3 minute read

The stress response is a physiological system, not a personality trait. When your brain perceives a threat, whether that is a deadline, a difficult conversation, a poor night of sleep, or a hard training session, it activates the same hormonal cascade. The hypothalamic-pituitary-adrenal (HPA) axis signals the adrenal glands to release cortisol. Glucose is mobilised. Processes such as digestion, immune regulation, and reproductive function may receive less physiological priority during periods of acute stress.

This is not a flaw. It is a survival system doing exactly what it was designed to do. The problem is not stress itself. It is a budget that is consistently spent and rarely replenished.

Your stress-response systems react to many different forms of demand, even when those demands do not feel stressful in the traditional sense. Work pressure, disrupted sleep, skipped meals, intense exercise, poor diet quality, long commutes, and an unending queue of small decisions all draw from the same account.

Research on allostatic load, the cumulative physiological cost of chronic stress exposure, shows that when the body is repeatedly activated without adequate recovery, the systems that manage stress become less efficient over time. The result is not simply feeling stressed. It is measurable dysregulation across cortisol rhythms, immune function, and metabolic health.

Most people only count the obvious withdrawals. The presentation that kept them up until midnight. The family crisis. The difficult performance review.

They do not count the rest.

In midlife, many people find the budget feels smaller.

Oestrogen plays a significant role in regulating HPA axis activity and supporting recovery after a stressor. As it declines through perimenopause and menopause, cortisol regulation becomes less precise and the time required to return to baseline after activation increases. Research suggests that in postmenopausal women, cortisol no longer follows as clear a daily rise and fall as it did previously.

Age-related testosterone decline may similarly reduce stress resilience and affect recovery, sleep, and body composition.

This is not decline for its own sake. It is a system with less buffer asking for more accurate accounting.

The presentation is familiar to many people at this life stage. Fatigue that sleep does not fully resolve. Cravings that feel difficult to explain through hunger alone. Motivation that has gone quiet. Difficulty recovering from exercise. Increased abdominal fat storage despite no obvious change in eating.

These are not character failings. They are downstream symptoms of a chronically overdrawn system.

The answer is not to generate more willpower. It is to audit where the budget is going and begin making consistent deposits.

Sleep is the highest-yield deposit available. During healthy sleep, activity of the body's stress-response systems is reduced and many key recovery processes occur. Chronic sleep restriction, often defined in research as fewer than seven hours per night for adults, is independently associated with elevated cortisol, increased insulin resistance, and reduced capacity to regulate stress the following day.

Everything else, nutrition quality, movement type, recovery practices, builds on that foundation. Address them in that order and the budget begins to recover.

You are not broken. You are overdrawn. That is a problem worth solving.

The first step is understanding where the withdrawals and deposits are really coming from.

Want to understand where your health actually stands right now?

McEwen, B.S. (1998). Stress, adaptation, and disease: Allostasis and allostatic load. Annals of the New York Academy of Sciences, 840(1), 33–44.

Seeman, T.E., Singer, B.H., Rowe, J.W., Horwitz, R.I., & McEwen, B.S. (1997). Price of adaptation: Allostatic load and its health consequences. Archives of Internal Medicine, 157(19), 2259–2268.

Hannibal, K.E., & Bishop, M.D. (2014). Chronic stress, cortisol dysfunction, and pain: A psychoneuroendocrine rationale for stress management in pain rehabilitation. Physical Therapy, 94(12), 1816–1825.

Genazzani, A.R., Pluchino, N., Luisi, S., & Luisi, M. (2007). Estrogen, cognition and a woman's risk of Alzheimer's disease. Annals of the New York Academy of Sciences, 1089(1), 239–254. (used for oestrogen's role in HPA axis modulation)

Spiegel, K., Leproult, R., & Van Cauter, E. (1999). Impact of sleep debt on metabolic and endocrine function. The Lancet, 354(9188), 1435–1439.

Liu, P.Y., Takahashi, P.Y., Yang, R.J., Iranmanesh, A., & Veldhuis, J.D. (2020). Age and time-of-day differences in the hypothalamo-pituitary-testicular, and adrenal, response to total overnight sleep deprivation. Sleep, 43(7), zsaa008. (directly compares older and younger men; replaces Leproult 2011)

Liu, P.Y., & Reddy, R.T. (2022). Sleep, testosterone and cortisol balance, and ageing men. Reviews in Endocrine and Metabolic Disorders, 23(6), 1323–1339. (comprehensive review specific to ageing male population)