Chris Kresser: I debated on how much detail to go into with this. The HPA axis is incredibly complex, and if you really dive into these papers, it’s an exercise in hair pulling because what becomes clear pretty quickly is that there are opposite things happening at the tissue level and then in the serum and then even in the urine. We’re measuring serum, we’re measuring saliva, we’re measuring urine, but that doesn’t necessary reflect what happens at the tissue level, and very often what is happening is somewhat opposive. For example, we might see impaired cortisol-to-cortisone metabolism at the tissue level, but there are other mechanisms that lead to higher levels of cortisone metabolites showing up in the urine. I decided to only focus on what I thought was practical in terms of helping you to make effective treatment decisions rather than going really deep into—obviously, with these questions—potentially confusing material. I’m glad you guys are paying close attention. If you want, you can read the full text of the papers that I linked to in the HPA axis dysfunction section for more info on all of these mechanisms and to better understand the differences and what’s happening at the tissue level versus in the serum and the urine and the saliva. Or you can not do that and just focus on what’s important in terms of your clinical approach. That depends on who you are and what your interest is and how much spare time you have on your hands. It’s super-complex. I’ve had a lot of conversations with Mark Newman from Precision Analytical about this, and we both joke around about how contradictory and complex the mechanisms are and the research is to interpret. It’s something that probably would take years to fully get a handle on, and unless you’re just really fascinated with this particular topic, I don’t think that’s an effective use of time in ADAPT and in general.