The Biological Dimension of Depression - Essay Example

The Biological Dimension of Depression Introduction The biological dimension of depression includes proven causes and predisposing factors. Althoughthe causes of depression have been studied for centuries, the mental and physical factors have dominated research. Studies on biological factors are not only a few but also less comprehensive, largely because they are very complex and intricate. In recent years, however, a lot of efforts have gone into investigating the biological causes, and researchers continue studying them extensively (Acton, 2013:21). Significant achievements have been recorded in the comprehension of brain function, the effects of hormones and neurotransmitters, and various other biological functions and how they may be associated with the onset of depression. Thesis Statement: Biological factors are one of the many causes of depression, and they require more attention than they currently receive. Discussion Because it is the body’s “command centre,” the brain controls all fundamental functions of the body. Researchers investigating clinical depression are fond of examining various aspects of brain function, including the parts of the limbic system and neurotransmitters’ role within neurons. Researchers who study clinical depression have been intrigued by a certain section of the brain known as the limbic system (Stein, Leventhal, and Trabasso, 2013:34). The limbic system is important in regulating emotions, responses to stress, and sexual and physical drives. The hypothalamus, the amygdala, and the hippocampus are the major parts of the limbic system that are linked to emotional stability and reaction, which are in turn closely associated with depression. The functions of the limbic system are so vital and intricate that they can influence an individual’s mood and conduct. Of the thirty known neurotransmitters, researchers have established links between clinical depression and the mechanism of three main ones: dopamine, serotonin, and norepinephrine. These neurotransmitters act on the parts of the brain that control emotions, sexual and physical drives, and stress responses (Beck and Alford, 2014:46). Parts that depression researchers have paid the most attention are the hypothalamus and the limbic system. Concepts regarding the effect of neurotransmitters on one’s mood have been derived from observation of the impacts of antidepressants on mitigating depression in some individuals. It is thought that antidepressants are effective because they control the level of certain neurotransmitters in the brain. In spite of this, the influence of neurotransmitters in the onset and alleviation of clinical depression is not very explicit. For example, studies have revealed that many depressed people have limited amounts of the neurotransmitter norepinephrine. Research also shows that some antidepressants can lead to an increase in the amount of norepinephrine in the brain. This can, in turn, alleviate symptoms of depression (Kahn, 2013:64). On the other hand, studies have revealed that some other depressed people have high quantities of norepinephrine. The scenario may also apply to other neurotransmitters. Another explanation for the ambiguous effects of neurotransmitters is associated with the fact that antidepressants are not effective for everyone. Studies show that due to the genetic makeup of some individuals, antidepressants do not work as intended (Kahn, 2013:67). In some cases, they do not work completely and produce negative effects that leave patients worse than they previously were. In case there was a direct causal correlation between depression and the amounts of neurotransmitters in the brain, we would anticipate a much higher success rate with treatments. In addition, although antidepressant drugs can have an instant impact on the amounts of neurotransmitters in the brain, it often requires a couple of weeks for a depressed person to feel better (Gilbert, 2014:21). The first inference that can be made here is that there seems to be a strong correlation between the levels of neurotransmitters in the brain and depression. The second hypothetical inference is that antidepressants are effective for many people, but there are doubts about the actual relationship between clinical depression and neurotransmitters. It is not clear whether fluctuations in levels of neurotransmitters lead to depression or depression leads to fluctuations in the level of neurotransmitters. Both statements may be true. Researchers think that behaviour can impact brain chemistry and vice versa. For example, many traumas can affect an individual’s brain, triggering clinical depression. On the other hand, the same individual could learn to alter depressed conduct and thoughts and manage stressful experiences (Becker and Kleinman, 2013:31). Doing this can also alter brain chemistry and reduce depression. Another biological aspect that research into the causes of depression focuses on is the endocrine system. Studies have revealed that many depressed people have abnormal amounts of some endocrine hormones in their blood in spite of having normal glands (Becker and Kleinman, 2013:34). Scholars believe that such hormonal imbalances may be linked to some symptoms of depression (e.g., insomnia and poor appetite) because they affect these functions. More leads in the relationship between the endocrine system and depression touch on the fact that people with specific endocrine disorders can develop depression, and some depressed people develop problems with their