INTRODUCTION
Basic Mechanisms of Stress
Even though we encounter stress in a negative way in our daily life, it is divided into two as good and bad stress in the literature. While good stress is the stress we experience while acting towards achieving a short-term and challenging job; Bad stress is referred to as a type of stress that is long-lasting, emotionally exhausting, and over which the person has no control. The most important indicator of the stress response is the activation of the autonomic nervous system and the hypothalamus-pituitary-adrenal (HPA) axis (McEwen, 2007). These two systems are activated in nature in response to deadly threats such as predators and natural disasters. Even if modern humans do not face such deadly threats today, stress is a part of life, especially for urban people. This is because the aforementioned mechanisms still have central roles in the human brain; but the threats that cause the evolution of these mechanisms are not encountered in urban life. This change in the lives of modern people has caused the events that we encounter as a matter of life and death in the evolutionary process to be replaced by factors such as life-long exams, noise pollution, economic problems, social exclusion and interpersonal conflict (Sapolsky, 2017). Therefore, city life activates these mechanisms, which have evolved to process momentary mortal threats, more frequently than in nature.
Studies to understand the damaging and protective factors that cause stress have led to the emergence of the terms allostatic and allostatic overload. While allostasis defines the emergence of processes such as the secretion of stress hormone to protect the self-balance (eng. homoestasis) in the face of a stressful situation; allostatic overload describes the damage caused by allostatic in the body (McEwen, 2007). These damages occur as a result of disturbances in allostatic processes, especially when stress hormone production is not stopped. However, the disorders caused by stress are not limited to the mentioned autonomic nervous system and HPA axis. Stressful events experienced by individuals have representations in the entire cortex through the hypothalamus; high-level cognitive activities such as attention and decision making It can cause damage even in the frontal area where it occurs (McEwen, 2007). This situation causes people to struggle with stress disorder during early life experience stressful-traumatic events and also leads to deterioration of cognitive functions in people (Brunson et al., 2005).
Researchers examining the relationship between aging and stress have put forward the weathering hypothesis (McEwen, 2007; Sapolsky, 2017). With this hypothesis, researchers suggested that stressful events accelerated aging. For example, Gerlach and McEwen (1972) observed adrenal steroids in the hippocampal formation where memory, spatial and contextual memory is processed. This observation showed that the factors that emerge as a result of the stress response affect the brain area where memory is stored and processed. The hippocampus is involved in terminating the stress response of the HPA axis, and it is known that damage to the hippocampus causes longer HPA axis responses as well as impairments in this termination task (Herrman & Cullinan, 1997; cited from McEwen 2007). This led to the hypothesis of glutocorticoid cascade (tr. glutocorticoid cascade) in aging and stress (Sapolsky, Krey & McEwen, 1986). This hypothesis suggests that the glutocorticoid hormone secreted in the adrenal cortex with aging causes damage that accumulates over time in the brain regions that stop this secretion process, and that this damage causes disturbances in the secretion arrest process with advanced age (Figure 1). While the researchers did not show the validity of the findings in primates and humans in 1986 rat studies, the hypothesis was shown to be valid in their later studies (Sapolsky, Krey & McEwen, 1986; McEwen, 2007). Similarly, Lupien et al. (1998; quoted from McEwen (2007)) predicted decrease in hippocampus volume with saliva cortisol level and associated this with poor performance on hippocampus-related memory tasks. Of course, the brain is a complex system and there are many factors that affect the amount and release of glutocorticoids. One of these factors is the 11-Hydroxysteroid Dehydrogenase-1 (11-HSD1) enzyme. This enzyme is deactivated 11-dehi It reactivates drocorticosterone and converts it to corticosterone and cortisone to cortisol. In other words, the increase in the amount of 11-HSD1 in the brain reactivates the inactive substances that cause the stress response and causes the stress response (McEwen, 2007). Yau et al. (2001) showed that rats with genetically deleted 11-HSD1 have less age-related cognitive dysfunction than natural phenotype rats.
