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  4. We refer to stress-induced pathology as HPA dysfunction, but the reality is that stressors affect us via two primary mechanisms: the HPA axis and the SAS.’ I understand these are intertwined, but my question is, isn’t it rather important to try to work out which one is dominantly out of whack in certain situations such as waking up in the middle of the night because the physiology will be a bit different? If cortisol is too high at night, isn’t that really different to if adrenaline is high at night? I know the long-term solutions will be the same, but in the short term in terms of which supplements to use, is there a difference?

We refer to stress-induced pathology as HPA dysfunction, but the reality is that stressors affect us via two primary mechanisms: the HPA axis and the SAS.’ I understand these are intertwined, but my question is, isn’t it rather important to try to work out which one is dominantly out of whack in certain situations such as waking up in the middle of the night because the physiology will be a bit different? If cortisol is too high at night, isn’t that really different to if adrenaline is high at night? I know the long-term solutions will be the same, but in the short term in terms of which supplements to use, is there a difference?

Chris Kresser: I haven’t found that to be an important clinical distinction. We talked a bit in the HPA axis unit about the differences between what you would do in a hypercortisolism state and a hypocortisolism state, and there aren’t a lot of good ways for testing outside of a research setting for SAS activation above and beyond the DUTCH testing that we’re already using and some of the other tests we talked about. Really, especially from a behavioral and lifestyle perspective, the changes that you’re going to suggest are largely the same, so I don’t think it makes a clinically meaningful difference.

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