Biological And Cognitive Explanations.

Introduction:

According to the American Psychiatric Association, depression is considered as the common as well as the serious psychological illness that poses adverse effects on thoughts, feeling, decision making and activities of the people. fortunately, this mental illness can be treated by applying proper psychotherapies and medications. Based on the who reports, each year, one in 16 adults (7%), is affected through depression. World Health Organisation also reports that more than 300 million people are currently suffering from depressional and other mental illness. Therefore, it is high time to understand the reason and outcomes of depression. This assignment is going to discuss and evaluate the two different explanation of depression. One is a biological explanation of depressional and the another is a cognitive explanation of depression. Through representing these two explanations, this essay is going to analyze the reason, pathology, and outcomes of depression, which will assist the learner to get proper knowledge regarding depression.

Outlining and evaluating the two explanation of depression:

Different research has been conducted to understand the actual reason behind depression and its possible adverse effect on the mental, physical, social and emotional health of the people. there is two major concepts such as Biological explanation and the cognitive explanation regarding the reason, pathophysiology, and outcomes of depressions.

The biological explanation of Depression:

As stated by Elder et al. (2017), Biological explanation or the Medical Model of depression represents the genetic and neurochemical interaction of different biological factors, which are associated with different psychological illness. American Psychiatric Association, focuses on the fact that genetic makeup and mutation in the neurotransmitter genes are considered to be associated with the psychological imbalance and depression. Researchers have also suggested a number of biological factors such and genes, malformation of eth brain structure and the biochemical imbalance contribute to their own way of developing depression, anxiety, and dementia. Biological researchers also suggested that the imbalances of the brain chemicals are considered to play important role in causing depression and other psychological disorders. Even, when considering the only one biological dimension of depression, the neurological issues in brain functions has been proved to play important role in occurring psychological disturbances.

As stated by Haberler (2017), the brain has the number of chemicals that are used to communicate with the different parts of the nervous system. In the nervous system, the nerve cells are called as neurons. Neuron communicates with each other through the neurotransmitter. The neurotransmitter is received as well as released through eth different neurons. Through the exchange of the neurotransmitter the nerve cells communicate with one another. Recent researches on the depression highlight the fact that depressional is associated with the imbalance of eth neurotransmitter in the brain, specialty the Serotonin, dopamine, and norepinephrine. However, it is quite difficult to determine the actual level if eth neurotransmitter in eth brain and their specific activities. Different biological studies have shown that the use of antidepressant medications act as the catalyst for the neurotransmitter which improves the activities and level of eth neurotransmitter inside the brain cells.

According to Karp (2016), Serotonin is one of the important neurotransmitters that is associated with different body functions such as easting, physical behavior, emotion, sexual behavior, mod, attitude and decision-making process. Serotonergic neurons are the parent cells for the Serotonin. Current biological and genetic researches suggest that decreases in the level of serotonin due to the reduced production of this neurotransmitter through the spermatogenic cells can cause depressions, anxiety, behavioral disorder, and other psychological disorders.

Neurotransmitter dysfunction has been considering as one of eth important cause of depression, through different researcher it is seen that Norepinephrine level in case of depressed people is lower than that in the normal people. As stated by Miller and Raison (2016), Norepinephrine is considered as the stress hormone which is secreted at the time of stress. When the brain perceives ant stressful event, this neurotransmitter is secreted from the brain cells and respond to the stress. During the stressful moment, Norepinephrine increase the heart rate, trigger the secretion of glucose into the blood and enhance the blood towards muscles. As stated by Temin (2016), recent researches have suggested that in the case of people with depressions and anxiety the level of Norepinephrine is lower than in eth normal people. due to the low level of Norepinephrine, people cannot deal with a stressful moment in a proper manner.

Due to the low level of Serotonin, people are suffering from suicidal thoughts, unorganized, and poor decision-making ability. in case of treating the patient with depression, most of the doctors recommend the antidepressant tablet Prozac, that blocks the reuptake of the Serotonin thereby increasing the serotonin level inside the brain.

