top of page

The Intersection of Obesity and Neurodivergence

Writer: Dean KilbyDean Kilby

A Compassionate, Evidence-Based Perspective


A stylized illustration of a brain with bright blue and orange interwoven lines against a dark background, creating a neon-like, technical effect.

Obesity and neurodivergence are complex, deeply personal experiences that can shape an individual’s life in profound ways. Emerging research suggests that obesity may contribute to neurodivergent phenotypes through neurobiological, genetic, and neuroendocrine pathways. However, it is crucial to approach this topic with both scientific rigour and compassion, recognising that no one is defined by their neurology or physiology. The human brain is plastic, capable of adaptation and transformation, and outcomes depend on the commitments we make rather than any fixed traits.



The Neurobiological Links Between Obesity and Neurodivergence


  1. Neuroendocrine Dysfunction and Brain Function

    Obesity has been linked to dysregulation in the hypothalamo-pituitary-adrenal (HPA) axis, a system that plays a crucial role in stress regulation, metabolism, and behaviour. Disruptions in this axis can affect mood, cognition, and impulse control—traits commonly seen in neurodivergent individuals (Perelló & Spinedi, 2004). Additionally, changes in leptin and insulin signalling, hormones critical for metabolism, can impact neuroplasticity and executive function, potentially influencing traits associated with ADHD, autism, and other neurodivergent profiles.

  2. Neuropeptide Y and Cognitive Function

    Neuropeptide Y (NPY) is a powerful neurotransmitter that regulates hunger, stress responses, and emotional processing. Overexpression of NPY, commonly seen in obesity, has been linked to alterations in reward-related brain circuits and impulse control (Kaga et al., 2001). Since these circuits overlap with pathways involved in attention, motivation, and executive functioning, obesity-related changes in NPY expression could contribute to neurodivergent traits.

  3. Structural and Functional Brain Changes

    Obesity has been associated with measurable changes in brain structure, particularly in the prefrontal cortex, hippocampus, and limbic system—regions responsible for executive function, memory, and emotional regulation (Vainik et al., 2017). These structural differences may contribute to difficulties in impulse control, working memory, and emotional processing, all of which are commonly seen in conditions such as ADHD and autism.

  4. Genetic Overlaps Between Obesity and Neurodivergence

    Genetic studies have found significant overlap between obesity-related genes and those associated with neurodevelopmental disorders. Children with genetic risk factors for obesity often show reduced cortical volume and increased impulsivity—traits commonly linked to ADHD and other neurodivergent conditions (Morys et al., 2022). Additionally, extreme obesity has been linked to genetic variants associated with neuropsychiatric conditions, suggesting a potential shared biological pathway (Stahel et al., 2019).



The Brain Is Plastic: No Identity Is Fixed


While these findings highlight the biological intersections between obesity and neurodivergence, it is essential to remember that no brain is fixed or “normal.” The human brain is neuroplastic, meaning it is constantly reshaping itself in response to experience, behaviour, and environment. This means that:


  • One is not defined by their neurology. Whether someone identifies as neurodivergent or not, their cognitive traits can shift over time based on lifestyle, interventions, and personal commitments.


  • Neuromodulation and behavioural strategies can shape outcomes. Techniques such as meditation, cognitive training, metabolic interventions, and even neuromodulation (e.g., transcranial stimulation) have shown promise in improving executive function, impulse control, and cognitive flexibility.


  • Health outcomes are driven by commitment, not identity. A person is not an ADHD brain or an obese body—they are a dynamic, adaptable individual capable of making changes based on their goals.



Compassion Over Stigma: Reframing the Conversation


Too often, discussions around obesity and neurodivergence carry stigma, implying fixed limitations rather than acknowledging the potential for change. Instead of viewing obesity as a cause of neurodivergence or vice versa, it is more helpful to see both as interconnected aspects of the human experience, influenced by biology, environment, and personal choices.


  • Blame is unhelpful; understanding is empowering. Recognising the biological links between obesity and neurodivergence does not mean resigning to fate—it means we can explore targeted, evidence-based strategies to support individuals in achieving their goals.


  • Support and autonomy go hand in hand. Every individual deserves respect and agency in their journey, whether they choose to embrace their neurodivergent traits, seek interventions, or pursue specific health outcomes.


  • There is no “normal” brain. The idea of a standard or ideal brain is a myth. Every person has a unique neurological makeup that can be shaped, adapted, and optimised according to their values and aspirations.



Conclusion: Outcomes Over Labels


The emerging evidence suggests that obesity can influence neurodivergent traits through genetic, neuroendocrine, and neurodevelopmental pathways.However, this does not mean that individuals are locked into a particular identity or experience. The human brain is adaptable, and outcomes depend on the specific goals one commits to rather than any predetermined neurological category.


Whether one identifies as neurodivergent, struggles with obesity, or simply seeks to understand these connections, the most important takeaway is that change is always possible. Through neuromodulation, behavioural strategies, and compassionate self-awareness, individuals can shape their own cognitive and health trajectories in ways that align with their personal aspirations.


No brain is broken. No brain is fixed. The only question is: What outcomes do you choose to create?



Simplr Health

Education • Understanding • Results

 

References

Kaga, T., Yamada, K., Hattori, E., Toyoshima, R., Iwayama, Y., Toyota, T., Minabe, Y., & Yoshikawa, T. (2001). Neuropeptide Y gene polymorphism and its impact on the risk of obesity and psychiatric disorders. Neuroscience Research, 41(3), 253-258. https://doi.org/10.1016/S0168-0102(01)00254-9


Morys, F., Nijenhuis, W., Vertes, P. E., O’Donoghue, M. C., Murray, G. K., & Vértes, P. E. (2022). Obesity-related genetic risk is associated with altered brain structure and impulsivity in children. Molecular Psychiatry, 27(4), 1718-1726. https://doi.org/10.1038/s41380-021-01162-4


Perelló, M., & Spinedi, E. (2004). Neuroendocrine and metabolic dysfunctions in obesity: A role for the hypothalamo-pituitary-adrenal axis? International Journal of Obesity, 28(3), 370-381. https://doi.org/10.1038/sj.ijo.0802569


Stahel, M. C., Xu, W., Metzger, I. V., Tönjes, A., Kovacs, P., Stumvoll, M., & Scholz, M. (2019). Severe obesity is associated with higher burden of rare variants in neurodevelopmental disorder genes. International Journal of Obesity, 43(8), 1527-1535. https://doi.org/10.1038/s41366-018-0242-6


Vainik, U., Baker, T. E., Dadar, M., Zeighami, Y., & Dagher, A. (2017). Neurobehavioral correlates of obesity are largely heritable. Proceedings of the National Academy of Sciences, 115(37), 9312-9317. https://doi.org/10.1073/pnas.1718206115

 
 
 

Kommentare


bottom of page