S-VV
Member
- Joined
- Jul 23, 2018
- Messages
- 599
Some ideas that came to mind:
An organism is always searching for a dynamic equilibrium (homeostasis) between itself and the environment (i.e. input = output). The lack of homeostasis directly threatens survival because it leads to the slowing down of life sustaining processes in one way or another.
The adaptation of the body to external factors is so important that in hospitals, most life-threatening situations are preceded with “compensated”, meaning the patient isn’t going to die, or “uncompensated”, meaning you probably need to start preparing a bed in the ICU.
Alterations in the environment, or stressors, place a demand on the body, and fulfilling that demand will return the body to homeostasis. The cumulative demands on the body are called the allostatic load.
When a stress cannot be compensated with the normal means of the body, adaptive mechanism spring into action. These mechanisms, broadly mediated by a series of related “stress hormones”, will improve short term survival at the cost of long term structure and function.
When an organism is engaged in an “allostatic struggle” with its environment, artificially supressing stress hormones will lead to detrimental results, unless the stressor is also removed. This is illustrated, for example, in Hans Selye`s experiments, where increasing cortisone in rats promotes short term survival.
All stress mediators can have positive effects, for example:
-Cortisol: Increasing blood glucose, decreasing excessive or unproductive inflammation, promoting pathogen tolerance
-Serotonin: Promotes protective torpor, adaptation to insurmountable social stress, enables to cope with chronic social defeat.
-Nitric Oxide: Increased vasodilation, blocks Complex IV leading to more O2 availability for other tissues
-Oestrogens: Increases intracellular water retention that can improve resistance to shock, promotes cell division via stabilization of mitotic apparatuses, maybe can “delete” epigenetic alterations
-Angiotensin II & Aldosterone: Increase kidney GFR and Na+ retention
-Acetyl-Choline: Decreases ATP expenditure via activation of parasympathetic efferents
-Endogenous opioids/cannabinoids: Analgesia, euphoria, oppose inflammation
However, over the long-term stress mediators damage the body, sometimes permanently. This is because the “supraphysiological” stress-resistance comes at the price of diverting available energy to essential processes, shutting down non-essential functions, generalized catabolism, decreased energy consumption etc.
Many people feel better with cortisol, SSRIs, low-carb diets, high intensity exercises and so on, while trying cyproheptadine (anti-serotonin), methylene blue (anti-NO), 17b-HSD inhibitors (anti-cortisol), clonidine (anti-adrenergic), aromatase inhibitors (anti-oestrogen) and other anti-adaptive hormone substances, leads to feeling acutely worse. This makes sense, because shutting down adaptive processes while still being subjected to the same allostatic load will lead to worse outcomes short-term, while it can reduce degeneration long-term, if the organism doesn’t cease to function due to allostatic overload.
An organism is always searching for a dynamic equilibrium (homeostasis) between itself and the environment (i.e. input = output). The lack of homeostasis directly threatens survival because it leads to the slowing down of life sustaining processes in one way or another.
The adaptation of the body to external factors is so important that in hospitals, most life-threatening situations are preceded with “compensated”, meaning the patient isn’t going to die, or “uncompensated”, meaning you probably need to start preparing a bed in the ICU.
Alterations in the environment, or stressors, place a demand on the body, and fulfilling that demand will return the body to homeostasis. The cumulative demands on the body are called the allostatic load.
When a stress cannot be compensated with the normal means of the body, adaptive mechanism spring into action. These mechanisms, broadly mediated by a series of related “stress hormones”, will improve short term survival at the cost of long term structure and function.
When an organism is engaged in an “allostatic struggle” with its environment, artificially supressing stress hormones will lead to detrimental results, unless the stressor is also removed. This is illustrated, for example, in Hans Selye`s experiments, where increasing cortisone in rats promotes short term survival.
All stress mediators can have positive effects, for example:
-Cortisol: Increasing blood glucose, decreasing excessive or unproductive inflammation, promoting pathogen tolerance
-Serotonin: Promotes protective torpor, adaptation to insurmountable social stress, enables to cope with chronic social defeat.
-Nitric Oxide: Increased vasodilation, blocks Complex IV leading to more O2 availability for other tissues
-Oestrogens: Increases intracellular water retention that can improve resistance to shock, promotes cell division via stabilization of mitotic apparatuses, maybe can “delete” epigenetic alterations
-Angiotensin II & Aldosterone: Increase kidney GFR and Na+ retention
-Acetyl-Choline: Decreases ATP expenditure via activation of parasympathetic efferents
-Endogenous opioids/cannabinoids: Analgesia, euphoria, oppose inflammation
However, over the long-term stress mediators damage the body, sometimes permanently. This is because the “supraphysiological” stress-resistance comes at the price of diverting available energy to essential processes, shutting down non-essential functions, generalized catabolism, decreased energy consumption etc.
Many people feel better with cortisol, SSRIs, low-carb diets, high intensity exercises and so on, while trying cyproheptadine (anti-serotonin), methylene blue (anti-NO), 17b-HSD inhibitors (anti-cortisol), clonidine (anti-adrenergic), aromatase inhibitors (anti-oestrogen) and other anti-adaptive hormone substances, leads to feeling acutely worse. This makes sense, because shutting down adaptive processes while still being subjected to the same allostatic load will lead to worse outcomes short-term, while it can reduce degeneration long-term, if the organism doesn’t cease to function due to allostatic overload.