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ADHD, Obesity, and Eating Disorders

ADHD, Obesity, and Eating Disorders

Author: Ulrich Brennecke
Review 10/2024: Waldemar Zdero, M.A. in Psychology

Eating disorders and obesity are common among people with ADHD.12
(E 2a): There was moderate evidence of an association between ADHD and disordered eating, most clearly for overeating. Symptoms of impulsivity were consistently associated with overeating and bulimia. Limited evidence of an association between hyperactivity symptoms and restrictive eating behaviors was found only among boys and men, but not among girls and women.(E 2a)3 (E 2a) (Review without meta-analysis, k = 75 studies)4 Limited evidence of an association between hyperactivity symptoms and restrictive eating behaviors was found only among boys and men, but not among girls and women. (E 2a)4
(ADxS assessment): It is not possible to determine from cross-sectional data whether ADHD contributes to eating disorders or vice versa.

Children with ADHD, as well as children with subclinical ADHD (ADHD that is too mild to be diagnosed), have an increased body fat percentage.5 According to a meta-analysis, the prevalence of ADHD among candidates for gastric bypass surgery (k = 14 studies with n = 24,455 adults and k = 3 studies with n = 299 adolescents), the prevalence of ADHD is three times higher among adults (8.94% to 9.90%) and six times higher among adolescents (28.73%).6

1. ADHD and Overweight/Obesity/Adiposity

1.1. ADHD Is Twice as Common in People with Obesity (Children: +20%, Adults: +55%)

The prevalence of ADHD is higher among people who are severely overweight than in the general population. In an extremely long-term study spanning 33 years, it was found that 41.4% of all men who had ADHD-C as children developed severe obesity as adults, while only 21.6% of those without a childhood ADHD diagnosis were affected. The doubling of the prevalence of obesity among people with ADHD is (albeit from extremely different baseline levels) in the U.S. from 21.6% without ADHD to 41.4% with ADHD7 as well as in Germany from 10.2% without ADHD to 22.1% with ADHD.8
Children with ADHD showed9

  • a significantly lower birth weight
  • a significantly higher likelihood of obesity among children aged 5 and older (OR 1.57 to 2.46, RR 0.98 to 2.29)
  • More severe ADHD symptoms in girls aged 7, 11, and 14 predicted significantly higher BMI-Z scores at ages 11, 14, and 17, respectively
  • More severe ADHD symptoms in boys aged 11 and 14 predicted significantly higher BMI-Z scores at ages 14 and 17, respectively

An Israeli cohort study found that obesity was nearly twice as common—at 13.5%—among adolescents with severe ADHD compared to those without the condition, and about 30% more common among those with mild ADHD than among those without the condition.10

A meta-analysis of 42 studies involving n = 728,136 participants found:11

  • Obesity increases the risk of ADHD by 20% in children (OR = 1.20) and by 55% in adults (OR = 1.55)
  • ADHD increases the risk of obesity by 40% in children (10.3% vs. 7.4%) and by 70% in adults (28.2% vs. 16.4%)

ADHD is a significant risk factor for the development of obesity.12 ADHD, alcohol dependence, insomnia, and heavy smoking are associated with an increased body fat percentage.13
Attention problems and hyperactivity were positively correlated with responsiveness to food, emotional overeating, the desire to drink, and a slowing of eating. Attention problems reduced the enjoyment of eating. Conversely, eating behavior does not appear to be a cause of ADHD.14 Being moderately overweight (not to the point of obesity) is also not thought to increase the likelihood of ADHD.8

A long-term cohort study in the United States found a linear correlation between the number of ADHD symptoms and waist circumference, BMI, obesity, diastolic blood pressure, and systolic blood pressure.15 An Israeli study also points to this.16
In a study of extremely obese children receiving inpatient treatment, the rate of ADHD comorbidity was 58%.17
Among 155 adult women in Brazil with a BMI > 39, an ADHD prevalence rate of 28.3% was found. Binge eating, bulimia, and depression were also more common than average.18 The likelihood of ADHD was thus 6.4 times higher than the expected prevalence of 4.4% among adults.
Similarly, the body mass index of people with ADHD is, on average, higher than average.19

