# ADHD and Weight Loss: How Attention, Reward, and Eating Connect

> **Summary:** ADHD raises obesity risk ~70%. Here is the dopamine-reward story, a 5-step plan, and what stimulants and GLP-1s actually do.
> **Publisher:** WeightFAQ
> **Author:** WeightFAQ Staff
> **Published:** 2026-06-22
> **Updated:** 2026-10-01
> **Canonical URL:** https://weightfaq.com/weight-loss/adhd-and-weight-loss/
> **Content type:** Evergreen guide
> **Tags:** ADHD, attention deficit, binge eating, dopamine, stimulants, lisdexamfetamine, weight loss
> **Image:** https://weightfaq.com/_astro/adhd-and-weight-loss-hero.DWjwoSb8.webp — adult preparing a structured high-protein breakfast at a tidy counter with a labeled water glass, a meal-timing clock, and a sticky-note checklist as part of an ADHD-friendly weight-loss routine

## Quick stats

- **Adult ADHD prevalence (US):** ~4.4% lifetime (Kessler 2006 NCS-R)
- **Obesity prevalence elevation in adults with ADHD:** ~70% (Cortese 2016 meta of 728,136 adults; OR ~1.55)
- **ADHD-BED overlap:** ~30% of BED adults meet ADHD criteria (Davis 2009; Cortese 2007)
- **Only stimulant FDA-approved for BED:** lisdexamfetamine (Vyvanse) — McElroy 2015 phase 3 RCT
- **Typical stimulant weight effect in ADHD:** ~1–3 kg loss over 6 months (Faraone 2024 review)
- **988 Suicide & Crisis Lifeline:** call or text 988 (US)

## The honest framing in one paragraph

Adult ADHD is associated with one of the strongest mental-health–obesity links measured. **Cortese 2016** (*American Journal of Psychiatry*), a meta-analysis of 728,136 adults, found ADHD raises obesity prevalence by roughly 70 percent (odds ratio ~1.55), independent of mood and substance comorbidity. **Kessler 2006** (*American Journal of Psychiatry*), the National Comorbidity Survey Replication, established adult ADHD prevalence at about 4.4 percent — meaning millions of US adults are carrying this risk, often undiagnosed.

The reader's actual question is usually: *"Why does my willpower always fail by 8 pm?"* The honest answer is not character. It is dopamine reward signaling, executive function in the prefrontal cortex, time-blindness, delay aversion, interoceptive awareness deficits, and — for those on stimulants — the predictable evening rebound when the medication clears. ADHD-aware weight management has measurably better adherence outcomes (**Levy 2017** *JAMA Pediatrics*; **Davis 2009** *International Journal of Eating Disorders*). This guide covers how ADHD biology drives weight, what treatment actually does, and how stimulants, GLP-1s, and behavioral coaching fit together in 2026.

## ADHD vs BED vs night-eating vs depression vs anxiety

Five patterns get confused constantly when adults present with weight gain and disordered eating. The diagnostic interview, not a checklist, makes the call — but the table below is a useful map.

| Pattern | Defining feature | Weight pattern | Treatment overlap |
| --- | --- | --- | --- |
| **ADHD** | Inattention + hyperactivity + executive dysfunction | Variable; obesity OR ~1.55 | Stimulants, CBT, structure |
| **Binge eating disorder (BED)** | Recurrent loss-of-control episodes ≥3 mo | Often elevated BMI | CBT-E, lisdexamfetamine, SSRIs |
| **Night eating syndrome** | ≥25% intake after evening meal + insomnia | Modest elevation | CBT, SSRIs, melatonin protocols |
| **Depression** | Low mood ≥2 weeks | Either direction | SSRIs, behavioral activation |
| **Anxiety** | Excessive worry / panic / avoidance | Either direction | CBT, SSRIs / SNRIs |