Recent researches suggest that there is a strong association between the elevated level of the cortisol and occurrence of depression in the people. Dexamethasone is generally recommended to the patient with depression, in order to reduce the level of eth Cortisol in the brain and maintaining the normal balance of this chemical.

As stead by Wakefield et al. (2017), Biological Theory of depression states that most of the researches support the genetic explanation of the depression. Genetic studies suggest that different genes are associated with influencing eth activities and secretion of the Serotonin and other neurotraumatic. For example, 5-HTT gene represents in either long or in short form. This gene is known as the Serotonin Transporter Gene, that is associated with different psychiatric disorders. It has been proved through the different biological research that, Serotonin and its transporter that transport the serotonin from the synaptic spaces to the presynaptic neurons are associated with the pathophysiology of different psychological disorders. Mutation in the 5-HTT or Serotonin transporter gene leads to massive changes in the functions of the serotonin transporter. There is two variant in the serotonin transporter gene variant, one is long and the other is the short variant. Repetition of codes in the promoter region of 5-HTT gene leads to abrupt changes in the structure and functions of the serotonin transporter, which is associated with depressional another psychiatric disease (Beck and Bredemeier, 2016). The recent studies have also shown that the repeat length valiant in the promoter region of the serotonin transporter gene is associated with the etiology of the different psychiatric disorders. The repeat the length variant also affect the Serotonin uptake thereby playing important role in developing post-traumatic stress as well as depression susceptibility among the people. due to the gene mutation of the neurotransmitter there occurs the chemical imbalance of the Serotonin, Norepinephrine, and dopamine, which leads to increase the risk of depression, suicidal attitude and unorganized behavior among in the people.

Cognitive explanation of Depression:

Cognitive explanation of psychiatric illness and depressional is based on eth fact that psychological disorders occur because of eth faulty thoughts and lack of thinking ability. the cognitive approach believes that human behaviour is controlled and influenced by the thoughts, perception, and decisions. As stated by Cheng (2015), the cognitive model of depression highlights the fact that irrational beliefs and thoughts are associated with psychiatric disorders and depression. There are different cognitive approaches that have been used in several times to explain the cause, pathology, and outcomes of depression.

In 1963 Beck developed a cognitive explanation of the psychiatric illness, especially of depression. Based on this model, people get depressed because of their thoughts and thinking process become biased towards the negative interpretation of the world and their thoughts lack the perceived sense of control. Beck explained the ‘Negative Triad', in which he explained the cognitive approach of understanding and evaluating the aspects of depression. The negative triads explain how the negative understating and expectation (schema) about everything can leads to depression. For example, negative thinkers always think that they can not do the easier task or they cannot cope up with the current situation. This negative thought leads to educational decision making, problem-solving and positive thinking ability which develop a high level of depression. As stead by Frost et al. (2015), Beck also explained that negative schema can be acquired during the childhood because of some traumatic incidents. There can be a different experience that can contribute to developing negative schemas such as parental rejection, childhood bullying, abuse, discriminating, violence, bereavement and consecutive failure in eth past. According to people with negative schemas are prevalent to make logical errors in their thinking, decision-making process.

Elise had proposed this cognitive model if depressional in 1962. The psychiatric disorder develops in eth Activating Stage (A) in early childhood such as the failure in the exam or childhood bullying in the school. According to Price et al. (2016), after the occurrence of activating stage (A), people set to the negative belief (B) in their mind, that affect their thoughts, feelings, and decisions. The beliefs can either irrational or rational. Rational belief assists the children to learn their drawbacks from the failure and prepare for the next time. Whereas the irrational belief leads to the logical errors into the thoughts, which damages the self-confidence of the children. Ellis stated that rational beliefs are associated with eth developing the healthy emotional outcomes, whereas the irrational beliefs lead to negative consequences (C), that can develop depressional and other psychological illness in the adult life. According to Haslam and Kvaale (2015), healthy emotional outcomes develop the adaptive consequences, that assist the children to develop their thoughts, decision, and skill to get the success. For example, proper revision and regular practice can assist the student to pass the exam. On the other hand, negative consequence leads to maladaptive psychological functions such as depression, anxiety, poor decision-making ability, and the suicidal approach.

