Stress: What It Actually Does to Your Body and Brain

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You know what stress feels like. The tension across your shoulders. The mind that will not switch off. The disproportionate response to a minor frustration at the end of a long day. The sense of being permanently slightly behind.

What most people do not know is what stress is actually doing — inside the body, inside the brain — when it has been present for long enough.

Stress is not a feeling. It is a physiological cascade. And when that cascade runs continuously, without adequate resolution, the consequences are not vague or metaphorical. They are measurable, documented, and significantly more far-reaching than most people appreciate until the damage is already done.

Up to now, you may have been managing stress as a psychological problem — trying to worry less, think differently, build resilience. But what if understanding the physiology changes what you actually do about it?

What stress actually is

The stress response is one of the most elegant systems in the human body. Faced with a threat — a predator, a social attack, a physical danger — the hypothalamus activates the HPA axis (hypothalamic-pituitary-adrenal axis) and the sympathetic nervous system simultaneously.

Adrenaline floods the system within seconds, producing the familiar fight-or-flight response: heart rate increases, breathing shallows, blood is redirected from digestive and reproductive organs to large muscle groups, pupils dilate, and pain sensitivity temporarily reduces. You are physiologically prepared to run or fight.

Cortisol follows within minutes, sustaining the response: glucose is mobilised for energy, immune function is temporarily suppressed (so that inflammatory responses do not slow you down in the moment), and non-essential functions — digestion, growth, reproduction — are deprioritised.

In the short term, this system is life-saving. It is also self-limiting: once the threat resolves, cortisol signals the hypothalamus to stand down, the sympathetic response decreases, and the parasympathetic nervous system restores baseline.

The problem is that modern stressors rarely resolve cleanly. A difficult relationship, an unmanageable workload, financial pressure, chronic pain, social threat — these are not predators that either catch you or do not. They persist. The system activates and stays activated. And a response designed to be temporary becomes, over months and years, a chronic physiological state.

What chronic stress does to the brain

The effects of chronic stress on the brain are not subtle, and they are not reversible by willpower.

The hippocampus shrinks. The hippocampus — central to memory formation, emotional regulation, and contextualising threat — is particularly vulnerable to prolonged cortisol exposure. Chronic stress produces measurable hippocampal volume reduction, impairing memory, increasing anxiety, and reducing the brain's capacity to put stressful experiences into proportion (McEwen, 2007). This is why chronic stress makes everything feel more threatening than it would otherwise — the brain's threat-contextualisation system is literally being degraded.

The amygdala becomes more reactive. While the hippocampus shrinks, the amygdala — the threat-detection system — becomes more sensitised under chronic stress. The result is a system that detects threat more readily and contextualises it less accurately: more reactive, less proportionate, slower to return to baseline.

The prefrontal cortex loses ground. The prefrontal cortex — responsible for rational thought, decision-making, impulse control, and emotional regulation — is functionally compromised by sustained cortisol exposure. The executive functions that allow you to think clearly, make good decisions, and regulate your emotional responses are exactly the functions that chronic stress impairs (Arnsten, 2009).

The practical consequence: the person under chronic stress is operating with a more reactive threat-detection system, a less effective regulatory system, and a degraded capacity for accurate contextualisation. They are not being irrational. Their brain has been physiologically reorganised by the stress they are carrying.

What chronic stress does to the body

The immune system. Cortisol is an immunosuppressant in the short term. Chronically elevated cortisol produces a paradoxical effect over time: immune dysregulation that increases susceptibility to infection, slows wound healing, and elevates pro-inflammatory cytokines — the same cytokines implicated in the neurobiological mechanisms of depression (Irwin & Cole, 2011). Chronic stress and chronic inflammation are closely linked, and both contribute to the physical conditions associated with poor mental health.

The cardiovascular system. Sustained sympathetic activation elevates blood pressure and heart rate, increases platelet aggregation, and contributes to arterial inflammation. Chronic stress is a significant independent risk factor for cardiovascular disease — not a contributing factor, but a direct one (Kivimäki & Steptoe, 2018).