A minority of studies found no link between ADHD and BMI. One study found no association between ADHD and BMI at ages 9 or 13. However, children with ADHD at age 9 were significantly more likely to be overweight or obese than children without ADHD. This was not attributed to ADHD, however, but rather to other child- and parent-related factors such as female gender, low physical activity, overweight or obese parents, and prenatal smoking during pregnancy.20 A smaller study of 76 adolescents found no overlap between obesity and ADHD or autism spectrum disorders.21 Another study found no correlation between ADHD and a high BMI, but did find a correlation between unhealthy eating habits and ADHD in adolescents.22

A meta-analysis found that the prevalence of ADHD among people with eating disorders ranged from 1.6% to 18%. Comorbid ADHD was more common in the AN-binge-eating/purging subtype and the bulimia subtype than in the restrictive anorexia subtype.
For people with ADHD, the meta-analysis found a lifetime prevalence of eating disorders ranging from 0 to 21.8% among women with ADHD.23

A study of n = 450,000 Europeans found that single-nucleotide polymorphisms that cause obesity also causally increase the risk of ADHD, depression, and bipolar disorder.24 Impulsivity in ADHD and an elevated BMI share genetic and neurophysiological correlates.25

Severe obesity is also associated with sleep apnea, reduced sleep duration, and other sleep problems.26
Conversely, sleep problems are the most common comorbidity associated with ADHD. See Sleep problems in ADHD as well as Comorbidity in ADHD, under “Sleep Problems.”
In adults without a diagnosis of ADHD, daytime sleepiness correlates with the severity of ADHD symptoms.27

1.2. ADHD Treatment Is Effective Against Obesity

ADHD treatment can lead to surprising success in weight loss among severely obese patients. Obese patients diagnosed with ADHD lost more than 12% of their body weight per year while taking standard ADHD medication.28
By way of comparison: according to current standards, obesity treatment is considered successful if weight gain does not exceed 5% per year.

Other studies also report a reduction in elevated BMI levels among people with ADHD following ADHD treatment.29

1.3. Is Gastric Bypass Surgery Less Effective for ADHD Symptoms?

A study found reduced weight loss following gastric bypass surgery among people with ADHD, a core symptom of ADHD.30

1.4. Obesity and Addictive Behavior

About half of all overweight people who have undergone gastric bypass surgery go on to develop another addiction. This is compelling evidence that being overweight can be a consequence of addiction.313233

It is well known that ADHD causes a significant disorder of the reward system, with the consequence that rewards that are further off in the future are significantly less appealing compared to those experienced by people without ADHD. Eating can provide this immediate gratification.

In ADHD, the overall risk of addiction is significantly increased. This applies to legal substances such as tobacco, caffeine, alcohol, or food, as well as illegal substances such as marijuana, amphetamines, or cocaine.
Nicotine and caffeine are stimulants, just like typical ADHD medications.
Amphetamines, cocaine, and marijuana are effective—in specific forms—as medications.

The difference between addictive substances and medications is that addictive substances (including nicotine) produce a rapid surge and target a very large number of receptors, whereas medications rise and fall slowly, occupy only a small portion of the receptors, and therefore do not cause intoxication-like states. As with any substance, the dose makes the poison.34

2. ADHD and Eating Disorders

Girls with ADHD are 3.6 times more likely to develop eating disorders than girls without ADHD.35

Leptin is an adipokine produced by adipose tissue that, as a hormone, plays a role in regulating feelings of hunger and satiety.36 As a result, leptin suppresses appetite.
Contradictory results were found in children with ADHD.

  • Serum leptin levels were significantly reduced, regardless of whether MPH was taken.37
  • Leptin levels increased (133%); further increased to 171% by MPH38

Ghrelin (Growth Hormone-Releasing) is an appetite-stimulating peptide produced in the stomach lining and the pancreas.
Contradictory results were also found in children with ADHD.

  • Serum ghrelin levels correlated with auditory attention and increased in a dose-dependent manner with MPH administration, but were reduced in cases of MPH side effects.37
  • Ghrelin levels increased 10-fold; MPH reduced ghrelin levels to 5 times those of the control group38

A study found that ADHD is associated with an increased risk of:39

  • Binge eating: OR=13.2 (1,320%)
  • Bulimia nervosa: OR=27.5 (2,750%)
  • recurrent binge eating: OR 5.8 (580%)

However, after taking depression, anxiety, alcohol consumption, and impulsivity into account, the increased risk was no longer significant:
Since impulsivity is a symptom of ADHD, we believe that adjusting for it skews the results. If study results on ADHD were adjusted for attention problems and hyperactivity/impulsivity, the findings would inevitably never be statistically significant.