Evidence-based reports suggest that, although the cognitive approach to explaining the depression is widely used by the psychologist, there are are some criticism regarding the relevance and appropriateness of the explanation. In order to evaluate and analyse the Cognitive approach of depression, Burke et al. (2015), mentioned that cognitive theory highlights the irrational thoughts and negative belief, that drives the individual towards different psychological illness such as depression, anxiety and restlessness. On supporting this viewpoint, several psychological types of research show that, while participants suffering from eth depression is reinforced with negative automatic thoughts, they are more depressed and anxious. This psychological disturbances through the negative thoughts and beliefs can be explained through the cognitive approach. On the contrary, Cheng (2015), argued that biological researches and genetic therapies have shown that, depression develops through the low level of the neurotransmitter Serotonin in the brain cells. Therefore, the cognitive approach that describes that negative and irrational thoughts are associated with the development of depression ignores the biological researches and theories. In this aspect, Haslam and Kvaale (2015) stated that cognitive approach highlights that if an individual thinks in a negative way he is prevalent to the risk of depression, this can lead to situational factors (family, background, social circumstances and culture) being overlooked.

Analysis of the Back's Triad Model also represents several strengths and drawbacks of the cognitive approaches in order to explain the depression. According to Beck and Bredemeier (2016), this model considers the negative thoughts and beliefs as responsible for leading people towards the negative interpretation of the world. Moreover, negative thoughts, irrational beliefs and the unorganized thinking process lead to a lack of a perceived sense of control. On the contrary, Tomlinson and Slater (2017) argued that this explanation has several criticisms by many biologist and therapists, in which they stated that cognitive therapy emphasizes on representing the strong association of mental dysfunction and the negative belief, that is considered as the drawback of cognitive approach by the several; biologist and psychotherapist. Recent biological researches show that an individual can have negative thoughts such as low self-esteem, self-criticism, unpleasant memories, self-blame and erroneous interpretation, then also they can have the proper brain functioning due to the appropriate level of the neurotransmitter Serotonin. According to De Raedt et al. (2015), although Cognitive Behavioural Therapy (CBT), is widely by a psychotherapist in order to treat the psychological disorders, it does not prove that only irrational belief and negative thoughts are associated with the development of depression. However, recent psychotherapists also suggest that, sometimes, CBT is unable to treat the depressional and anxiety of patients, due to the decreasing amount of neurotransmitter into the brain cells. In this aspect, Cheng (2015), stated that sometimes the people who are suffering from poor parental support, tormented family conditional and lack of social support can be highly prevalent to the psychological disorders. Cognitive approach overlooked these situation factors such as culture, family background, educational background and social situation, which play the important roles in influencing the mental processes of the human being.

Therefore, from the above-mentioned analysis and evaluation of the cognitive approach if depression, it can be stated that, although cognitive approach has wide ranges of benefit to improve the psychological condition of the patient, it has several drawbacks in explaining the actual cause of depression. On the other hand, the cognitive approach assists physicians and therapist to use Cognitive Behavioural Theory (CBT) and Rational Emotional Behavioural Therapy (REBT) in order to treat psychological disorders. therefore, it can be stated that, although there are several criticisms regarding the explanation of the cognitive approach, it can be used in a positive way to the depression and other psychological illness.

Conclusion:

From the above discussion, it can be concluded that depressional is the psychological; disorder that adversely affects the thoughts, beliefs and perfectional of the people. different approaches are established to explain the reason, outcomes and pathopsychological of depression. There are two most important approaches for depressional such as biological approach and cognitive approach. Biological approach highlights the genetic dysfunction, mutational and neurotransmitter dysfunction are associated with the depression. On the other hand, the cognitive approach considers the wrong thoughts and logical error in the thinking process as important factors associated with eth depression. However, this study has concluded that it is high time to reduce the ever-increasing risk of depressional by analyzing the reason, cause, and pathophysiology of depression.

