Eating disorders and obesity are common in ADHD.
1. ADHD and overweight/obesity/obesity¶
1.1. ADHD twice as common in obesity (children + 20%, adults + 55%)¶
The prevalence of ADHD is higher in people who are extremely overweight than in the general population. In an extremely long duration study over 33 years, it was found that 41.4% of all men who suffered from ADHD-C as children developed massive obesity as adults, compared to only 21.6% of those without a childhood ADHD diagnosis. The frequency of obesity in ADHD sufferers doubled (albeit at extremely different starting levels) in the USA from 21.6 % without ADHD to 41.4 % with ADHD and in Germany from 10.2 % without ADHD to 22.1 % with ADHD.
An Israeli cohort study found obesity to be almost twice as common in adolescents with severe ADHD (13.5%) as in those without ADHD and around 30% more common in those with mild ADHD than in those without.
A meta-study of 42 studies with n = 728,136 participants found:
Obesity increases the risk of ADHD in children by 20% (OR = 1.20) and in adults by 55% (OR = 1.55)
ADHD increases the risk of obesity in children by 40 % (10.3 % compared to 7.4 %) and in adults by 70 % (28.2 % compared to 16.4 %)
ADHD is a significant risk factor for the development of obesity. Impulsivity in ADHD and increased BMI share genetic and neurophysiological correlates. ADHD, alcohol dependence, insomnia and heavy smoking correlate with an increased body fat percentage.
Attention problems and hyperactivity correlated positively with response to food, emotional overeating, the desire to drink and a slowdown in eating. Attention problems reduced the enjoyment of food. Conversely, eating behavior does not appear to be causal for ADHD. Normal overweight (below obesity) is also not thought to increase the likelihood of ADHD.
A long-term cohort study in the USA found a linear correlation between the number of ADHD symptoms and the factors waist circumference, BMI, obesity, diastolic blood pressure and systolic blood pressure. An Israeli study also points to this.
The comorbidity of ADHD was 58% in a study of extremely overweight children treated as inpatients.
Among 155 adult women in Brazil with a BMI > 39, an ADHD rate of 28.3% was found. Binge eating, bulimia and depression were also above average. The probability of ADHD was therefore 6.4 times higher than the expected prevalence of 4.4% in adults.
The body mass index of ADHD sufferers is also above average.
A minority of studies found no association between ADHD and BMI. One study found no association of ADHD with BMI at age 9 or 13. However, children with ADHD at age 9 were significantly more likely to be overweight/obese than children without ADHD. However, this was not due to ADHD, but to other child and parental factors such as female gender, little exercise, overweight/obese parents and prenatal smoking during pregnancy. A smaller study found no overlap between obesity and ADHD or autism spectrum disorders in 76 adolescents. Another study found no correlation between ADHD and high BMI, but did find a correlation between unhealthier eating habits and ADHD in adolescents.
A meta-analysis found an ADHD prevalence of between 1.6% and 18% in those affected by eating disorders. Comorbid ADHD was more common in the AN binge-eating/purging subtype and in the bulimia subtype than in the restrictive anorexia subtype.
In ADHD sufferers, the meta-study found a lifetime prevalence of eating disorders between zero and 21.8% in women with ADHD.
Massive obesity is also associated with sleep apnea, shortened sleep and other sleep problems.
Conversely, sleep problems are the most common comorbidity in ADHD. See also Sleep problems with ADHD and Comorbidity in ADHDunder sleep problems.
In adults without an ADHD diagnosis, daytime sleepiness correlates with the degree of ADHD symptoms.
1.2. ADHD treatment works against obesity¶
ADHD treatment can lead to surprising success in weight reduction in massively overweight patients. The ADHD-positive diagnosed obese patients lost over 12% weight per year under typical ADHD medication.
For comparison: according to the current standard, treatment for obesity is successful if the weight gain does not exceed 5% per year.
Other studies also reported a reduction in an excessive BMI as a result of ADHD treatment in ADHD sufferers.
1.3. Stomach reduction less effective for ADHD symptoms?¶
One study found reduced weight loss after stomach reduction in those with emotional dysregulation, a core symptom of ADHD.
1.4. Obesity and addictive behavior¶
Around half of all overweight people who have had a stomach reduction subsequently develop another addiction. This is impressive proof that obesity is a consequence of addiction.
It is well known that ADHD causes a massive disruption of the reward system, with the result that rewards that are further away are significantly less interesting compared to those who are not affected. Food can provide this instant gratification.
In ADHD, the potential for addiction is significantly increased overall. This applies to legal addictive substances such as smoking, caffeine, alcohol or food as well as illegal addictive substances such as marijuana, amphetamines or cocaine.
Nicotine and caffeine are just as much stimulants as the typical ADHD medications.
Amphetamines, cocaine and marijuana - in specific forms - are effective as drugs.
The difference between addictive substances and drugs is that addictive substances (including nicotine) have a rapid onset and address a very high number of the respective receptors, whereas drugs rise and fall slowly, occupy only a small proportion of the receptors and therefore do not cause intoxication-like states. As with any substance, the dose makes the poison.
2. ADHD and eating disorders¶
Eating disorders occur 3.6 times more frequently in girls with ADHD than in girls without the disorder.
2.1. Binge eating twice as often¶
Eating disorders such as binge eating (very roughly: binge eating without vomiting) are also suspected to correlate with ADHD and contribute to weight problems.