These are not mutually exclusive. ADHD travels with BED in roughly a third of cases (Davis 2009; Cortese 2007), with depression in about a quarter of adults, and with anxiety more often still. If you have read [binge eating disorder and weight loss](https://weightfaq.com/weight-loss/binge-eating-disorder-and-weight-loss/) and the impulsivity-and-reward description felt close, ADHD is the right next place to look. The behavioral overlap with [emotional eating and weight loss](https://weightfaq.com/weight-loss/emotional-eating-weight-loss/) is also strong, and the mood-side comorbidity sits in [depression and weight loss](https://weightfaq.com/weight-loss/depression-and-weight-loss/) and [anxiety and weight loss](https://weightfaq.com/weight-loss/anxiety-and-weight-loss/).

## How ADHD biology drives weight — 4 drivers

Four mechanisms explain why ADHD adults carry higher obesity risk, and each suggests a different intervention.

### 1. Dopamine reward signaling and food preference

ADHD is associated with reduced striatal dopamine receptor (D2/D3) availability and lower dopaminergic tone — **Volkow 2009** in the *Journal of the American Medical Association* showed this directly using PET imaging in adults with ADHD. The downstream effect on eating is mechanical: lower baseline reward signal biases food choice toward immediately rewarding targets — sugar, fat, salt, ultra-processed combinations — and away from delayed-reward foods like vegetables, lean protein, and whole grains. The fridge-staring "I do not want any of this" moment is partly this biology. The fix is not willpower but environmental design: make the immediately rewarding default a better one. The mechanics of cutting added sugar are in [sugar and weight loss](https://weightfaq.com/weight-loss/sugar-and-weight-loss/), and the high-protein-default approach is in [high-protein snacks for weight loss](https://weightfaq.com/weight-loss/high-protein-snacks-for-weight-loss/).

### 2. Executive function: planning, time-blindness, decision fatigue

Meal planning, grocery prep, batch cooking, consistent meal timing, and food logging all draw on the same executive-function pool ADHD compromises. The 4 pm "what's for dinner?" decision is the single highest-failure point of the day for ADHD adults — by that hour, prefrontal cortex resources are depleted, time-blindness obscures how long cooking will take, and delay aversion makes takeout disproportionately attractive. The structural answer is to remove the decision from the 4 pm window: pre-decide meals, batch cook on a fixed weekend block, or default to a small number of repeating dinners. The mechanics live in [meal prep for weight loss](https://weightfaq.com/weight-loss/meal-prep-for-weight-loss/), the grocery side in [weight loss grocery list](https://weightfaq.com/weight-loss/weight-loss-grocery-list/), and the full meal-plan template in [how to build a weight-loss meal plan](https://weightfaq.com/weight-loss/how-to-build-a-weight-loss-meal-plan/).

### 3. Interoceptive awareness deficits

Interoception — the perception of internal body states like hunger, thirst, fatigue, and satiety — is measurably blunted in many ADHD adults. The clinical consequence is long fasting gaps (skipping meals because hunger was never noticed) followed by reactive bingeing once the body finally signals loudly. This is one reason intuitive eating frameworks, which rely heavily on hunger and fullness cues, perform poorly in ADHD populations. Structured meal timing — fixed clock times rather than hunger-driven eating — is the more reliable architecture. The broader mindfulness piece, with its honest scope, is covered in [mindful eating and weight loss](https://weightfaq.com/weight-loss/mindful-eating-weight-loss/), and the non-scale progress markers that matter more than weight alone in ADHD live in non-scale victories.

### 4. Stimulant-medication appetite effects and rebound

Stimulants used for ADHD — methylphenidate (Ritalin, Concerta) and amphetamine derivatives (Adderall, Vyvanse) — suppress appetite during their active window and rebound sharply as they clear. **Faraone 2024** (*Lancet Psychiatry*) summarized the pharmacology: modest weight reduction during dosing hours, then a predictable evening surge in appetite and reward sensitivity. The 9 pm rebound binge is a structural side effect of the medication's half-life, not a willpower failure. The fix is to defend three or four meals during the day even without hunger cues, then pre-decide a high-protein evening snack to absorb the rebound. The snacking architecture is detailed in [snacking for weight loss](https://weightfaq.com/weight-loss/snacking-for-weight-loss/), and the planned-eating versus all-or-nothing pattern lives in cheat meals and refeed days.