The gut. The gut-brain axis is bidirectional: the brain communicates with the gut via the vagus nerve and the enteric nervous system, and the gut communicates back. Chronic stress disrupts gut motility, alters the gut microbiome, and increases gut permeability — producing the gastrointestinal symptoms (IBS, nausea, disrupted appetite) that accompany significant stress, and contributing to the inflammatory processes that affect mental health (Cryan et al., 2019).

Sleep. Elevated cortisol disrupts the sleep architecture described in the previous blog in this series. Cortisol and melatonin are antagonistic — one signals alertness, the other signals sleep. Chronic stress maintains cortisol at levels that interfere with sleep onset and sleep quality, which produces its own cascade of consequences for mental health.

Reproductive and metabolic function. Chronic stress suppresses reproductive hormone production and disrupts insulin sensitivity. The connections between chronic stress, hormonal disruption, and metabolic syndrome are well-documented and clinically significant — particularly for women navigating perimenopause alongside high occupational or relational demand.

The stress-mental health connection

Stress is not the same as anxiety or depression. But it is one of the most consistent precipitants of both.

Prolonged stress sensitises the HPA axis — making it more reactive to subsequent stressors and slower to return to baseline. This sensitisation is one of the mechanisms underlying the development of anxiety disorders: the threat-response system has been calibrated by experience to activate more readily and recover more slowly (Lupien et al., 2009).

The relationship between chronic stress and depression involves multiple pathways: neuroinflammation, hippocampal volume reduction, HPA axis dysregulation, sleep disruption, and the behavioural withdrawal that often accompanies sustained stress exposure. Depression is not caused by stress in a simple linear way — many people experience significant stress without developing depression — but stress is among the most consistently identified precipitating factors, particularly in the context of a sensitised stress-response system and insufficient recovery.

Burnout — the endpoint of prolonged occupational and relational stress — is addressed in a separate article in this series. What is worth noting here is that burnout is not simply extreme tiredness. It is a specific physiological and psychological state produced by sustained stress without adequate recovery, and its treatment requires addressing the physiology, not only the psychology.

Why "just relax" does not work

The advice to manage stress through relaxation, perspective, and attitude is not wrong. It is incomplete.

A nervous system that has been in chronic sympathetic activation does not relax because it has been told to. The prefrontal cortex that would normally modulate the stress response is the same system that chronic stress has been degrading. Trying to think your way to calm when the brain has been physiologically reorganised by stress is like trying to use a tool that the stress has already damaged.

Effective stress management has to work at the level of the physiology — not instead of psychological approaches, but before and alongside them. The autonomic nervous system needs to experience actual safety, not the idea of safety. That requires bottom-up approaches: movement, breathing, co-regulation, sleep, reduction of the actual stressor load.

Cognitive approaches — reframing, perspective-taking, cognitive restructuring — have a role. They are more effective when the nervous system is regulated enough to engage them. The sequence matters.

What actually helps

Reduce the load where possible. This sounds obvious. It is consistently under-prioritised because the dominant stress management narrative focuses on coping with stress rather than reducing it. A structural review of workload, relational demands, and recovery time is a legitimate clinical intervention — not a concession or a failure of resilience.

Physiological downregulation. Extended exhale breathing, slow rhythmic movement, cold water exposure to the face, and co-regulation with safe others all activate the parasympathetic nervous system and reduce cortisol. These are not relaxation techniques. They are physiological interventions with measurable effects on HPA axis activity.

Sleep. As covered in the previous article in this series — sleep is the primary mechanism by which the brain clears cortisol, restores prefrontal function, and resets the stress-response system for the following day. Treating sleep as optional under conditions of high stress is the equivalent of running an engine without oil.

Movement. Regular aerobic exercise reduces baseline cortisol, increases hippocampal neurogenesis (partially reversing the hippocampal shrinkage associated with chronic stress), and supports the parasympathetic recovery that chronic stress prevents (Cotman et al., 2007). The effect requires consistency rather than intensity.

Social connection. Co-regulation — the direct effect of a regulated nervous system on another nervous system via the social engagement system — is one of the most powerful and most underutilised stress buffers available. Isolation compounds stress physiologically, not only emotionally.

