Essay On Chronic Stress

Through my research I wanted to learn about exactly what anti-depressants do chemically . I also wanted to determine what role genetics, heredity, environment, and biological factors play in depression. Though I was not able to answer all of these questions, I learned a lot about depression and even developed some theories of my own. For a long time, I have thought of some forms of depression as a weakness. I truly believed that in many cases it could be controlled by the depressed person themself. I also felt that environmental and personal factors played were the basis for depression. However, through what we have learned in class and from my research, I have come to realize that this theory is not completely true. Mood is a generalized control mechanism like sleep. Eating also exhibits many characteristics of generalized control mechanisms. Mood can be affected by sensory input and the I-function, but it is also autonomous in that it can vary independent of sensory input. This internal variation is pharmacologically dependent. Changes in a persons pharmacological makeup can cause mood changes, sleep disturbances, and even depression. The I-function influences mood manipulation but cannot determine mood. Though you may want to be in a good mood, make a conscious effort to think RhappyS thoughts, and may not have serious stressors in your life, you may still suffer clinical depression as a result of a chemical imbalance in your system. Depression can be physical and

These adaptive mechanisms can become maladaptive if unresolved after precipitating events have passed, leading to interferences in emotional regulation (Liston, McEwen, & Casey, 2009; Juster et al., 2011). Imaging studies show alterations in the brain structures that assist in regulation of the stress response—the amygdala, hippocampus, and prefrontal cortex—due to prolonged exposure to stress (Carrion et al. 2010; Rao et al. 2010). The over activation of this fear circuitry in the brain can lead to distorted processing, contributing to depression (Thienkrua et al., 2006; Neria, Besser, Kiper, & Westphal, 2010; Rao et al., 2010), anxiety (Derryberry and Reed, 2002; Goldin et al., 2009; Graham and Milad, 2014), and mood impairments (Kobasa, 1979; Linehan, 1993; Haller and Miles, 2004). These cognitive changes can also contribute to insomnia, chronic pain, addictive disorders, impairment of immunity, and development of coping mechanisms such as smoking, use of alcohol or drugs, overeating, and other survival mechanisms (Raja, 2012). The allostatic load of a chronically over-activated hypothalamus-pituitary-adrenal system can lead to development of comorbid health conditions such as cardiovascular disease,

Psychology, as most know, is the study of the mind and personal or group thoughts, feelings, and emotions in humans and animals. Scientists study, analyze, and investigate many areas of psychology, but the causes and effects of mood disorders and emotion irregularities are still unrecognized. Many studies were an attempt to find more information on mental illnesses. One of the most common illnesses in the United States is depression, also; it is the most often recognized mental illness in the world. What most clinicians don’t know, however, is what happens in the brains of patients before, during, and after depressive episodes.

The CNS instantly tells the rest of your body what to do, marshaling all resources to the cause. In the brain, the hypothalamus gets the ball rolling, telling your adrenal glands to release adrenaline and cortisol. When the perceived danger is gone, the CNS should tell all systems to go back to normal. It has done its job. If the CNS fails to return to normal, or if the stressor doesn’t go away, it begins to take its toll on the body. Symptoms of chronic stress include irritability, anxiety, and depression. A person may suffer from constant headaches or even insomnia. Chronic stress is a factor in some behaviors like overeating or not eating enough, alcohol or drug abuse, or social withdrawal. Let’s take a closer look on the different mental disorders that are directly linked to chronic stress. The first, and probably the must harmful, depression. Byproducts of stress hormones can act as sedatives (chemical substances which cause us to become calm or fatigued). When such hormone byproducts occur in large amounts (which will happen under conditions of chronic stress), they may contribute to a sustained feeling of low energy or depression. One could argue that it is normal to experience a range of moods, both high and low, in everyday life. While some "down in the dumps" feelings are a part of life, sometimes, people fall into depressing feelings that persist and start interfering with their ability to complete daily activities, and this isn’t normal. The term Major Depression is used to describe such periods of extended, and profound depression. Symptoms of Major Depression may include: sleep problems, fatigue, and feelings of worthlessness. It can also cause an inability to concentrate or make decisions, agitation, restlessness, and irritability. Depression is also associated with an increase in suicidal

Neurotransmitters are chemical messengers that carry messages between neurons and affect behaviour, mood and thought. Two of the neurotransmitters that play a role in depression are norepinephrine and serotonin (Shives 2005). In depression, neurons don’t produce enough neurotransmitters. Shives (2005) states as a result, membrane channels don’t open, nerve messages are not communicated, and areas of the brain affecting emotion may not receive stimulation (Shives 2005). The hormonal system known as the hypothalamic-pituitary-adrenal axis, that regulates the body’s response to stress, is overactive in many people with depression. The hypothalamus increases production of corticotrophin releasing factor when a person’s physical or psychological well-being is threatened (Shives 2005). Elevated levels of corticotrophin releasing factor lean to an increase in hormone secretion by the piturity and adrenal glands which prepares the body for defensive action (Shives 2005). The chronic overactivity of the hypothalamic-pituitary-adrenal axis may occur following a traumatic experience this may contribute to the onset of depression (Shives 2005).

The physiological and behavioral effects of early life stress (ELS) on the developing and adult brain are a subject of great interest in the field of neuroscience today. The ability to delineate the mechanisms and structures that are affected during postnatal exposure to chronic stress has the potential to provide invaluable insight into the development of a multitude of neuropsychiatric disorders. While we have come to understand a few of the mechanisms involved in many of these illnesses – such as the significance of the serotonin (5-hydroxytryptamine, 5-HT) neurotransmitter in many depression cases – the complex nature of these disorders and our ability to effectively treat them remains elusive. Such an understanding of how the brain adapts and differentially develops as a result of chronic stress, particularly in early life, may also be able to broaden our understanding of the way in which the brain codes and responds to a variety of emotional triggers.