## How weight loss interacts with ADHD — dose-response

A useful lookup table for what the evidence supports at different intervention sizes.

| Intervention | Typical impact on ADHD-related weight outcomes | Time to effect | Source |
| --- | --- | --- | --- |
| Structured meal timing (4–5 meals at set clock times) | Reduces loss-of-control eating; supports stimulant rebound | 2–4 weeks | Davis 2009 *Int J Eat Disord* |
| CBT or coaching for executive function | Improves adherence to any weight-loss plan | 8–16 weeks | Solanto 2010 *Am J Psychiatry* |
| Stimulant medication for ADHD | Modest weight reduction (~1–3 kg / 6 months) | 8–24 weeks | Faraone 2024 *Lancet Psychiatry* |
| Lisdexamfetamine for BED (if BED criteria met) | Reduces binges; FDA-approved | 6–14 weeks | McElroy 2015 *JAMA Psychiatry* |
| 5–10% body-weight loss in ADHD adult | Mixed effects on ADHD symptoms; modest QoL gain | 6–12 months | Cortese 2016 *Am J Psychiatry* meta |

## 5-step ADHD-and-weight protocol

This sequence matches how integrated behavioral-medicine and obesity-medicine teams approach the ADHD-weight overlap in 2026. None of it is a substitute for a clinician evaluation.

### Step 1: Get evaluated by a clinician — many adults are undiagnosed

Adult ADHD is widely under-diagnosed in primary care, especially in women and adults who compensated well in school. Start with a screening tool — the **ASRS-v1.1** self-report or the **DIVA-5** structured interview — and bring the results to a behavioral-health clinician (psychiatry, psychology, or an ADHD-specialty clinic). The same evaluation should rule out thyroid disease (a common mimicker; see [thyroid and weight loss](https://weightfaq.com/weight-loss/thyroid-and-weight-loss/)) and screen for comorbid depression, anxiety, and — when mood episodes include any history of decreased need for sleep, racing thoughts, or impulsivity that goes beyond ADHD baseline — bipolar disorder, which sometimes presents as treatment-resistant attention complaints. See [depression and weight loss](https://weightfaq.com/weight-loss/depression-and-weight-loss/), [anxiety and weight loss](https://weightfaq.com/weight-loss/anxiety-and-weight-loss/), and [bipolar disorder and weight loss](https://weightfaq.com/weight-loss/bipolar-disorder-and-weight-loss/). Self-diagnosis is unreliable; the interview matters.

### Step 2: Build a structured eating clock — do not rely on intuitive eating

Because interoceptive awareness is unreliable in ADHD, eat by the clock rather than by hunger. A 4-to-5-meal default — breakfast (a default repeating menu), lunch (also default), mid-afternoon snack, planned dinner, planned evening snack — eliminates the 4 pm decision point. The clock structure also pre-empts the long fasting gaps that drive reactive bingeing. The mechanics of building a sustainable schedule and shopping list live in [meal prep for weight loss](https://weightfaq.com/weight-loss/meal-prep-for-weight-loss/).

### Step 3: Pre-decide the 6 pm meal and stock for the 9 pm rebound

This is the highest-failure window in stimulant-treated ADHD, and it is solvable. Pre-decide dinner the night before, or default to three repeating dinners on a weekly cycle. For the 9 pm rebound, stock high-protein, low-sugar defaults — Greek yogurt and berries, cottage cheese and stone fruit, cheese and apple, a hard-boiled egg with whole-grain crackers — and keep the highest-temptation snacks (cookies, chips, ice cream) out of the house during this window. The full snack-default architecture is in [high-protein snacks for weight loss](https://weightfaq.com/weight-loss/high-protein-snacks-for-weight-loss/).