Another study found a 97% increase in the risk of eating disorders associated with ADHD (HR 1.97) and a 183% increase associated with ASD (HR 2.82). This study also found that anxiety and depression could account for 44% to 100% of the association between ADHD or ASD and eating disorders.40

2.1. Avoidant/Restrictive Food Intake Disorder (ARFID) (+870%)

Avoidant/Restrictive Food Intake Disorder (ARFID) is an eating disorder characterized by an extremely limited variety and/or amount of food. It is associated with serious consequences for physical and mental health.41
With ARFID, the risk of

  • ADHD increased by 870% (OR 9.7)
  • ASS increased by 1,270% (P/E ratio 13.7)

2.2. Bulimia is 6 to 8 times more common in women with ADHD (+500 to 700%)

Bulimia (bulimia nervosa; very broadly defined as binge eating followed by purging) is found in 11% to 12% of adult women with ADHD (according to DSM-III-R criteria), compared to about 1% to 3% of women without ADHD. No differences are observed among men and children.42 Assuming a 1.5% prevalence of bulimia nervosa43, this would result in an 8-fold increase in the prevalence among people with ADHD.
A meta-analysis reported that nearly all studies found that stimulants had a positive effect on eating behavior in people with bulimia.44

2.3. Anorexia is 2.2 times more common in people with ADHD (+120%)

The likelihood that girls and women with ADHD will develop anorexia (very broadly defined as the pursuit of extreme thinness) is “only” 2.2 times higher than for girls and women without ADHD.45

2.4. Binge eating is twice as common (+100%)

Eating disorders such as binge eating (roughly defined as episodes of excessive eating without vomiting) are also suspected of being linked to ADHD and of contributing to weight problems.4647

In obese patients (BMI > 30), ADHD doubles the likelihood of developing binge eating and increases the likelihood of developing other eating disorders.48

Among 150 adult women with a BMI over 39, the prevalence of ADHD was found to be 28.2%. Binge eating, bulimia, and depression were also more common than average.18

2.5. Food addiction (+66%)

Food addiction was 66% more common among n = 139 children with parent-reported ADHD than among those without the condition.49
Surprisingly, food addiction, as measured by the YFAS50, increased with each quartile of executive function level, with the associations being stronger at higher levels.

2.6. Compulsive snacking (grazing) increases the risk of ADHD by a factor of 8 (+700%)

Grazing is the unstructured, repeated consumption of small amounts of food over an extended period of time outside of scheduled meals and snacks and/or not in response to feelings of hunger or fullness. Grazing has two subtypes:

  • compulsive snacking
    • Feeling that you can’t resist or stop grazing
    • Prevalence in the general population: 10.2%
    • ADHD prevalence among people with ADHD: approximately +800% (OR 8.94)51
    • correlates with
      • more severe psychopathology associated with the eating disorder
      • increased psychological distress
      • lower psychological quality of life
      • lower treatment success rates in patients with high body weight
  • non-compulsive subtype
    • that is, repeated, distracted eating
    • Prevalence in the general population: 38% to 90%

3. ADHD and Diabetes

Of 677,587 German children and adolescents, 16,833 were diagnosed with ADHD (2.5%), while 3,668 were being treated with insulin for type 1 diabetes mellitus (0.05%). In the subgroup of children with diabetes, 153 children (4.2%) also had a diagnosis of ADHD. This suggests that people with ADHD have a significantly higher prevalence of type 1 diabetes, and vice versa.52

4. Cortisol, Metabolism, and Body Fat

Glucocorticoids (such as cortisol) play a central role in the regulation of carbohydrate metabolism by influencing gluconeogenesis.53

Glucocorticoids also initiate and regulate a wide variety of digestive enzymes54, the expression of membrane-bound transporter proteins55, as well as proteins that play a key role in gluconeogenesis.56