The independent variable in this experiment was whether the rat was raised in isolation with no toys or in group with toys and which cage they were tested in whether it was the home cage or a new cage. The dependent variable was how many times rats in each scenario stuck their noses in the candles flame. Results showed that almost every rat stuck their nose into the flame in pure curiosity however, rats raised in a restricted environment and placed in a new environment stuck their noses in almost double the amount of times than any other rat did. These results indicate that rats raised in isolation handle stress differently and that those in isolation have poor pain avoidance. I liked this study because it shows that curiosity is prominent in rats as in humans although it only takes us one time to realize something hurts to not do it again. It also shows that something raised in isolation reacts to stress in a negative way and proceeds to harm themselves and with this evidence we can maybe understand why depression can lead to

The experiments conducted used mice in two groups, an experimental group that underwent chronic early life stress and a control. Hormone production analysis for each subject occurred as the experiment proceeded. The mice underwent object recognition tasks, followed by sucrose and forced swim tests to quantify the effects of depression and anhedonia. Reduction of CRH production then occurred via short-hairpin RNA intervention in target mice. The mice were then retested, and given a social play test. The experiment then analyzed the synapse function of the control and CES mice. Cell imaging determined neuron expression, with further testing being conducted that focused on the analysis of microglial cells in a developing fetus.

showed that prenatal stress decreases cell turnover and proliferation in the hypothalamus of adult rats, which reduces structural plasticity and reduces the response to stress in adulthood. This study also showed that when prenatally stressed rats were stressed in adulthood the females showed an increase in corticotropin-releasing hormone suggesting it to be an up-regulation in the hypothalamic-pituitary adrenal axis. Males showed no elevation of corticosterone levels. Increase in adrenocorticotropic hormone with no effect of adult stress and a decrease in the corticotropin-releasing hormone mRNA in the hypothalamus showed a down-regulation. The author concludes that this makes prenatally stressed females less reactive to later life stressors than

The rats which were depressed were lethargic and lacked survival instincts when tested however with therapy in the form of a rat sized playground they began to show signs of recovery within a month despite their genes. This experiment was also reversed to try to cause depression and was successful “the stressed control rats displayed depressed behaviors when placed in a tank of water. They simply floated- despair behavior- and didn’t try to escape”(3). The science is improving nevertheless humans are complex creatures and hard to study; the experiments conducted on rats cannot be replicated in humans therefore the research has to take a path of observation and

Among them is the chronic mild stress (CMS) procedure devised by Willner (Willner 1995; Papp et al.1996). In the CMS model, chronic sequential exposure of rats to a variety of mild stressors induces changes in hypothalamic-pituitary adrenal axis, weight body and adrenal glands (Harro et al.2001), all these symptoms are consistent with human depression. It leads to increased activity of the HPA axis, including adrenal hypertrophy and corticosterone hypersecretion (Vollmayr et al . 2003). Which results in an increased release of adrenocorticotropic hormone (ACTH) from the anterior pituitary and glucocorticoids from the adrenal cortex (S. El Fazaa et al.

In experimental animals, stress has been demonstrated to contribute to atrophy of the hippocampus similarly to depression (Sapolsky, 2000). Chronic stress paradigms in animals show many of the primary behavioural characteristics of depression and respond to antidepressant treatment (Willner, 2005). The exact reasons are not yet fully understood but any comprehensive model of the pathophysiology of depression needs to include the role of stress plays in the etiology of the mental illness. There is also an increased appreciation of the impact stress has on mechanisms of neuroplasticity. Evidently an intimate relationship must exist between the effects of stress, mechanisms of neuroplasticity, and the pathophysiology of depression and the role

Anxiety is a frequent consequence of chronic stress. In humans, stressful life events may lead to anxiety even in the absence of a chronic physiological stress response [1]. Many studies have been conducted to identify the role of different factors that contribute to the development of depression and anxiety [2, 3].It has been reported that decrease anxiety related behavior in humans and animals. Exposure to stress is a main environmental risk factor associated with the occurrence of depression [4, 5,6]. And its may be the most important environmental factor affecting feeding behavior, metabolism, and neuroendocrine functions [7] and [8]. Among trusty models of depression, chronic mild stress (CMS) model of depression

In this journal, Hammen (2015) mentions different articles that include studies done with samples of various age groups, such as children, adolescents, and adults, on the role of stress, which has been thought to be mainly derived from depression for long periods of time. Nevertheless, the range of the role of stress has been expanded and applied to other psychological disorders over time, as well as to the wide variety of experiments on human stress processes and the study of various conceptual models (Hammen, 2015). Therefore, Hammen (2015) questions how the results from a collection of articles on stress can be combined to draw a more unified conclusions, and how these conclusions can be beneficial towards understanding and making improvements

There is a very complex relationship between stressful situations, our mind and body’s reaction to stress and the onset of depression. Some people develop depression after going through stressful events in their lives, such as the death of someone close, loss of job and other negative and traumatic problems that can cause large amount of stress (Prentiss, 2009). These problems make us experience a mixture of physical and emotional effects that can create stress as a positive or negative feeling. The human body is designed to experience and react to stress; it can be both a positive and negative influence. Positive stress can give a person the drive and