The Hypothalamic-Pituitary-Adrenal (HPA) Axis and it's Role in the Stress Response

Last week, I talked about cortisol and its role in the body's negative feedback loop.

In order to see what happens when excess cortisol occurs, let's circle back and take a look at where stress originates, physiologically, before the cortisol is actually created.

Much of what I see online, especially in the social media realm, relates to the impact excess cortisol has on our systems, then connecting those dots, rather than tracing it all back to the core neurological things they have in common.

I'm not saying there's anything "wrong" with this, but that is more of a treatment perspective - trying to find ways to eradicate or treat those resulting illnesses/issues - whereas I'm looking at it from a preventative and management perspective - how can we at least put a stop in the dam of cortisol while managing where we currently are? I can't heal or treat those results of chronic stress like diabetes and autoimmune illnesses, but my literal job as a certified health coach is to help manage them through lifestyle ie movement, nutrition, and stress management.

SO.

Because a picture can say a thousand words, I'm including a photo from my certified health coaching text that depict things succinctly.

Okay, now I want to point out a couple of things...

The amygdala is what will initially trigger the hypothalamus once a threat is recognized.

Autistics have BOTH hyper-aroused amygdalas AND a reduced volume hypothalamus. This means we are both triggered more often, and our hypothalamus is operating at a reduced capacity from the start. And remember, Autistics are also born with larger amygdalas that they grow into so... potential for greater hyper-arousal in early years. Everything else cascades from here.

When levels of cortisol become regularly resistant to the HPA axis's negative feedback loop, this is when we can develop HPA axis dysfunction, cortisol-related symptoms/illnesses, etc.

This is also why, when I see illnesses and issues that have things like a reduced volume hypothalamus or hyper-aroused limbic system in common, I see those as the connectors, not necessarily the things that occur much further down the line. This is why I'm so adamant about working on reducing and eliminating triggers and stressors from the onset whenever possible, and am so passionate about nervous system regulation "basics" like breath work that can be done by anyone.

The last thing I want to note is that the timeframe between being triggered and secreting stress hormones is called our "window of tolerance" and is something I'll talk a bit more about next. By reducing triggers and stressors, we're trying to increase our window of tolerance which will allow us more time to bring ourselves back to parasympathetic activation before the cascade of stress effects hit our bauties.

Oh my gosh, I went into another rabbit hole while writing this and I'm going to have to make it a separate post but there are a couple of studies showing proof of dysregulation even after cortisol is regulated and that regulated ACTH levels may have the greatest impact on HPA axis functioning and cortisol secretion. HOLY MOLY.

Okay, with that, I will leave this with one more random thought: much of the research related to these effects focuses on stress hormone levels and all research points to the much higher rate of autoimmune illnesses among AFAB, but I feel like there's something large missing... I wonder how much is being overlooked in research considering the role and impact that menstrual hormones have with stress hormones? In ALL of the research I've done over the last year about stress and hormones and the brain, NONE factor in reproductive hormone cycles unless the study is specifically about cycles....

Until next time.

Stay regulated,

Shauna