Welcome back, readers, and happy Monday! Yes, I’m dreading the start of the week too. It’s the start of long, stressful days full of work and responsibility. Dare I say that Monday is our nation’s symbol of stress?
Now, in the short-term, stress is good! We like stress. It is our evolutionary response that yells at our brain to make that crucial decision “fight or flight” (or, I suppose in our case, flee, considering we don’t have wings or feathers). However, more and more people are experiencing stress on a daily basis, whether that’s at work, school, home or a combination of those. This is where we have a problem.
You see, our brain does a whole lot for us and that includes the hefty ordeal of dealing with stress. To manage this momentous task, a few key structures band together in the name of the Hypothalamus-Pituitary-Adrenal axis (HPA) (the lovely diagram to the left provides a visual). When the brain senses a stressful situation, the hypothalamus releases corticotropin-releasing hormones (CRH), activating the anterior pituitary to release adrenocorticotropic hormones (ACTH), then activating the adrenal cortex to release glucocorticoid hormones. Stay with me here. These glucocorticoid hormones include what we call cortisol. It’s responsible for telling the other structures to shut off, helping our bodies maintain a homeostatic state (a stable equilibrium).
Okay, I know that was a lot, so let’s recap. Essentially each structure in this axis releases a hormone that triggers the next structure to release their hormone until we come to the Adrenal cortex. The critical hormone released here is cortisol, which is what shuts everything down when we have reached a stable state again (the stressful situation has subsided and we feel that we can breath again–perhaps your boss went back into his office, so you can slouch back and relax).
Yay! We love cortisol! Until there is way too much (unfortunately, the saying “you can never have too much of a good thing” does not apply in this situation). Excessive cortisol over long periods of time (the “chronic” aspect of chronic stress) severely damages and alters our brain in size, function, and structure. It breaks synapses and kills cells; it shrinks some structures while enlarging others. Critically important is the shrinking of the hippocampus and boost of activity within the amygdala: over time, this activity increases neural connections in this latter structure responsible for fear, essentially developing a cycle whereby our stress response is heightened and releases more cortisol. These structural changes then influence functions of the brain, where studies have seen a loss of sociability, a loss of memory, and an inability to learn new things.
Unfortunately, the effects of chronic stress on our hippocampus can lead to many severe mental disorders, such as major depression, bipolar, Cushing’s disease, alzheimers and post-traumatic stress disorder (PTSD). Studies on PTSD patients show that they suffer from the cognitive deficits seen of chronic stress on the brain. This includes lack of attention or focus and loss of memory.
After all of this negativity, let’s end on a positive note. There are things that we can all do to help our brains relax, lowering cortisol levels. Think of it as preventative medicine. If you’re an active person, you enjoy being outdoors or hitting the weights, fantastic! Exercise is a great way to reduce stress. If exercise isn’t your thing, no worries. Try meditation! There are plenty of YouTube videos and podcasts that will walk you through practice. You don’t even need to leave your room for that one! Stay inside, and deep breaths!
Now, let’s get out there and kick BUTT!
References (scientific writings and other links to click)
Bremner, J. D. (1999). Does stress damage the brain. Biological Psychiatry, 45(7), 797–805. https://doi.org/10.1016/S0006-3223(99)00009-8
McEwen, B. S. (2008). Central effects of stress hormones in health and disease: Understanding the protective and damaging effects of stress and stress mediators. European Journal of Pharmacology, 583(2–3), 174–185. https://doi.org/10.1016/j.ejphar.2007.11.071