people, your prescriber, and it's an important clinical information. Second, of course, take nutrition seriously in a way you might be tempted not to.

18:29
ADHD stimulant medications already suppress appetite, sometimes significantly. GLP-1 medications add a potent second layer of appetite suppression. In the context of a brain that needs consistent fuel to produce neurotransmitters and maintain function, under-fuelling is a real and underappreciated risk in this combination. Clearly protein intake uh especially matters. Adequate protein supports dopamine and noradrenaline synthesis.

18:56
both of which are already the sticking point in ADHD. And this isn't a situation where eating very few calories is inherently better. Structured eating, deliberate protein targets, and not relying on hunger cues to tell you when to eat is particularly important. Thirdly, understand what is actually driving the eating behavior. If food functions primarily as reward seeking and the issue is strong cue reactivity, you walk past a bakery and feel an almost impulsive pull,

19:26
you see something on social media and immediately want it, food is about stimulation and novelty. GLP-1s are likely addressing a meaningful part of the problem. If food is primarily serving as an emotional regulation, it's what you reach for when stressed, overstimulated, bored, or anxious, or low mood, GLP-1s may reduce the behavior without addressing the driver. That underlying emotion dysregulation, which is extremely common in adult ADHD, still needs attention.

19:56
and the medication might create some breathing room, but the work does still need to happen. Fourth, I don't know, I imagine this is the case, but ADHD is likely on the screening radar for anyone presenting with obesity and binge type eating. The research has cleared that ADHD is substantially overrepresented in this group. Outcomes from standard behavioral weight loss programs are consistently worse in adults with ADHD. And this may be because the programs aren't designed for a brain that regulates

20:24
attention and behavior differently. So understanding the neurobiological driver changes the treatment approach and sets more realistic expectations. What I will say though is, and this is what I want to finish on, is that, you know, there's a lot of uncertainty here because this is a space where the mechanisms are, you know, it's pretty interesting, but the clinical trial data is pretty thin as well. So there are no dedicated trials of GLP-1 receptor agonists in adults with ADHD.

20:53
The Mendelian randomization data, that genetic variant data that found causal signals for bulimia nervosa and several psychiatric conditions didn't find a significant signal for ADHD. And that's an important thing to note. It suggests that whatever benefit GLP-1s might offer in this population probably isn't operating on ADHD-caused symptoms directly, but on the comorbid reward and hedonic behavioral layer. There's also the

21:23
pharmacovigilance data on psychiatric adverse events with GLP-1 medications, which do show signals for anxiety, depression, and sleep disturbance. And these are already overrepresented in adults with ADHD, and they interact with that dopamine regulation. Of course, I don't want to overstate it. The absolute rates are totally low, but the population we're talking about is already carrying elevated baseline risks for these outcomes. So they just warrant

21:52
monitoring, I think, in this space. And there's no data on the combination of ADHD stimulant medications and GLP-1 receptor agonists. Both are acting on the central nervous system. Both involve dopamine, but that interaction hasn't been studied formally. I mean, maybe it's coming or maybe I've missed something. I know it's probably quite likely, but I haven't seen much here. So bottom line, ADHD is far more than just that attention problem.

22:22
It's also a reward system disorder and the hedonic behaviors that travel with it, like the food struggles, the impulsivity, the difficulty moderating anything rewarding, these are neurologically connected to the same dopamine deficit that drives those attention difficulties. And GLP-1 receptor agonists act directly on those brain circuits involved in reward and hedonic behavior. They reduce that Q-reactivity, quiet food preoccupation,

22:51
and appear to have genuine effects on compulsive eating patterns, not just hunger. So for adults with ADHD, whose primary struggle is in that reward seeking behavior cluster, there is that real biological rationale for benefit. But because the medications reduce dopamine reward signaling and ADHD already involves insufficient dopamine tone in a substantial proportion of people who have it, then that is something that deserves more attention.

23:18
And this whole area in GLP-1s is moving fast. So I bet over the next few years, we will see dedicated research in this population, because of course, more and more people are being diagnosed as well. So we'll get a much clearer picture of who benefits and who doesn't, and what monitoring is appropriate. But for now, of course, because you've been diagnosed with ADHD, it doesn't take these medications off the table at all. And I don't doubt that your prescriber is aware of,

23:46
everything that is sort of going in and going on with you. But just understanding the mechanism, watching carefully, keeping nutrition a priority is a practical path forward, I think. So that's, as I understand it, what we know about the intersection between GLP-1 agonist and ADHD. I'd love to hear if you've got experience or if you know anything about this, I'd love to hear from you.

24:13
You can catch me over on Instagram, threads and X @mikkiwilliden, over on Facebook @mikkiwillidenNutrition, or head to my website, mikkiwilliden.com and see that little banner there that says sign up to the Mastering Your Maintenance Diet webinar. Click on that. If you want to have real food freedom, that's lifelong. All right, guys, you have the best week. See you later.