Psychological intervention. CBT addresses the cognitive patterns that amplify stress responses — catastrophising, all-or-nothing thinking, overestimation of threat. ACT addresses the relationship to stress: accepting its presence without being controlled by it, and acting in accordance with values rather than in the direction stress dictates. Both are evidence-based for stress-related presentations and are most effective when combined with the physiological approaches above.

If you are also neurodivergent

Neurodivergent adults carry a specific and significantly underacknowledged stress load.

The chronic effort of masking — managing sensory sensitivities, translating implicit social expectations, performing neurotypicality in professional and social environments — maintains sympathetic activation at a level that would be recognised as significant stress in any other context. This is not metaphorical. It is a physiological reality with the same consequences for the HPA axis, the immune system, and the brain as any other form of chronic stress.

The consequences accumulate in ways that the person often does not attribute to stress — because the masking effort is not experienced as stressful in the moment. It is simply the cost of being in the world. Autistic burnout is, in significant part, the endpoint of this accumulated physiological load.

For ADHD adults, the chronic experience of executive function demands exceeding executive function capacity — the gap between what is required and what the neurological system can reliably produce — is itself a sustained stressor that the standard stress management literature does not account for.

Resources for late-diagnosed neurodivergent adults navigating stress and burnout are available at Mindpath Academy.

When to seek professional support

Stress warrants professional attention when it is:

• Producing significant physical symptoms — disrupted sleep, gastrointestinal complaints, chest tightness, fatigue — that are not explained by a medical condition

• Significantly affecting your mood, relationships, or functioning

• Accompanied by anxiety or depression that is not resolving with self-directed approaches

• Connected to a work environment or relationship that is not safe or sustainable

• Producing thoughts of escape, self-harm, or not wanting to be here

A GP is the starting point for ruling out medical contributors and considering medication where indicated. A clinical psychologist can provide assessment and evidence-based treatment for stress-related presentations including anxiety, burnout, and depression.

→ The Stress Reset Workbook A 20+ page clinical workbook covering your personal stress audit, the physiology of your stress response, evidence-based regulation tools, and a structured plan for reducing your stress load and building sustainable recovery. $4.99.

→ Book a single coaching session with Dr Melanie du Preez One session. No package required. A clinical conversation about what is driving your stress response and where to start.

References

Arnsten, A. F. T. (2009). Stress signalling pathways that impair prefrontal cortex structure and function. Nature Reviews Neuroscience, 10(6), 410–422. https://doi.org/10.1038/nrn2648

Cotman, C. W., Berchtold, N. C., & Christie, L. A. (2007). Exercise builds brain health: Key roles of growth factor cascades and inflammation. Trends in Neurosciences, 30(9), 464–472. https://doi.org/10.1016/j.tins.2007.06.011

Cryan, J. F., O'Riordan, K. J., Cowan, C. S. M., Sandhu, K. V., Bastiaanssen, T. F. S., Boehme, M., Codagnone, M. G., Cussotto, S., Fulling, C., Golubeva, A. V., Guzzetta, K. E., Jaggar, M., Long-Smith, C. M., Lyte, J. M., Martin, J. A., Molinero-Perez, A., Moloney, G., Morelli, E., Morillas, E., … Dinan, T. G. (2019). The microbiota-gut-brain axis. Physiological Reviews, 99(4), 1877–2013. https://doi.org/10.1152/physrev.00018.2018

Irwin, M. R., & Cole, S. W. (2011). Reciprocal regulation of the neural and innate immune systems. Nature Reviews Immunology, 11(9), 625–632. https://doi.org/10.1038/nri3042

Kivimäki, M., & Steptoe, A. (2018). Effects of stress on the development and progression of cardiovascular disease. Nature Reviews Cardiology, 15(4), 215–229. https://doi.org/10.1038/nrcardio.2017.189

Lupien, S. J., McEwen, B. S., Gunnar, M. R., & Heim, C. (2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience, 10(6), 434–445. https://doi.org/10.1038/nrn2639

McEwen, B. S. (2007). Physiology and neurobiology of stress and adaptation. Physiological Reviews, 87(3), 873–904. https://doi.org/10.1152/physrev.00041.2006