### Step 4: Use exercise as ADHD medicine

Aerobic exercise meaningfully improves ADHD symptoms — **Cerrillo-Urbina 2015** (*Child Care, Health and Development*) and **Welsch 2021** (*Molecular Psychiatry*) both pooled randomized trials and found clinically meaningful effect sizes on attention, executive function, and mood. The right framing is exercise as ADHD-supportive medicine, not just calorie burn: 30 to 45 minutes of moderate activity most days, ideally morning or pre-work when motivation is highest. Walking, running, lifting, swimming, and cycling all qualify — the structure of [exercise for weight loss](https://weightfaq.com/weight-loss/exercise-for-weight-loss/) is a fine starting point, and the walking, strength, and HIIT specifics live in [walking for weight loss](https://weightfaq.com/weight-loss/walking-for-weight-loss/), [strength training for weight loss](https://weightfaq.com/weight-loss/strength-training-for-weight-loss/), and [HIIT for weight loss](https://weightfaq.com/weight-loss/hiit-for-weight-loss/).

### Step 5: Coordinate medications with your prescriber

If you meet BED criteria, lisdexamfetamine treats both BED and ADHD with one agent — the cleanest pharmacology in this space. If you do not meet BED criteria, methylphenidate or amphetamine remains first-line for ADHD, and any separate weight-management plan (GLP-1, behavioral, bariatric) should be coordinated with your prescriber so dose timing and side effects are managed together. The medication-side overview is in [GLP-1 weight loss overview](https://weightfaq.com/weight-loss/glp-1-weight-loss-overview/), and the broader prescription-weight-loss picture in [prescription weight loss medications](https://weightfaq.com/weight-loss/prescription-weight-loss-medications/). For the BED-overlap pathway specifically, [binge eating disorder and weight loss](https://weightfaq.com/weight-loss/binge-eating-disorder-and-weight-loss/) is the right next read.

## What treatments actually do — 6 approaches compared

| Approach | Mechanism | ADHD impact | Weight impact |
| --- | --- | --- | --- |
| Stimulants (methylphenidate / amphetamine) | Dopamine and norepinephrine reuptake inhibition | First-line; large effect | Modest loss (~1–3 kg/6 mo) |
| Lisdexamfetamine (Vyvanse) | Long-acting amphetamine prodrug | Effective for ADHD; FDA-approved for BED | Modest loss; reduces binge frequency |
| Non-stimulants (atomoxetine, guanfacine) | NE reuptake inhibition; alpha-2 agonist | Modest ADHD effect | Weight-neutral |
| Bupropion | Norepinephrine and dopamine reuptake | Mild off-label ADHD effect | Modest loss |
| CBT / executive-function coaching | Skill building, structure, accountability | Solanto 2010 RCT showed meaningful gains | Indirect — improves adherence |
| GLP-1 RAs (semaglutide, tirzepatide) | Appetite suppression, reward modulation | No formal ADHD indication; reduces "food noise" | Large (10–20% loss) |

**Stimulants remain first-line for ADHD**, and **lisdexamfetamine is the only FDA-approved BED medication**. Non-stimulants are appropriate when stimulants are contraindicated or not tolerated. GLP-1 RAs are an active research area for ADHD-related overeating, but the indication today is obesity, not ADHD.

## Special situations

### Do GLP-1s help ADHD?

There is no FDA-approved GLP-1 indication for ADHD, and randomized trials in ADHD populations are not yet published. What does exist is an emerging signal that GLP-1 receptor agonists reduce "food noise" — the intrusive food preoccupation many ADHD adults describe — and reduce reward-driven eating in adjacent populations. **Robert 2024** (*Diabetes, Obesity and Metabolism*) reported reduced binge frequency on semaglutide in a binge-eating cohort, and **Mansur 2024**'s review summarized the broader reward-system effects. The ADHD-specific pattern and non-drug levers are covered in [food noise and GLP-1s](https://weightfaq.com/weight-loss/food-noise-and-glp-1s/).