endocrine systems in spite of having normal glands. The endocrine system generally maintains normal hormonal levels through a process via a complex feedback process, just like a domestic thermostat. The endocrine system constantly monitors and regulates the body’s hormonal levels (Durbin, 2014:104). When a particular hormone increases to a specific level, the gland halts its production and secretion. In depressed persons, this feedback mechanism may not work like it should. Hormonal imbalance may be linked to fluctuations in brain chemistry that are observed in clinical depression. The endocrine system is linked to the brain through the hypothalamus that regulates many fundamental body functions. The hypothalamus also controls the pituitary gland that, in turn, regulates other glands’ hormonal secretion. When managing the endocrine system, the hypothalamus uses some neurotransmitters (serotonin, dopamine, and norepinephrine) that researchers have associated with depression (Getz, 2014:22). These neurotransmitters all play a role in the regulation of hormone function. The onset of clinical depression may be an indication of an abnormality present in organs that secrete hormones (Getz, 2014:23). Such abnormalities include Addison’s disease, thyroid conditions, and Cushing’s syndrome. About fifty percent of clinically depressed individuals exhibit abnormal levels of a hormone called cortisol. This hormone is produced by the adrenal glands and may continue being produced even when an individual already has over-the-top levels. Cortisol is thought to be associated with clinical depression because the abnormal levels often drop to normal levels once depression subsides. The hypothalamus is the likely suspect when it comes to abnormal levels of cortisol (Kosciejew, 2012:35). This is because it triggers the mechanism that results in the production of cortisol. First, it secretes corticotrophic-releasing hormone (CRH). Second, the pituitary gland is then stimulated into releasing adrenocorticotrophic hormone (ACTH), which “instructs” the adrenal glands to produce cortisol (Kosciejew, 2012:37). In a healthy endocrine system, the hypothalamus checks the amount of cortisol present in the blood. When the level increases the hypothalamus suppresses its effect on the pituitary gland in the secretion of CRH. When the levels of cortisol drop, the hypothalamus “instructs” the pituitary gland to secrete more CRH. In depressed individuals, the hypothalamus can indefinitely “direct” the pituitary to secrete CRH irrespective of the existing levels of blood cortisol. Other researches on cortisol show that the timing of the secretion of this hormone could be problematic in depressed people (Muir, 2012:39). Those who are not depressed produce cortisol at specific times of the day. The levels are usually at their peak at around 8:00 a.m. and 4:00 p.m., and then drop to their lowest at night (Muir, 2012:41). This normal fluctuation in the hormone does not happen in some depressed people. For example, they might exhibit a stable cortisol level throughout, or extremely high levels in the middle of the night. A dexamethasone suppression test (DST) can be used to measure cortisol level (Kosciejew, 2012:49). Although it is not a measure of depression because some depressed people may not be diagnosed based on the test results, it is applicable in confirming diagnoses of depression in some individuals. There is compelling evidence that genetic dispositions are highly influential in an individual’s chances of developing depression (Kosciejew, 2012:26). Melancholic depression, bipolar disorder, and psychotic depression are types of depression that one can be predisposed to due to genetic factors. So far, no single gene has been identified as having a role in an individual’s chances of developing depression (Durbin, 2014:29). However, a combination of genes has been found to be responsible for triggering depression. In addition, research has revealed that susceptibility to depression may be hereditary. For example, studies conducted by the American Psychological Association (APA) show that genetic predisposition to depression is around forty percent if a biological parent is or has been depressed. The remaining sixty percent is caused by factors in a person’s own environment. It is unlikely that depression will develop without stressful life experiences, but the chances of developing depression due to such events have a strong genetic element. Researchers often examine illness patterns in patients to measure their heritability. In other words, they can determine what proportion of patients’ causes of depression is genetic, by studying illness patterns in their families. In some cases, this has involved finding depressed people with twins, and then establishing whether or not the twin is also depressed (Gotlib and Hammen, 2014:24). Identical twins often share all their genes, while non-identical twins share fifty percent of their genes. If genetics is to be blamed, a patient’s identical twin should be more susceptible to depression than a non-identical twin. This is often the scenario for major depression. For severe depression, genetic risk factors are responsible for between 40 and 50 percent (or higher) of depression cases (Gotlib and Hammen, 2014:27). This could signal that in the majority of depression cases, around fifty percent is caused by genetic factors while the other fifty percent is not linked to genes but physical or psychological factors. It could also imply that in some instances the chances of becoming depressed are