Prevalence of Attention DeficitHyperactivity Disorder in Women Who are Obese

Introduction

National Health Week (April 13-20, 2003) focused on the issue of obesity. I thought it would be interesting to look at the prevalence of ADHD in women who are obese. The issue of eating disorders and obesity in women with ADHD was first raised by Dr. John Fleming, Ph.D., and Lance Levy in the chapter on eating disorders and ADHD in Understanding Women with ADHD.

Fleming and Levy reported on their work in an obesity clinic in Canada. They found that women who were least successful in losing weight in their eating disorders treatment program had a much higher incidence of undiagnosed ADHD than in the general population.

Dr. Fleming wrote that he believed this pattern had several causes, all related to ADHD. For example, changing unhealthy patterns of overeating or binge eating requires planning and consistency – two capacities that are compromised by the executive functioning challenges associated with ADHD. After interviewing these women, the study concluded that many ate out of boredom and need for stimulation. One new approach at the clinic was to help them develop healthier sources of stimulation. It was postulated that because ADHD is a disorder of self-regulation, this might lead to problems with eating patterns.

Further Research

These findings have recently been replicated by Dr. Jules R. Altfas (Behavioral Medical Center for Treatment and Research, Portland, Oregon, USA) and published in BMC Psychiatry September 2002. Altfas’ study explored the prevalence and characteristics of patients with obesity, who were unable to lose weight or maintain a weight loss.

For this study, the clinical records of 215 patients (90% female) receiving obesity treatment during 2000 were reviewed. Data collected and analyzed included age, sex, beginning and ending body mass index (BMI), number of clinic visits, and months of treatment. Subjects were characterized by a variable level of obesity and ADHD symptoms and divided into one of three categories.

Classification Abbreviation
ADHD AD
some ADHD symptoms (ADSx)
non-ADHD (NAD)
Classification Abbreviation
overweight Ov
moderate to severe obesity I-II
extreme obesity III

The most important results of this study were the prevalence of ADHD (27.4%) in the sample, and the surprisingly strong association between ADHD and Obesity III. Nearly half, (42.6%), of patients with Obesity III had ADHD. That is, the ADHD population was concentrated in the obesity class having the highest mortality and morbidity risks, and greatest need for effective treatment.

Moreover, at all levels of obesity patients with ADHD symptoms were less successful at losing weight than non-ADHD peers. Compared to patients without ADHD, they had a significantly higher starting BMI (39.6 vs. 34.2), yet lost less weight (2.6 vs. 4.0 kg/m2). Greater contrast is found within the Obesity III category. Those without ADHD achieved more than twice the weight loss (7.0 vs. 2.9 kg/m2), while mean weight loss for those with ADHD symptoms (ADSx) did not differ significantly from those with ADHD (2.3 vs. 2.6 kg/m2), implying that the presence of even “subthreshhold” ADHD symptoms reduces the effectiveness of obesity treatment. In other words, in patients with ADHD and obesity, treatment outcome has stronger association with symptoms of ADHD than level of obesity.

The results also showed that those with ADHD actually attended more visits than those without (56.0 vs. 39.4 mean total visits), persisting over a longer span of time. Even though all three groups had similar rates of clinic visits on a monthly basis (AD 1.5 visits/month, ADSx 1.2 and NAD 1.4), patients without ADHD lost the most weight (NAD lost 0.14 BMI/month, ADSx 0.075 and AD 0.067).

It is also important to note that the 27.4% prevalence of ADHD in obese patients is considerably higher than found in the general adult population, (reported as 4.7% by Murphy and Barkley in 1996).

Why Might ADHD and Obesity Be Related?

The reasons for a strong association between ADHD and obesity (particularly extreme obesity) are unknown, but there are a number of reported findings that appear to be relevant and certainly interesting. For one, evidence exists that variations of dopamine receptor (DR) genes affect both conditions. In obesity, DRD2 and DRD4 genes, and in ADHD, the DRD4 gene, have been implicated in the transmission of, or predisposition to, the disorders, raising the possibility that similar, overlapping or shared DR functioning (or dysfunction) in these disorders is related to their co-occurrence.

DRD2 and a range of dopamine and other genes have been associated with a “reward deficiency syndrome” in which insufficient dopamine-mediated “natural” reward leads to use of “unnatural” rewards, such as substances, gambling, risk taking and inappropriate eating. This syndrome is associated with obesity, and common in ADHD. The DRD4 gene has been associated with “novelty seeking” traits, said to be greater in substance abusers, and individuals with both DRD2 and DRD4 genetic variations may be especially prone to multiple difficulties (e.g., having both ADHD and “reward deficiency syndrome”), further suggesting obesity and ADHD could share neurobiological attributes.

A recent study showed the availability of striatal DRD2 receptors was decreased as a function of increasing BMI, supporting the idea that reward-seeking behavior plays a role in the onset or continuation of obesity. In other studies, administration of D2 agonists resulted in decreases in hyperinsulinemia associated with obesity, and it is known that the brain is richly supplied with insulin receptors, including the cortex and striatal areas, suggesting an intriguing link between insulin resistance, characteristic of obesity, and dopamine-mediated psychiatric symptoms, including ADHD.

Conclusion

The association has important implications not only for treating obesity, but also for the diagnosis and treatment of ADHD. These findings may also have implications for the understanding of the etiology of obesity as well as the treatment of obesity. The nature of the connections between attention and obesity is still unclear, but the results may point to attentional components and impulsivity playing a role in the onset or continuation of obesity. Attentional mechanisms may be linked in some way to metabolic and energy storage regulation through dysregulation of common dopamine pathways. The finding of coexisting obesity and ADHD clearly needs to be replicated in larger and more systematic studies.

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