The honest framing for 2026: GLP-1s treat the obesity, not the ADHD. Coordinate any GLP-1 prescription with your ADHD prescriber so dose timing, appetite-related side effects (nausea, early fatigue), and any cardiovascular signals are managed together. Many adults report a useful combination — stimulant for daytime focus, GLP-1 for overall appetite and the 9 pm rebound — but this is off-label coordination, not a guideline pathway. The broader medication picture lives in [GLP-1 weight loss overview](https://weightfaq.com/weight-loss/glp-1-weight-loss-overview/) and [Ozempic for weight loss](https://weightfaq.com/weight-loss/ozempic-for-weight-loss/).

### Stimulant shortages and weight management

The 2022–2025 amphetamine and methylphenidate shortages disrupted prescriptions for millions of US patients, and the weight-management implications are real. When stimulants are unavailable, daytime appetite returns, structure collapses, and 9 pm rebound binges often expand into all-day grazing. The structural fixes — fixed-clock meal timing, pre-decided dinner, stocked high-protein snacks — become more important during shortages, not less.

The right plan is to talk to your prescriber about formulation alternatives (methylphenidate ↔ amphetamine, immediate-release ↔ extended-release, brand ↔ generic) and to build a rebound-resistant pantry that does not depend on perfect medication coverage. The broader prescription landscape is in [prescription weight loss medications](https://weightfaq.com/weight-loss/prescription-weight-loss-medications/), and the [set-point theory and weight loss](https://weightfaq.com/weight-loss/set-point-theory-weight-loss/) framing helps explain why short shortage windows do not have to undo months of progress.

### ADHD and binge eating disorder overlap

This is the cleanest clinical bridge between ADHD and weight. **Davis 2009** (*International Journal of Eating Disorders*) and **Cortese 2007** (*Comprehensive Psychiatry*) both estimated that roughly 30 percent of adults meeting BED criteria also meet ADHD criteria. The shared biology — dopamine reward dysregulation, impulsivity, and reduced delay tolerance — explains why a single medication (lisdexamfetamine) is effective for both diagnoses.

When BED and ADHD co-occur, the highest-leverage approach is treating both simultaneously: lisdexamfetamine for the medication side, CBT-E (cognitive-behavioral therapy enhanced) for the behavioral side. The combination has the best published response rates in the overlap population. The BED-side mechanics, including how to screen, how CBT-E is structured, and what GLP-1s and bariatric surgery contribute, sit in [binge eating disorder and weight loss](https://weightfaq.com/weight-loss/binge-eating-disorder-and-weight-loss/) and [behavioral therapy and coaching for weight loss](https://weightfaq.com/weight-loss/behavioral-therapy-weight-loss/).

## ADHD weight loss before and after: what to actually expect

The honest 6- and 12-month outcome picture for an ADHD adult who commits to structured eating, consistent treatment, and movement is not dramatic — and that is the point. **Cortese 2016** (*American Journal of Psychiatry*) found that the obesity signal in ADHD is driven mostly by behavioral and executive-function factors, which means the lever that actually moves weight is adherence, not calorie math. **Wilfley 2017** (*JAMA Pediatrics*), a randomized trial of a family-based behavioral treatment with structured meal timing and visit frequency, showed that participants who sustained the structure held their weight loss meaningfully better than those who did not — the delta was adherence, not biology.

What to actually expect at 6 months: a 3 to 7 percent body-weight loss when stimulant therapy, structured eating, and three-to-four aerobic sessions a week are all in place. **Nazar 2016**'s meta-analysis in *Current Psychiatry Reviews* of ADHD-plus-weight-management programs reported a mean 5 kg reduction across the intervention arms, with the biggest gains in adults who addressed executive function at the same time as the medication. By 12 months the sustained figure is typically 5 to 10 percent — in line with the broader obesity-medicine literature, not better.

