Under-fuelling, cortisol and the persistence of hunger

Restriction is an experience as well as an energy calculation

EPK asks whether a dietary approach supplies enough energy for a person to function and remains tolerable over time. Hunger, fatigue and preoccupation with food are relevant outcomes alongside changes in body mass. Human studies show that restriction can affect stress and appetite regulation, although the response depends on the intervention and population.

Separating calorie restriction from calorie monitoring

Tomiyama and colleagues randomly assigned 121 women to four conditions for three weeks: calorie restriction, calorie monitoring, both, or neither. Restriction involved 1,200 kcal/day. Restriction increased total salivary cortisol output, while monitoring increased perceived stress. The design helped separate the biological response to eating less from the psychological burden of tracking intake. [1]

This experiment supports the possibility that restrictive dieting can carry physiological and psychological costs. It did not establish that cortisol caused later weight regain, and its short duration does not tell us how every person responds to longer-term dieting.

Why cortisol is not a universal verdict on dieting

A six-month CALERIE investigation found little effect on salivary cortisol despite sustained restriction and weight loss. This is an important comparison with the shorter trial. Differences in participants, severity, timing and measurement can produce different results. Restriction can increase cortisol; it does not invariably do so. [2]

Cortisol is part of normal regulation and its concentration alone is not a diagnosis of harmful stress. An EPK evaluation would need repeated measurements alongside sleep, hunger, mood, activity and functional outcomes.

Hunger can persist after weight loss

Sumithran and colleagues enrolled 50 adults with overweight or obesity in a ten-week very-low-energy weight-loss programme. At follow-up a year after initial weight loss, hunger and several appetite-regulating hormones remained different from baseline. These findings show a biological pressure towards regain, rather than demonstrating that every participant regained weight or that all diets fail. [3]

Appetite hormones and stress hormones should not be collapsed into one mechanism. Lower leptin and changes in ghrelin and gut signals concern appetite regulation; cortisol concerns a different, interacting system. The practical relevance is that sustaining a lower body mass may require continued effort even after the initial diet ends.

A direct connection to athletic function

In a randomised crossover experiment in 12 female endurance athletes, 14 days of low energy availability increased cortisol and impaired exercise performance. Some impairment remained after three days of refuelling. The result links inadequate fuelling with measurable functional costs, but it cannot be assumed to describe every non-athlete or every modest deficit. [4]

What this contributes to EPK

These studies support testing whether meeting individual energy needs reduces persistent hunger and improves function compared with continued restriction. They do not establish a universal kcal/kg threshold or validate EPK itself. The research question is whether a sustainable intake can improve lived experience and performance, with body composition tracked as one outcome among several.

For EPK–001 and EPK–002, the relevant outcomes include adherence, hunger and behavioural stability. For EPK–004 and EPK–005, they include fatigue, movement and recovery. A useful trial would record the prior duration of restriction and distinguish restoration to energy balance from deliberate overfeeding.

Related working papers

Read the relevant PDFs: EPK–001 to 007 are the revised version 1.2 papers; EPK–008 to 010 are version 1.0 supplements. Earlier PDFs and DOI records remain on the paper archive.