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Reference list:

• Beck, A.T. and Bredemeier, K., 2016. A unified model of depression: Integrating clinical, cognitive, biological, and evolutionary perspectives. Clinical Psychological Science, 4(4), pp.596-619.
• Burke, T.A., Stange, J.P., Hamilton, J.L., Cohen, J.N., O'Garro‐Moore, J., Daryanani, I., Abramson, L.Y. and Alloy, L.B., 2015. Cognitive and emotion‐regulatory mediators of the relationship between behavioral approach system sensitivity and nonsuicidal self‐injury frequency. Suicide and Life‐Threatening Behavior, 45(4), pp.495-504.
• Cheng, Z.H., 2015. Asian Americans and European Americans’ stigma levels in response to biological and social explanations of depression. Social psychiatry and psychiatric epidemiology, 50(5), pp.767-776.
• De Raedt, R., Vanderhasselt, M.A. and Baeken, C., 2015. Neurostimulation as an intervention for treatment resistant depression: from research on mechanisms towards targeted neurocognitive strategies. Clinical Psychology Review, 41, pp.61-69.
• Drysdale, A.T., Grosenick, L., Downar, J., Dunlop, K., Mansouri, F., Meng, Y., Fetcho, R.N., Zebley, B., Oathes, D.J., Etkin, A. and Schatzberg, A.F., 2017. Resting-state connectivity biomarkers define neurophysiological subtypes of depression. Nature medicine, 23(1), p.28.
• Elder, G.H., 2018. Children of the great depression. Routledge. Chukhraev, N., Vladimirov, A., Zukow, W., Chukhraiyeva, O. and Levkovskaya, V., 2017. Combined physiotherapy of anxiety and depression disorders in dorsopathy patients. Journal of Physical Education and Sport, 17(1), p.414.
• Frost, A., Hoyt, L.T., Chung, A.L. and Adam, E.K., 2015. Daily life with depressive symptoms: Gender differences in adolescents' everyday emotional experiences. Journal of Adolescence, 43, pp.132-141.
• Haberler, G., 2017. Prosperity and depression: A theoretical analysis of cyclical movements. Routledge.
• Haslam, N. and Kvaale, E.P., 2015. Biogenetic explanations of mental disorder: The mixed-blessings model. Current Directions in Psychological Science, 24(5), pp.399-404.
• Karp, D.A., 2016. Speaking of sadness: Depression, disconnection, and the meanings of illness. Oxford University Press.
• Kaser, M., Deakin, J.B., Michael, A., Zapata, C., Bansal, R., Ryan, D., Cormack, F., Rowe, J.B. and Sahakian, B.J., 2017. Modafinil improves episodic memory and working memory cognition in patients with remitted depression: a double-blind, randomized, placebo-controlled study. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 2(2), pp.115-122.
• Kertz, S.J., Belden, A.C., Tillman, R. and Luby, J., 2016. Cognitive control deficits in shifting and inhibition in preschool age children are associated with increased depression and anxiety over 7.5 years of development. Journal of abnormal child psychology, 44(6), pp.1185-1196.
• Miller, A.H. and Raison, C.L., 2016. The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nature Reviews Immunology, 16(1), p.22.
• Price, R.B., Rosen, D., Siegle, G.J., Ladouceur, C.D., Tang, K., Allen, K.B., Ryan, N.D., Dahl, R.E., Forbes, E.E. and Silk, J.S., 2016. From anxious youth to depressed adolescents: Prospective prediction of 2-year depression symptoms via attentional bias measures. Journal of abnormal psychology, 125(2), p.267.
• Temin, P., 2016. Great Depression. In Banking Crises (pp. 144-153). Palgrave Macmillan, London.
• Wakefield, J.C., Horwitz, A.V. and Lorenzo-Luaces, L., 2017. 8 CHAPTER Uncomplicated Depression as Normal Sadness: Rethinking the Boundary Between Normal and Disordered Depression. The Oxford handbook of mood disorders, p.83.

