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Stress damage due to early / prolonged stress

Stress damage due to early / prolonged stress

Stressors activate the various stress systems in humans, which act in parallel. The most important of these are the autonomic nervous system (sympathetic/parasympathetic nervous system), which is activated quickly by electrical nerve impulses, and the HPA axis, which is activated slowly by hormones. The HPA axis releases stress hormones in a relay, starting with CRH and vasopressin, followed by ACTH and ending with cortisol. At higher levels, these trigger stress symptoms (which is healthy up to this point). However, they have a neurotoxic effect if they are released over a long period of time.1234 If the levels are too low, the stress symptoms and stress reactions are not formed sufficiently and the HPA axis cannot be shut down properly if the cortisol release is too low.
The HPA axis / stress regulation axis

The neuroplastic effect of prolonged stress was described as an allostatic concept as early as 1988.56
Prolonged stress leads to an allostatic overload7 (acute pathological consequences of allostatic reactions), which causes changes in the following brain regions, among others, which in turn changes behavior and physiological reactions:

  • Hippocampus (volume reduction)
    • Cognitive impairments
    • Depression
    • Impairment of self-esteem
  • Amygdala
  • PFC

Stress exposure has very different effects depending on the age of the individual.8910

Different types of stressors and different types of exposure to stressors have different effects:

  1. Stress by age at exposure - early childhood stress
  2. Stress by duration: Long-lasting, chronic stress
  3. Stress by type of stressor
  4. Stress effect by gender
  5. Diagnosis of stress system damage
  6. Resilience, increased sensitivity, genetic disposition and maternal care

  1. Sapolsky, Pulsinelli (1985): Glucocorticoids potentiate ischemic injury to neurons: therapeutic implications. Science 229:1397–1400

  2. Leverenz, Wilkinson, Wamble, Corbin, Grabber, Raskind, Peskind (1999): Effect of chronic high-dose exogenous cortisol on hippocampal neuronal number in aged nonhuman primates. J Neurosci 1999;19(6):2356–61.

  3. Sapolsky (1996): Why stress is bad for your brain. Science 1996;273(5276):749–50.

  4. Starkman, Giordani, Berent, Schork, Schteingart (2000): Elevated cortisol levels in Cushing’s disease are associated with cognitive decrements. Psychosom Med 2001;63(6):985–93.

  5. Sterling, Eyer (1988): Allostasis: a new paradigm to explain arousal pathology. In: Fisher S, Reason J, eds. Handbook of Life Stress, Cognition and Health. New York, NY: John Wiley & Sons; 1988:629–649.

  6. McEwen (2006): Protective and damaging effects of stress mediators: central role of the brain; Dialogues Clin Neurosci. 2006 Dec; 8(4): 367–381. PMCID: PMC3181832

  7. Doom, Gunnar (2013): Stress physiology and developmental psychopathology: past, present, and future. Dev Psychopathol 2013;25(4 0 2):1359–73.

  8. Bloomfield, McCutcheon, Kempton, Freeman, Howes (2019): The effects of psychosocial stress on dopaminergic function and the acute stress response. Elife. 2019 Nov 12;8:e46797. doi: 10.7554/eLife.46797. PMID: 31711569; PMCID: PMC6850765.

  9. Brake, Zhang, Diorio, Meaney, Gratton (2004): Influence of early postnatal rearing conditions on mesocorticolimbic dopamine and behavioural responses to psychostimulants and stressors in adult rats. Eur J Neurosci. 2004 Apr;19(7):1863-74. doi: 10.1111/j.1460-9568.2004.03286.x. PMID: 15078560.

  10. Meaney, Brake, Gratton (2002): Environmental regulation of the development of mesolimbic dopamine systems: a neurobiological mechanism for vulnerability to drug abuse? Psychoneuroendocrinology. 2002 Jan-Feb;27(1-2):127-38. doi: 10.1016/s0306-4530(01)00040-3. PMID: 11750774.

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