Adrenal Function Profile (Salivary Diurnal Cortisol & DHEA)

Salivary cortisol tracks the unbound, diffusible fraction of circulating cortisol, which enters saliva passively and independently of corticosteroid-binding globulin, so a salivary value is not directly comparable with a total serum cortisol. Output is governed by the hypothalamic-pituitary-adrenal axis and rises sharply in the first 30–45 minutes after waking (the cortisol awakening response), making the morning specimen the peak of the diurnal rhythm and the point most sensitive to how soon after waking the sample was taken.

The waking value anchors the diurnal curve and indexes the top of the daily rhythm. A robust morning rise is the expected physiological pattern; a blunted or absent morning peak is interpreted in functional practice as reduced HPA-axis reactivity, though this reading is not a recognised endocrine diagnosis. Genuine morning hypocortisolism suggestive of adrenal insufficiency must be confirmed with serum morning cortisol and dynamic testing rather than inferred from saliva.

By late morning to early afternoon the awakening surge has resolved and cortisol is on the descending limb of the circadian curve. The midday specimen samples this intermediate point and, together with the morning and evening values, defines the slope of the daytime decline that the profile is designed to capture.

The midday point is used chiefly to describe the shape of the fall from the morning peak rather than as a standalone diagnostic value. A disproportionately high or flat midday result contributes to the functional picture of a disrupted rhythm but carries no independent validated threshold.

In the early evening cortisol approaches but has not yet reached its circadian nadir. The evening sample captures the later daytime decline and, with the bedtime specimen, documents whether the expected approach to a low night-time value is preserved.

The evening value refines the descending slope and the transition toward the night nadir. Persistent evening elevation is read functionally as failure of the rhythm to wind down, often in the context of stress or disrupted sleep, but it is interpreted as a pattern rather than a diagnosis.

The late-evening to bedtime specimen samples the circadian nadir, when HPA-axis drive is normally at its lowest. Loss of this low point — a failure to suppress cortisol at night — is the physiological hallmark of endogenous hypercortisolism and the basis of the one clinically validated use of salivary cortisol.

Late-night salivary cortisol is an established, guideline-endorsed first-line screen for Cushing's syndrome: an elevated bedtime value with loss of the normal nadir warrants formal confirmatory evaluation. This validated use should be weighted quite differently from the broader, functional interpretation of the diurnal curve in which the same specimen also participates.

DHEA is the principal adrenal androgen precursor; the salivary measurement is taken to reflect its free, diffusible fraction. In adrenal profiling it is measured as a counterpoint to cortisol — both are cortical steroids, and their relative output is used in functional practice to characterise overall adrenocortical activity. Salivary DHEA shows its own age-related decline and some diurnal variation, so the collection time is recorded.

Within this profile, salivary DHEA is used as a functional index of adrenal androgen output and as the denominator of a cortisol-to-DHEA relationship. It is important to be clear that serum DHEA-sulphate is the standardised, validated marker of adrenal androgen status; the salivary measure and any derived ratio are functional-medicine constructs without mainstream endocrine endorsement, and a low or high salivary DHEA does not establish a recognised diagnosis.

The ratio expresses adrenal glucocorticoid output relative to adrenal androgen output from a single collection set. Because it is a derived quantity, it inherits the collection-timing and contamination sensitivities of both inputs and amplifies any error in either.

Functional and integrative practitioners use the ratio as a summary index of a presumed stress state, on the premise that chronic HPA-axis activation shifts steroidogenesis toward cortisol. There is no mainstream validation of the ratio for diagnosis or management, and it should be framed as a hypothesis-generating, exploratory metric rather than a clinical endpoint.