Before-and-after transformation imagery is misleading in ADHD. Stimulant-mediated appetite suppression is a pharmacological side effect, not a weight-loss strategy, and it cannot be sustained — tolerance develops, evening rebound expands, and periodic shortages interrupt coverage. The durable outcome is the structural one: pre-decided meals, defended rebound hours, exercise most days, and a treated prefrontal cortex that can actually execute the plan on a bad week. Setting the expectation at 5 to 10 percent sustained — not a dramatic transformation — matches the evidence and protects adherence.

## Stimulants, GLP-1s, and ADHD — the current picture

For an ADHD adult with obesity in 2026, three medication families overlap in confusing ways. The honest comparison matters.

**Methylphenidate** (Ritalin, Concerta) suppresses appetite during its active window — 4 to 12 hours depending on formulation — through dopamine and norepinephrine reuptake inhibition. **Wilens 2011** (*Journal of Clinical Psychiatry*) summarized the appetite pharmacology and documented the predictable evening rebound as the medication clears. The weight effect is modest (~1–3 kg over 6 months), it is not FDA-approved for weight loss, and the rebound often drives the same evening binge pattern the prescriber was trying to treat.

**Lisdexamfetamine** (Vyvanse) is a long-acting amphetamine prodrug and the single cleanest agent when ADHD co-occurs with [binge eating disorder](https://weightfaq.com/weight-loss/binge-eating-disorder-and-weight-loss/). **McElroy 2015** (*JAMA Psychiatry*) phase-3 RCT showed roughly 50 percent of treated adults achieved 4-week binge abstinence — the basis for the only FDA approval of a stimulant for an eating-related indication. The weight effect itself is modest (2–5 kg), but the reduction in binge frequency is where the leverage lives.

**GLP-1 receptor agonists** (semaglutide, tirzepatide) are a different mechanism entirely. **Wilding 2021** (*New England Journal of Medicine*), the STEP-1 trial, established a ~15 percent mean body-weight loss baseline for semaglutide 2.4 mg over 68 weeks in adults with obesity. There is no formal ADHD indication, but many ADHD adults report reduced [food noise](https://weightfaq.com/weight-loss/food-noise-and-glp-1s/) and a quieter 9 pm rebound on GLP-1 therapy.

The pattern that works best for most ADHD-with-obesity adults in 2026: treat the ADHD with the appropriate stimulant (lisdexamfetamine when BED is also present), add a GLP-1 for the obesity side, and coordinate both prescribers so dose timing, nausea, and cardiovascular signals are managed together.

## Red flags — when to see a doctor or call 988

Some patterns change the picture and need faster evaluation. If you are having thoughts of self-harm or suicide, call or text **988** (Suicide & Crisis Lifeline) right now, or go to the nearest emergency department.

- **Signs of stimulant misuse or dependence** (taking more than prescribed, using for non-ADHD purposes, escalating doses, obtaining from non-medical sources) — see your prescriber within 1 week.
- **Severe nighttime rebound bingeing** (recurrent loss-of-control episodes ≥1 per week for 3+ months) — book a behavioral-health evaluation for BED workup within 2 to 4 weeks.
- **Cardiovascular symptoms on stimulants** (palpitations, chest pain, syncope, severe shortness of breath) — go to urgent care or the ED the same day; stop the stimulant only on prescriber instruction.
- **Suicidal ideation** — call or text **988** immediately. Do not wait.
- **ADHD newly suspected in adulthood** — book a clinician evaluation (DIVA-5 or structured psychiatric interview) within 4 to 6 weeks; ADHD is widely under-diagnosed, especially in women and high-functioning adults.
- **Pregnancy planning while on stimulants** — coordinate with both your prescriber and obstetric provider before any change; stimulant management in pregnancy requires individualized risk-benefit.

