Eating Disorders and Obesity Share Surprising Root Causes

The Problem with Labels

Here is a paradox that should unsettle anyone who thinks we understand eating disorders and obesity.

In 2006, a group of researchers gathered in Port Douglas, a small town in tropical north Queensland, Australia. They were members of the Eating Disorder Research Society, and they had an idea that seemed almost heretical at the time. They wanted to write a handbook that treated eating disorders and obesity as two sides of the same coin. Not as separate problems with separate causes, separate treatments, and separate stigmas. But as conditions that share deep, hidden roots.

The result, published in 2008 and now in its third edition in 2024, is a 59-chapter, 70-author handbook edited by Stephan Herpertz, Martina de Zwaan, and Stephan Zipfel. It is not a pop science book. It is a dense reference work for clinicians and researchers. But buried in its pages is a finding that changes how we should think about both conditions.

The authors found that anorexia nervosa and severe obesity are not polar opposites. They are cousins. They emerge from the same disrupted relationship between the brain, the body, and the environment. And the implications for treatment are radical.

What If We Have Been Asking the Wrong Question?

For decades, we have treated eating disorders and obesity as if they belong to different galaxies. Anorexia is a psychiatric illness. Obesity is a metabolic disease. One gets sympathy and research funding. The other gets judgment and diet plans. But the handbook's authors argue this division is not just wrong. It is harmful.

Herpertz and his colleagues point to a growing body of evidence that both conditions share core features: disordered eating, body image disturbance, and a profound dysregulation of the brain's reward and inhibition systems. The difference is not in the kind of problem but in the direction it takes. One person restricts. Another binges. Both are trapped.

Consider this: in the general population, the lifetime prevalence of binge eating disorder is about 2 to 3 percent. But among people seeking treatment for obesity, that number jumps to 20 to 30 percent (Herpertz et al., 2024). That is not a coincidence. It is a signal that we have been ignoring.

The Brain Does Not Know Your BMI

The handbook draws on neuroscience that has quietly accumulated over the last two decades. The key player is the dopaminergic reward system, the same circuitry that makes chocolate taste good and cocaine feel euphoric. In people with anorexia, this system is underactive. Food does not feel rewarding. In people with obesity, it is also underactive, but for a different reason. Chronic overeating desensitizes the system, so you need more food to get the same hit.

The endpoint is the same: a brain that cannot regulate its own intake. One person starves. The other gorges. Both are trying to solve the same problem of a broken reward system.

Herpertz and his colleagues describe this as a "transdiagnostic" framework. The term is jargon, but the idea is simple. Instead of asking "Does this patient have anorexia or obesity?" we should ask "What is the underlying mechanism driving their disordered eating?" The answer might be the same for both.

The Numbers That Matter

The handbook is not a single study. It is a synthesis of hundreds of studies. But here are some of the findings that the authors highlight:

• ▸Among patients with bulimia nervosa, 30 to 50 percent have a history of obesity (Herpertz et al., 2024).
• ▸Among patients with binge eating disorder, 40 to 60 percent are obese (Herpertz et al., 2024).
• ▸The heritability of anorexia is estimated at 50 to 60 percent. The heritability of obesity is 40 to 70 percent. These numbers overlap (Herpertz et al., 2024).
• ▸Both conditions are associated with elevated rates of anxiety, depression, and substance use disorders (Herpertz et al., 2024).

These are not small overlaps. They are the kind of numbers that should make researchers in both fields sit up and take notice. But they rarely do, because the two fields have been siloed for so long.

How the Silos Were Built

To understand why this matters, you have to understand how we got here.

In the 1970s and 1980s, eating disorders were seen as rare, mysterious conditions affecting mostly young white women. Obesity was seen as a lifestyle problem affecting people who ate too much and moved too little. The research communities grew separately. Eating disorder researchers focused on psychology and trauma. Obesity researchers focused on metabolism and genetics.

The handbook traces this history. The authors note that it was only in the 1990s that binge eating disorder was formally recognized as a distinct diagnosis. Before that, people who binged were either classified as having bulimia (if they purged) or as having obesity (if they did not). There was no category for the person who binged without purging and was not necessarily overweight.

This category error has real consequences. A person with binge eating disorder who is normal weight gets referred to a psychiatrist. A person with binge eating disorder who is obese gets referred to a bariatric surgeon. They have the same problem. They get completely different treatments.

What the Research Actually Shows

The handbook is careful not to overstate its claims. The authors do not say that eating disorders and obesity are the same disease. They say they share "common etiological factors." Let me translate: they come from the same soil but grow into different plants.