  • Cortisol increases the reward value of pleasurable or compulsive activities (consuming sucrose, fat, and drugs, or participating in bike races). This motivates the consumption of “comfort food.”57
  • Cortisol increases abdominal fat deposits throughout the body. This causes57
    • inhibition of catecholamines in the brainstem and
    • inhibition of CRH expression in the hypothalamus, which has consequences for ACTH
  • Cortisol acts on adipose tissue via insulin58
    Possible consequences:
    • visceral obesity58
    • Insulin resistance58
    • Dyslipidemia58
  • Cortisol increases adrenaline-induced lipolysis (fat breakdown, fat digestion).5960
    This impairment may be further exacerbated by reduced ACTH levels.61
    It is possible that this correlation is reversed in severely obese individuals (see below).
  • While chronic stress and high levels of glucocorticoids increase body weight gain in rats, in humans this leads either to increased food intake and weight gain or to decreased food intake and weight loss.5762
  • Several studies show a correlation between the cortisol stress response and the waist-to-hip ratio, such that a low cortisol stress response is associated with a low waist-to-hip ratio (less pronounced waist), whereas a high cortisol stress response is associated with a high waist-to-hip ratio (pronounced waist).636465
  • Abnormalities in lipid metabolism (hypertriglyceridemia), which occur more frequently in Type A personalities, can be corrected by administering ACTH, but not by administering cortisol.66
    The described effect of ACTH would be consistent with the hypothesis that the HPA axis is underactive in Type A.
    For people with Type A ADHD (also known as ADHD-HI, or ADHD with hyperactivity), a genetic predisposition or chronic stress could be a factor
    → have led to a prolonged increase in CRH release,
    → which triggers CRH receptor downregulation,
    → which causes the pituitary gland to be underactive,
    → which triggers a decrease in ACTH secretion,
    → which causes reduced adrenal gland activity,
    → which has consequences for reduced cortisol secretion,
    → which is why, when the HPA axis is activated at the end of a stress response, only the MR receptors—but not the GR receptors—are targeted,
    → which results in the HPA axis not being properly shut down.
  • In healthy individuals, norepinephrine levels in the OFC and amygdala correlate with activation of the HPA axis. In severely obese individuals, however, this correlation is reversed.67
    The endocrine stress responses involving norepinephrine and cortisol occur in parallel. In ADHD-HI (with hyperactivity), therefore, not only is the cortisol stress response reduced, but so is the norepinephrine stress response.
  • Obesity is characterized by high levels of oxidative stress and inflammation.68 Inflammation is inhibited by cortisol. A weak cortisol stress response results in reduced anti-inflammatory effects.

5. Links Between ADHD and Eating Disorders

5.1. Emotional Dysregulation and Impulsivity

Symptoms of emotional dysregulation and impulsivity appear to be an important link between eating disorders (particularly binge eating) and ADHD.69

5.2. Dopamine

ADHD, like obesity, is characterized by abnormalities in dopamine levels.70 While disordered eating in women correlated with elevated plasma dopamine levels, blood dopamine levels were reduced in men with eating disorders.71

Dopamine follows a circadian rhythm. Disorders in the circadian rhythm can contribute to metabolic syndrome.
A high-fat diet reduces the circadian peak of dopaminergic activity in the central nervous system’s pacemaker circuits and increases noradrenergic and serotonergic inputs to the ventromedial hypothalamus (VMH), which, through several downstream neuroendocrine events, leads to the cardiometabolic syndrome (hypertension, obesity, insulin resistance, glucose intolerance, dyslipidemia), while feeding behavior remains unchanged.72
The loss of the circadian peak in dopaminergic input to the SCN promotes noradrenergic/serotonergic hyperactivity in the VMH as well as NPY and CRH hyperactivity in the PVN, which triggers the insulin resistance syndrome.73 This physiological survival response system to low or no food availability (“therapeutic triad”) transforms into a “treacherous triad” when it occurs chronically rather than seasonally (low circadian peak dopamine activity in the SCN, increased NE/S activity in the VMH, and increased NPY/CRH activity in the PVN). This is more than sufficient to trigger and sustain the cardiometabolic syndrome.72
This is where treatment with the short-acting dopamine agonist bromocriptine comes into play; it is administered 2 hours after waking up.74

5.3. Stress

A study found no association between ADHD and stress-induced eating. Stress was not associated with the occurrence or amount of eating. Impulsivity, whether as a trait or a state, had no influence on the relationship between stress and eating.75

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