Should Psychiatrists “Own” and Fully Embrace Obesity as a Brain-Based Disorder?

Obesity remains one of the most complex and rapidly evolving public health challenges in the United States. Psychiatrists frequently address the emotional, cognitive, and behavioral drivers of weight gain. Yet our field seldom engages with a critical question: if these processes fall squarely within psychiatry’s domain, should psychiatry be more formally involved in obesity care? This is not a call for ownership it is an invitation for reflection.

A growing body of research highlights the brain’s central role in regulating appetite, processing stress, and modulating reward. Neuroimaging studies show altered activation in the hypothalamus, insula, and reward circuits among individuals with obesity.¹ Traumatic stress, early adversity, chronic sleep disruption, and mood disorders further influence neurobiological pathways that shape eating behaviors and heighten vulnerability to weight gain.² These mechanisms overlap with circuits involved in addiction, affect regulation, impulsivity, and reward sensitivity core areas of psychiatric expertise.

Novel medications for obesity, including GLP-1 receptor agonists and emerging multi-agonists, act partly through central appetite and reward circuits.³ Patients describe experiences that sound familiar to psychiatric clinicians: decreased craving, altered reward patterns, improved cognitive control, and unexpected emotional shifts during weight loss.⁴ This raises important questions:

• Should residency programs include structured teaching on the neurobiology and psychiatric dimensions of obesity?
• Should collaborative care models integrate psychiatric expertise into obesity treatment pathways, rather than relying on ad-hoc consultation?
• How do we safeguard against malpractice while still offering evidence-based, compassionate care?

As obesity treatment increasingly centers on the brain, psychiatry’s potential role becomes harder to overlook.

Reframing obesity as a disorder with neurobiological foundations does not diminish personal responsibility or environmental realities. Nor should it reduce a person to their neurocircuitry. Instead, this approach fosters a more compassionate and comprehensive understanding of why weight change is difficult and why relapse is common.⁵

This reframing also surfaces key ethical questions:

• Can psychiatric framing reduce stigma and self-blame?
• Could it unintentionally reinforce medicalization or bias?
• How do we integrate neuroscience with culturally informed, trauma-sensitive care?
• How do we avoid pathologizing normal variation while validating lived experience?

These questions require nuance, humility, and interdisciplinary collaboration.

Psychiatry Is Already Involved, Just Not Formally

Psychiatrists routinely treat conditions deeply intertwined with obesity: binge-eating disorder, mood disorders, trauma-related dysregulation, chronic stress, insomnia, impulsivity and ADHD, and antipsychotic-induced weight gain.⁶ These are core areas of practice. The gap is not exposure but intentionality.

As science increasingly ties obesity to brain-behavior interactions, psychiatry may be at an inflection point. Integrating psychiatric expertise into obesity care could improve outcomes, reduce stigma, and address long-standing disparities particularly in communities disproportionately affected by both obesity and mental-health challenges.⁷

Perhaps this moment calls for collective reflection:

• What is psychiatry’s role in obesity?
• What should it be?
• And are we prepared to thoughtfully explore that possibility?

These questions do not demand immediate answers, but they are worth asking as the field evolves.

Finally, as a reminder: it took decades for our field to fully embrace addiction as a brain disease. Obesity may be undergoing a similar transition. Psychiatry can and should be part of this national conversation. Not to dominate it, but to deepen it.

References

1. New CDC data show adult obesity prevalence remains high. Centers for Disease Control and Prevention. September 12, 2024. Accessed January 5, 2026. https://www.cdc.gov/media/releases/2024/p0912-adult-obesity.html

2. Liu W, Li N, Tang D, et al. Multimodal neuroimaging of obesity: from structural-functional mechanisms to precision interventions. Brain Sci. 2025;15(5):446.

3. Dallman MF. Stress-induced obesity and the emotional nervous system. Trends Endocrinol Metab. 2010;21(3):159-165.

4. Podolsky MI, Raquib R, Shafer PR, et al. (2025). Factors associated with semaglutide initiation among adults with obesity. JAMA Netw Open. 2025;8(1):e2455222.

5. Thomsen RW, Mailhac A, Løhde JB, et al. Real-world evidence on the utilization, clinical and comparative effectiveness, and adverse effects of newer GLP-1RA-based weight-loss therapies. Diabetes Obes Metab. 2025;27 Suppl 2(Suppl 2):66-88.

6. Matikainen-Ankney BA, Kravitz AV. Persistent effects of obesity: a neuroplasticity hypothesis. Ann N Y Acad Sci. 2018;1428(1):221-239.

7. Rajan TM, Menon V. Psychiatric disorders and obesity: a review of association studies. J Postgrad Med. 2017;63(3):182-190.

8. Leutner M, Dervic E, Bellach L, et al. Obesity as pleiotropic risk state for metabolic and mental health throughout life. Transl Psychiatry. 2023;13(1):175.