The soil includes:

• ▸Genetic vulnerability. Certain gene variants increase the risk for both conditions. The FTO gene, for example, is strongly linked to obesity. But it also appears to influence eating behavior in ways that could predispose someone to binge eating (Herpertz et al., 2024).
• ▸Childhood trauma. Adverse childhood experiences, especially emotional abuse and neglect, are risk factors for both eating disorders and obesity. The mechanism is thought to be dysregulation of the stress response system (Herpertz et al., 2024).
• ▸Dieting history. This is the counterintuitive one. Restrictive dieting is a risk factor for both obesity and eating disorders. The more you try to control your weight, the more likely you are to lose control entirely (Herpertz et al., 2024).
• ▸Body dissatisfaction. This is the most obvious shared factor, but it is also the most neglected. Both groups of patients hate their bodies. The difference is that one group tries to shrink their body through restriction, and the other feels hopeless about ever changing it.

The Treatment Implications

If the root causes are shared, then treatment should be shared too. But it is not.

The standard treatment for anorexia is cognitive behavioral therapy (CBT) plus medical monitoring to prevent refeeding syndrome. The standard treatment for obesity is a combination of diet, exercise, and sometimes bariatric surgery. These are not the same. They are not even in the same building.

The handbook argues for a transdiagnostic approach. The authors point to evidence that CBT adapted for eating disorders is effective for many patients with obesity who have binge eating disorder. The same techniques that help an anorexic patient learn to eat regularly can help an obese patient learn to stop bingeing.

But there is a catch. Most obesity treatment programs do not screen for eating disorders. And most eating disorder treatment programs do not address obesity. Patients fall through the cracks.

What This Research Does Not Prove

I need to be honest with you. The handbook is a synthesis, not a definitive study. It is based on observational and correlational data. The authors cannot prove that eating disorders and obesity share a single cause. They can only show that they share many correlates.

There is also a political problem. The eating disorder community has fought hard to be taken seriously as a psychiatric condition. Some researchers worry that lumping eating disorders with obesity could undermine that progress. Obesity is still heavily stigmatized. If anorexia is seen as "just another form of obesity," it might lose the sympathy it has fought for.

The authors acknowledge this tension. They do not resolve it. They simply present the evidence and let the reader decide.

The Missing Piece

One of the most provocative sections of the handbook deals with what the authors call "the obesity paradox." In epidemiological studies, people with anorexia have the highest mortality rate of any psychiatric disorder. People with severe obesity also have elevated mortality, but not as high. Why?

The answer, the authors suggest, may be that anorexia kills through starvation, while obesity kills through metabolic complications. But both are forms of malnutrition. One is too little food. The other is too much of the wrong food. Both are failures of the body's ability to regulate energy balance.

This is not just a scientific question. It is a moral one. If we accept that both conditions are biological, not moral failures, then we have to change how we treat people. No more blaming the anorexic for refusing to eat. No more blaming the obese person for eating too much. Both are trapped in a system they did not choose.

The Biology of Blame

The handbook includes a chapter on neurobiology that is worth reading for its sheer detail. The authors describe how the hypothalamus, the brain's energy center, is dysregulated in both conditions. In anorexia, it is hyperactive, constantly signaling that the body is in danger of starvation. In obesity, it is hypoactive, failing to register that the body has enough energy stores.

But here is the twist. Both patterns can be triggered by the same environmental factor: chronic stress. When you are under chronic stress, your hypothalamus changes its set points. It becomes less sensitive to signals of fullness and more sensitive to signals of threat. You either eat too little or too much, depending on your biology and history.

This is not a choice. It is a biological adaptation to a toxic environment.

What This Actually Means

Let me give you the takeaways that matter for your life, your work, or your understanding of these conditions.

• ▸Stop treating eating disorders and obesity as opposites. They share more than they differ. If you work in healthcare, screen for both in every patient. A person with obesity may have an eating disorder. A person with anorexia may have a history of obesity. Do not assume.

• ▸Dieting is not the solution. Restrictive dieting is a risk factor for both conditions. The evidence is clear: the more you restrict, the more likely you are to binge. The answer is not more control. It is better regulation.

• ▸Treat the brain, not just the body. Both conditions are brain disorders. They are not willpower problems. They are not lifestyle choices. They are dysregulations of the reward, inhibition, and stress systems. Treatment should target these systems, not just the symptoms.

• ▸Screen for childhood trauma. Adverse childhood experiences are a major risk factor for both conditions. If you are treating someone for an eating disorder or obesity, ask about their history. It may be the key to their recovery.

• ▸Stop blaming patients. The evidence is overwhelming that both conditions have strong biological and genetic components. Blaming people for their weight or their eating is like blaming them for their eye color. It is not just wrong. It is counterproductive.

The Future

The handbook ends with a call for integration. The authors want a future where eating disorder clinics and obesity clinics are the same place. Where patients are assessed for both conditions simultaneously. Where treatment targets the underlying mechanisms, not the surface symptoms.

That future is not here yet. But the evidence for it is. And as the authors note, the idea was born in a small Australian town in 2006. It has taken nearly two decades to mature. But it is ready.

The question is whether we are ready to listen.