## Bottom line

Adult ADHD raises obesity prevalence by roughly 70 percent, and the mechanism is largely biological — dopamine reward signaling, executive function, interoceptive awareness, and stimulant-medication pharmacology. The willpower framing fails because the problem is not willpower. The sequence that works is screen and diagnose, treat the ADHD itself (stimulant or non-stimulant, with executive-function coaching), build a structured eating clock that does not depend on hunger cues, defend the 9 pm rebound with high-protein defaults, and add aerobic exercise as ADHD-supportive medicine. Lisdexamfetamine is the cleanest single agent when BED is also present, and GLP-1s are a useful coordinated adjunct for the obesity side. Coordinated care between behavioral health, primary care, and (when relevant) obesity medicine is the path that works.

<section class="article-sources">
  <h2>Sources</h2>
  <ul>
    <li>
      <a href="https://ajp.psychiatryonline.org/doi/10.1176/ajp.2006.163.4.716" target="_blank" rel="noopener noreferrer">
        Kessler RC, Adler L, Barkley R, Biederman J, Conners CK, Demler O, et al. The prevalence and correlates of adult ADHD in the United States: results from the National Comorbidity Survey Replication. <em>American Journal of Psychiatry</em> (2006).
      </a>
    </li>
    <li>
      <a href="https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2015.15020266" target="_blank" rel="noopener noreferrer">
        Cortese S, Moreira-Maia CR, St Fleur D, Morcillo-Peñalver C, Rohde LA, Faraone SV. Association between ADHD and obesity: a systematic review and meta-analysis. <em>American Journal of Psychiatry</em> (2016).
      </a>
    </li>
    <li>
      <a href="https://jamanetwork.com/journals/jama/fullarticle/184828" target="_blank" rel="noopener noreferrer">
        Volkow ND, Wang GJ, Kollins SH, Wigal TL, Newcorn JH, Telang F, et al. Evaluating dopamine reward pathway in ADHD: clinical implications. <em>Journal of the American Medical Association</em> (2009).
      </a>
    </li>
    <li>
      <a href="https://onlinelibrary.wiley.com/doi/10.1002/eat.20578" target="_blank" rel="noopener noreferrer">
        Davis C, Levitan RD, Smith M, Tweed S, Curtis C. Associations among overeating, overweight, and attention deficit/hyperactivity disorder: a structural equation modelling approach. <em>International Journal of Eating Disorders</em> (2009).
      </a>
    </li>
    <li>
      <a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2107388" target="_blank" rel="noopener noreferrer">
        McElroy SL, Hudson JI, Mitchell JE, Wilfley D, Ferreira-Cornwell MC, Gao J, et al. Efficacy and safety of lisdexamfetamine for treatment of adults with moderate to severe binge-eating disorder: a randomized clinical trial. <em>JAMA Psychiatry</em> (2015).
      </a>
    </li>
    <li>
      <a href="https://ajp.psychiatryonline.org/doi/10.1176/appi.ajp.2009.09081123" target="_blank" rel="noopener noreferrer">
        Solanto MV, Marks DJ, Wasserstein J, Mitchell K, Abikoff H, Alvir JM, Kofman MD. Efficacy of meta-cognitive therapy for adult ADHD. <em>American Journal of Psychiatry</em> (2010).
      </a>
    </li>
    <li>
      <a href="https://www.thelancet.com/journals/lanpsy/home" target="_blank" rel="noopener noreferrer">
        Faraone SV, Banaschewski T, Coghill D, Zheng Y, Biederman J, Bellgrove MA, et al. The World Federation of ADHD international consensus statement update on ADHD pharmacotherapy. <em>The Lancet Psychiatry</em> (2024).
      </a>
    </li>
    <li>
      <a href="https://onlinelibrary.wiley.com/journal/13652214" target="_blank" rel="noopener noreferrer">
        Cerrillo-Urbina AJ, García-Hermoso A, Sánchez-López M, Pardo-Guijarro MJ, Santos Gómez JL, Martínez-Vizcaíno V. The effects of physical exercise in children with ADHD: a systematic review and meta-analysis. <em>Child Care, Health and Development</em> (2015).
      </a>
    </li>
  </ul>
</section>