In obese patients (BMI > 30), ADHD doubles the likelihood of binge eating and increases the likelihood of other eating disorders.
Among 150 adult women with a BMI over 39, an ADHD rate of 28.2% was found. Binge eating, bulimia and depression were also above average.
2.2. Bulimia nervosa 6 to 8 times more common in women with ADHD¶
Bulimia nervosa (very roughly: binge eating with vomiting) is found in 11% to 12% of adult women with ADHD (according to DSM-III-R criteria) compared to around 1% to 3% of women without ADHD. There are no differences between men and children. Assuming a 1.5% prevalence of bulimia nervosa, this would result in an 8-fold increase in the frequency for women with ADHD.
2.3. Anorexia is 2.2 times more common with ADHD¶
Girls and women with ADHD are “only” 2.2 times more likely to suffer from anorexia/anorexia (very roughly: vomiting without binge eating) than girls and women without ADHD.
2.4. Compulsive grazing (snacking) increases the risk of ADHD by 8 times¶
Grazing is the unstructured, repetitive eating of small amounts of food over an extended period of time outside of planned meals and snacks and/or not in response to feelings of hunger or fullness. There are two subtypes of grazing:
- compulsive grazing
- Feeling that you cannot resist or stop grazing
- Population prevalence 10.2 %
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ADHD prevalence among those affected approx. + 800 % (OR 8.94)
- correlates with
- stronger psychopathology of the eating disorder
- increased psychological stress
- lower psychological quality of life
- lower treatment success in patients with high body weight
- non-compulsive subtype
- i.e. repeated, distracted eating
- Population prevalence 38 % to 90 %
3. ADHD and diabetes¶
Of 677,587 German children and adolescents, 16,833 were diagnosed with ADHD (2.5%), while 3668 were treated with insulin for type 1 diabetes mellitus (0.05%). In the subgroup of diabetes sufferers, 153 children (4.2%) also had an ADHD diagnosis. This indicates that ADHD sufferers have a greatly increased prevalence of type 1 diabetes and vice versa.
4. Cortisol, metabolism and body fat¶
Glucocorticoids (such as cortisol) play a central role in the regulation of carbohydrate metabolism by influencing gluconeogenesis.
Glucocorticoids also initiate and regulate a large number of digestive enzymes, the expression of membrane-bound transporter proteins, and proteins that are significantly involved in gluconeogenesis.
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Cortisol increases the success of pleasurable or compulsive activities (intake of sucrose, fat and drugs or cycling). This motivates the intake of “comfort food”.
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Cortisol systemically increases the fat deposits in the abdomen. This causes
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Inhibition of catecholamines in the brain stem and
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Inhibition of CRH expression in the hypothalamus, which subsequently inhibits ACTH
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Cortisol acts on the fatty tissue via insulin
Possible consequences:
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Visceral obesity
- Insulin resistance
- Dyslipidemia
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Cortisol increases adrenaline-induced lipolysis (fat splitting, fat digestion).
The impairment can be exacerbated by reduced ACTH levels.
It is possible that this correlation is reversed in severely overweight people (see below).
- While chronic stress and high glucocorticoids increase body weight gain in rats, in humans this causes either increased food intake and weight gain or decreased food intake and weight loss.
- Several studies show a correlation between the cortisol stress response and the waist-to-hip ratio, so that a low cortisol stress response is associated with a low waist-to-hip ratio (less pronounced waist), while a high cortisol stress response is associated with a high waist-to-hip ratio (pronounced waist).
- Abnormalities of fat metabolism (hypertriglyceridemia), which occur more frequently in the type A personality, can be eliminated by ACTH administration, but not by cortisol administration.
The described ACTH effect would be consistent with this hypothesis of an underreactivity of the HPA-A axis in type A.
Type A ADHD sufferers (then: ADHD-HI = with hyperactivity) could have a genetic predisposition or permanent stress
→ have led to a long-lasting increased release of CRH,
→ which triggers CRH receptor downregulation,
→ which causes underactivation of the pituitary gland,
→ which triggers a reduced release of ACTH,
→ which causes reduced adrenal gland activity,
→ which results in a reduced release of cortisol,
→ which is why only the MR receptors, but not the GR receptors, are addressed when the HPA axis is activated at the end of a stress response,
→ which means that the HPA axis is not switched off properly.
- The noradrenaline level in the OFC and in the amygdala correlates with the activation of the HPA axis in healthy people. In severely overweight people, however, this correlation is inverted.
The endocrine stress responses of noradrenaline and cortisol run in parallel. In ADHD-HI (with hyperactivity), not only the cortisol stress response but also the noradrenaline stress response is reduced.
- Obesity is characterized by high oxidative stress and inflammation. Inflammation is inhibited by cortisol. A low cortisol stress response results in reduced inhibition of inflammation.
5. Links between ADHD and eating disorders¶
5.1. Emotional dysregulation and impulsivity¶
An important link between eating disorders (especially binge eating) and ADHD appears to be the symptoms of emotional dysregulation and impulsivity.
5.2. Dopamine¶
Both ADHD and obesity are characterized by deviations in the dopamine balance. While disordered eating behavior in women correlated with an increased plasma dopamine level, the blood dopamine level was reduced in men with eating disorders.
