Adaptogens

“Adaptogen” is not a marketing coinage. It is a term from Soviet pharmacology, introduced by Nikolai Lazarev in 1947 and given formal criteria by Israel Brekhman and Igor Dardymov: a substance must produce a non-specific increase in resistance to varied stressors, must have a normalising action — correcting in either direction rather than pushing one way — and must not appreciably disturb normal physiological function at effective doses.

Those criteria are the useful part, because they are testable and most products in this category are not tested against them.

The proposed mechanisms

The best-developed account is that adaptogens act on the stress-response system rather than on any single organ. Three strands recur.

The hypothalamic–pituitary–adrenal axis is the primary target: constituents are proposed to modulate cortisol release and to blunt the exaggerated response to a stressor while not suppressing baseline function — which is what “normalising” would mean physiologically.

A second strand concerns molecular chaperones. Several adaptogen constituents induce heat-shock protein 70, which stabilises proteins under stress and is itself a general stress-resistance mechanism. This is a plausible route to non-specific resistance, which is the criterion hardest to explain otherwise.

A third involves stress-activated kinase signalling and neuropeptide Y. These are supported mainly by cell and animal work.

The constituents are named, and that matters

Rhodiola rosea is standardised on salidroside and rosavins; Withania somnifera on withanolides; Eleutherococcus senticosus on eleutherosides; Panax ginseng on ginsenosides. These are specific molecules with measurable content, which makes the central quality question concrete rather than rhetorical.

Extract standardisation is where the evidence base fractures. Different studies use different plant parts, extraction solvents and marker concentrations, so two trials of “ashwagandha” may not be testing the same preparation. This is not a minor caveat: it is the main reason the literature is difficult to synthesise, and it is why a positive result for one branded, characterised extract does not transfer to another product from the same species.

The test a reader can apply

Clinical trials in this area use defined doses of characterised extracts — typically hundreds of milligrams daily of a standardised preparation. A functional beverage or blended supplement often contains a fraction of that, sometimes an order of magnitude less, and frequently as an unstandardised powder rather than a marker-standardised extract.

So the checkable question is: which species, which plant part, standardised to what marker at what percentage, at what milligram dose per serving, compared against the dose used in the trials being cited. That comparison resolves most claims in this category without needing to adjudicate the pharmacology at all.

What the evidence supports

Human trials exist, most substantially for Rhodiola in fatigue and for Withania in stress and sleep measures. They are generally small, short, and heterogeneous in preparation and outcome measure, and the outcomes are frequently self-reported. Some show effects; the body of evidence is not strong enough to treat any of these as established, and regulatory authorities in major markets have not authorised health claims for the category.

The honest summary: a defined pharmacological concept with plausible and partly characterised mechanisms, an evidence base limited by standardisation, and a marketplace in which the dose is often the weakest link.