Cortisol, ADHD, and perimenopause, understanding the stress system

Cortisol is the body’s key stress hormone, released by the adrenal glands as part of the hypothalamic-pituitary-adrenal (HPA) axis to help us respond to demands, threats and pressure. It plays an essential role in waking up, mobilising energy, supporting attention and orchestrating the physiological stress response.

Cortisol itself is not harmful. Its function is adaptive and protective when stress is short lived and the HPA axis can reset after demand. The problem arises when stress becomes chronic and the HPA axis stays activated or dysregulated. Prolonged stress can alter typical cortisol rhythms, leading to a flattened diurnal pattern and persistent dysregulation, which in turn is associated with impaired cognitive and emotional functioning as well as poorer physical health outcomes (Lei et al., 2025; Patel, 2025).

Chronic HPA axis activation also interacts with immune and inflammatory systems, which can further undermine health and resilience (Nunez et al., 2025). This pattern of chronic strain is known as allostatic load, the cumulative “wear and tear” on physiological systems due to repeated stress activation over time (McEwen & Stellar, 1993, cited in general stress literature).

Cortisol and ADHD

ADHD is not caused by cortisol, but many people with ADHD live with high baseline psychological and physiological load due to a more stress-sensitive nervous system, frequent executive functioning demands, emotional regulation challenges and social-environmental pressures. Some evidence suggests that HPA axis function differs in people with ADHD, with hypoactivity of basal secretion and altered stress responsiveness in some individuals (Fulun et al., 2025). Cortisol reactivity to stress has also been shown to differ in adults with ADHD compared with non-ADHD controls, with stronger or prolonged responses to stress in some contexts (Raz et al., 2015).

A meta-analysis of studies measuring cortisol in people with ADHD noted lower basal cortisol levels in youth with ADHD, particularly in the morning, which may reflect altered HPA axis regulation (Chang et al., 2021). Other research indicates that cortisol responses to acute psychosocial stress are heterogeneous in individuals with ADHD and may be influenced by psychiatric comorbidities (Bernhard et al., 2021). Taken together, these findings support the idea that stress hormone regulation and HPA axis function are not typical in many people with ADHD and may contribute to challenges in stress tolerance, cognitive performance and emotional regulation.

Cortisol in perimenopause and menopause

Perimenopause and menopause involve significant changes in reproductive hormones, notably oestrogen and progesterone. These fluctuations do not directly increase cortisol production, but they can reduce the body’s resilience to stress and can alter brain systems that regulate mood, cognition and stress responses. Recent reviews indicate that hormonal transitions in midlife can influence the HPA axis and emotional regulation pathways, which may increase vulnerability to psychological symptoms including anxiety, depression and perceived stress (Lang et al., 2025; Kuck et al., 2024).

Some studies also suggest links between estradiol fluctuations and cortisol levels in perimenopausal women with depressive symptoms, supporting the idea that interactions between sex hormones and the stress system can affect wellbeing (Liang et al., 2024). These interactions do not imply that cortisol is an ovarian hormone, but that the overall regulatory system for stress becomes more sensitive when sex hormone support changes.

What chronic stress and cortisol dysregulation feel like

When the stress response system is persistently activated or unable to settle quickly after demand, people commonly report:

• Feeling exhausted yet unable to rest fully
• Difficulty sleeping or disturbed sleep patterns
• Brain fog and memory issues
• Reduced stress tolerance and quicker overwhelm
• Heightened irritability and anxiety
• Greater challenges with executive function and sustained attention

These symptoms are consistent with chronic HPA axis strain and allostatic load, rather than a lack of willpower or motivation. Dysregulated stress physiology affects cognition, mood and energy, and can make everyday functioning more effortful.

Supporting the stress system

Supporting the stress system is not about relaxation alone. It is about reducing chronic load externally and internally, improving recovery capacity, and regulating demand signals before they escalate into prolonged stress responses.

Key elements include:

• Prioritising quality sleep and regular rest patterns
• Managing chronic demands and unrealistic expectations
• Building routine, regular nourishment to support metabolic and nervous system stability
• Integrating gentle, consistent movement rather than sporadic extremes
• Recognising early signals of stress overload before collapse
• Setting boundaries and intentional pauses in the day

These strategies aim to reduce chronic HPA axis activation and improve the body’s ability to reset between demands.

There are also medical and nutritional factors that can influence stress physiology, but these need individual consideration and are a subject in their own right.

References

Bernhard, A., Mayer, J.S., Fann, N. and Freitag, C.M., 2021. Cortisol response to acute psychosocial stress in ADHD compared to conduct disorder and major depressive disorder: systematic review. Neuroscience and Biobehavioral Reviews [online]. Available at: doi:10.1016/j.neubiorev.2021.XXXX (accessed Month Year).

Chang, J.P.C., et al., 2021. Cortisol and inflammatory biomarker levels in youths with ADHD: a meta-analysis. Translational Psychiatry [online]. Available at: doi:10.1038/s41398-021-01550-0 (accessed Month Year).

Fulun, L., et al., 2025. Hypothalamic-pituitary-adrenal axis dysfunction in children with ADHD: systematic review. Journal of Psychiatric Research [online]. Available at: PubMed ID 40974807 (accessed Month Year).

Kuck, M.J., et al., 2024. Stress, depression, anxiety across menopausal stages. Frontiers in Psychiatry [online]. Available at: doi:10.3389/fpsyt.2024.1323743 (accessed Month Year).

Lang, X.L., et al., 2025. From physiology to psychology: integrated review of menopause syndrome mechanisms. Frontiers in Neuroscience [online]. Available at: PMC article (accessed Month Year).

Liang, G., et al., 2024. Menopause-associated depression: impact of oxidative stress and interactions with cortisol. Biomedicines [online]. Available at: doi:10.3390/biomedicines12010184 (accessed Month Year).

Lei, A.A., Phang, V.W.X., Lee, Y.Z., Kow, A.S.F., Tham, C.L., Ho, Y.C. and Lee, M.T., 2025. Chronic stress-associated depressive disorders: impact of HPA axis dysregulation and neuroinflammation. International Journal of Molecular Sciences, 26(7), p.2940.

Patel, H., 2025. Assessment of HPA axis function in chronic stress: correlation with cortisol rhythms and immune markers. Healthcare Bulletin [online]. Available at: article (accessed Month Year).