Childhood Adverse Experiences and Stress
So far, their neurobiological basis In addition to the factors we discussed, the experiences of the person or animal also contribute to aging caused by stress (McEwen, 2007). Positive and negative events experienced at work, school or in a romantic relationship can affect people's reactions to events in a negative or positive way. For example, the behavior of people who have been betrayed in a romantic relationship in their next relationship will be shaped according to these experiences. Experiences at an early age affect this formation more seriously (McEwen, 2007). Felitti et al. (1998) associated adverse childhood experiences with risk factors such as early death and hypertension. 52.1% of 9508 people who participated in this study in the United States (USA) stated that they had experienced one of the negative experiences described in the study. It has been reported that individuals who experience 4 or more of the categories of negative childhood experiences (CSF) are 4 to 12 times more likely to turn to one of the important risk factors such as drug use, suicide attempt and being diagnosed with depression. These studies show that the imbalance in the stress mechanism at an early age is associated with many lethal risk factors.
It is known that almost all patients receiving psychiatric treatment in the USA were abused as children (Kaufman, 1999). These children are at higher risk of having PTSD in adulthood than healthy children. Another finding related to the neurobiological factors discussed in the previous section is also stated in this report by Kaufman (1999). According to De Bellis and Putnam (1994), the urine of abused children is compared to non-abuse children. la higher levels of cortisol were found. This shows that the previously mentioned HPA axis is more active in abused children and its function of inhibiting the stress response is impaired. These findings can also be explained by relating abused children's perception of events that are perceived as normal by healthy people as threats. In parallel, studies in baby rats have shown that disruptions in the care of their mothers have serious psychological effects (McEwen, 2007). For example, it has been shown that pups who lack maternal care die earlier and experience cognitive decline earlier. In addition, it was observed that exploratory behavior decreased in rats with a lack of maternal care (McEwen, 2007). It has been revealed that puppies with good maternal care are prone to neophilic behavior (Cavigelli & McClintock, 2003). Conversely, offspring lacking maternal care have been shown to be neophobic rats. It has been shown that the HPA axis of neophobic rats is more sensitive and their exploration behavior of new situations is reduced (McEwen, 2007). In one study, rats were taught the relationship between odor and electric shock using the fear conditioning method, and corticosterone levels of the rats were increased when the odor emerged (Sullivan et al., 2000). In the continuation of this study, the mothers of the baby rats were left with them and the odor stimulus was given again. It was observed that the HPA axis of the rats with their mothers was inhibited and stress response did not occur. This showed evidence that the presence of the mother reduces stress.
The stressors discussed so far have both short-term and chronic effects. For example, a cockroach seen in the kitchen immediately creates a stress response and raises the heart rate and blood pressure. This response adapts after a while and prevents these responses from remaining in the middle for a long time. However, the chronic emergence of the stress response continuously raises blood pressure and heart rate, and this causes pathophysiological consequences such as embolism over time (McEwen, 2007).
At this point, allostasis and essence mentioned at the beginning of this article We return to the concepts of nge. It is the defense mechanism of the organism that actually elicits the acute and chronic stress responses just mentioned. However, uncertainties in stressful events, especially in the complex social world of people, destabilize this protection mechanism. This disturbance of balance is also seen in the animal studies just mentioned. When laboratory animals are exposed to events that will cause intense stress response for a long time, it becomes difficult for the stress mechanism to return to self-balance. This experimental situation allowed the human-stress relationship to be studied in the laboratory. In all of the mentioned studies, it is seen that allostatis is higher than normal. It is seen that stressful events of much higher intensity than the person or animal can control or make sense of for the moment cause the mechanisms in the brain to perform the opposite actions required to restore the balance, higher than normal. These allostatic factors affecting the HPA axis, on the other hand, were seen to cause damage in areas such as the hippocampus and frontal cortex, where stress regulation takes place in long-term conditions.
Sleep and Stress
An example of this situation is insomnia caused by stress (McEwen, 2007). Allostatis leads to the production of proinflammatory cytokines to relieve poor sleep quality and the stress response caused by insomnia. But one of the most common causes of insomnia and poor quality sleep is stress itself. The allostatic load that arises as a result of this insomnia caused by stress also leads to harmful conditions in terms of health. Therefore, the response to inhibition of stress caused by insomnia causes an increase in stress. The reason for this is that the brain is both the mechanism that governs all these processes and is also an element that is affected by the situations produced by these mechanisms. As the neuroendocrine, immune and autonomic systems are regulated in the brain, stress-induced changes in the brain cause many different effects on health (McEwen, 2007). For example, reducing the sleep time to 4 hours increases blood pressure in people,
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