almost 100% genetic, and in some situations it has absolutely no links to genetics. The answer to this is yet to be found. It is also possible to examine adoption histories, to determine whether an adopted child’s predisposition to depression is higher if the biological parent suffered from depression. This appears to be the cases. People with family histories of major depression are probably 2 or 3 times more likely to become depressed compared to the normal person (Lawlor, 2012:39). This is around 20-30% versus 10%. The scenario is slightly different if one’s parent or sibling has suffered from multiple bouts of depression (recurrent depression) and if the condition started quite early in life (e.g., in the twenties, adolescence, or childhood). This type of depression is far less prevalent. The precise proportion of the population affected is unknown, but it could be between three and five percent. However, the offspring and siblings of people who have or are suffering from this type of depression probably acquire it four or five times faster than the average individual (Preece and Upton, 2014:13). Research shows that just like other afflictions like alcoholism and diabetes, there might be a “depression gene,” and scientists are working to prove its existence (Preece and Upton, 2014:15). The number of genes that cause depression is still unknown, but it is highly unlikely that any single gene leads to depression in any large group of people. It is, for this reason, safe to say that nobody just gets depression passed on to them by their parents. Every individual inherits a distinct assortment of genes from their parents, and some assortments can increase the risk of an offspring developing the disease. Major depression is related to bipolar disorder. Most individuals who suffer from depression lack manic episodes. Major depression is a phrase commonly used by practitioners to denote depression that lacks manic symptoms (Preece and Upton, 2014:42). Most people with manic symptoms also suffer from major depression. The term bipolar disorder or manic depression – is used for this attribute. Bipolar disorder and major depression are the two primary mood disorders (Lewis, 2012:19). Most people suffering from major depression lack close relatives suffering from bipolar disorder. However, the relatives of patients with bipolar disorder are more likely to develop both bipolar disorder and major depression (Lewis, 2012:24). In the case of anxiety disorders and major depression, it is likely that there are genetic developments that can increase the risk of developing both anxiety disorders (e.g., social phobia, generalised anxiety disorder, and panic disorder). Practitioners use jargons like neuroticism and adverse affectivity to identify this pattern, and people who suffer from it are also at a greater risk of developing major depression. However, majority of individuals who develop major depression do not exhibit this personality prior to the onset of their depression (Read and Dillon, 2013:25). In recent times, scientists have proved that physical alterations in the body can trigger mental changes. Medical conditions like stroke, hormonal disorders, cancer, Parkinson’s disease, and cardiac arrest can lead to depressive thoughts and depression itself (Read and Dillon, 2013:27). Such grave conditions can make the sick individual apathetic and hesitant to show concern for her physical needs. The result is a longer recuperation period. In addition, a serious loss, stressful events, undesired changes to life patterns or emotional problems can cause depressive situations. All factors considered a cocktail of genetic, environmental, or psychological factors is associated with the development of depression. Conclusion Most people are unaware that there are biological factors that cause depression. In fact, the common notion is that non-genetic and non-biological factors are the only causes of depression (Sharpley, 2013:43). This has led to numerous misdiagnoses of depression, often involving its strict association with non-genetic and non-biological causes. A patient may present depressive symptoms that are largely or strictly biological, and may be misdiagnosed or poorly treated because of preset mentalities to the classification of symptoms and the development of possible interventions (Sharpley, 2013:45). It is time for researchers to adopt a more serious approach to studying the biological factors that cause depression, by dedicating more time and resources to this kind of investigation. References Acton, A. (2013) Issues in biological and life sciences research: 2013 edition, New York, ScholarlyEditions. Beck, A. & Alford, B. (2014) Depression causes and treatment (Second ed.), Philadelphia, University of Pennsylvania Press. Becker, J. & Kleinman, A. (2013) Psychosocial aspects of depression, Hillsdale, N.J., Routledge. Durbin, C. (2014) Depression 101, New York, Springer Publishing Company. Getz, G. (2014) Applied biological psychology, New York, NY, Springer Publishing Company, LLC. Gilbert, D. (2014) Depression the evolution of powerlessness, Hoboken, Taylor and Francis. Gotlib, I. & Hammen, C. (2014) Handbook of depression, third edition (3rd ed.), New York, Guilford Publications. Kahn, J. (2013) Angst: Origins of anxiety and depression, New York, Oxford University Press. Kosciejew, R. (2012) Unusual reality of depression, S.l., Authorhouse. Lawlor, C. (2012) From melancholia to Prozac: a history of depression, Oxford, Oxford University Press. Lewis, B. 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