Bibliography:

• Beck, A.T. and Bredemeier, K., 2016. A unified model of depression: Integrating clinical, cognitive, biological, and evolutionary perspectives. Clinical Psychological Science, 4(4), pp.596-619.
• Belzung, C., Willner, P. and Philippot, P., 2015. Depression: from psychopathology to pathophysiology. Current opinion in neurobiology, 30, pp.24-30.
• Cai, N., Chang, S., Li, Y., Li, Q., Hu, J., Liang, J., Song, L., Kretzschmar, W., Gan, X., Nicod, J. and Rivera, M., 2015. Molecular signatures of major depression. Current Biology, 25(9), pp.1146-1156.
• Cheng, Z.H., 2015. Asian Americans and European Americans’ stigma levels in response to biological and social explanations of depression. Social psychiatry and psychiatric epidemiology, 50(5), pp.767-776.
• Czéh, B., Fuchs, E., Wiborg, O. and Simon, M., 2016. Animal models of major depression and their clinical implications. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 64, pp.293-310.
• De Raedt, R., Vanderhasselt, M.A. and Baeken, C., 2015. Neurostimulation as an intervention for treatment resistant depression: from research on mechanisms towards targeted neurocognitive strategies. Clinical Psychology Review, 41, pp.61-69.
• Drysdale, A.T., Grosenick, L., Downar, J., Dunlop, K., Mansouri, F., Meng, Y., Fetcho, R.N., Zebley, B., Oathes, D.J., Etkin, A. and Schatzberg, A.F., 2017. Resting-state connectivity biomarkers define neurophysiological subtypes of depression. Nature medicine, 23(1), p.28.
• Elder, G.H., 2018. Children of the great depression. Routledge. Chukhraev, N., Vladimirov, A., Zukow, W., Chukhraiyeva, O. and Levkovskaya, V., 2017. Combined physiotherapy of anxiety and depression disorders in dorsopathy patients. Journal of Physical Education and Sport, 17(1), p.414.
• Frost, A., Hoyt, L.T., Chung, A.L. and Adam, E.K., 2015. Daily life with depressive symptoms: Gender differences in adolescents' everyday emotional experiences. Journal of Adolescence, 43, pp.132-141.
• Gururajan, A., Clarke, G., Dinan, T.G. and Cryan, J.F., 2016. Molecular biomarkers of depression. Neuroscience & Biobehavioral Reviews, 64, pp.101-133.
• Haslam, N. and Kvaale, E.P., 2015. Biogenetic explanations of mental disorder: The mixed-blessings model. Current Directions in Psychological Science, 24(5), pp.399-404.
• Karp, D.A., 2016. Speaking of sadness: Depression, disconnection, and the meanings of illness. Oxford University Press.
• Kaser, M., Deakin, J.B., Michael, A., Zapata, C., Bansal, R., Ryan, D., Cormack, F., Rowe, J.B. and Sahakian, B.J., 2017. Modafinil improves episodic memory and working memory cognition in patients with remitted depression: a double-blind, randomized, placebo-controlled study. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, 2(2), pp.115-122.
• Kelly, J.R., Borre, Y., O'Brien, C., Patterson, E., El Aidy, S., Deane, J., Kennedy, P.J., Beers, S., Scott, K., Moloney, G. and Hoban, A.E., 2016. Transferring the blues: depression-associated gut microbiota induces neurobehavioural changes in the rat. Journal of psychiatric research, 82, pp.109-118.
• Kertz, S.J., Belden, A.C., Tillman, R. and Luby, J., 2016. Cognitive control deficits in shifting and inhibition in preschool age children are associated with increased depression and anxiety over 7.5 years of development. Journal of abnormal child psychology, 44(6), pp.1185-1196.
• Kiecolt-Glaser, J.K., Derry, H.M. and Fagundes, C.P., 2015. Inflammation: depression fans the flames and feasts on the heat. American Journal of Psychiatry, 172(11), pp.1075-1091.
• Milaneschi, Y., Lamers, F., Peyrot, W.J., Abdellaoui, A., Willemsen, G., Hottenga, J.J., Jansen, R., Mbarek, H., Dehghan, A., Lu, C. and Boomsma, D.I., 2016. Polygenic dissection of major depression clinical heterogeneity. Molecular psychiatry, 21(4), p.516.
• Miller, A.H. and Raison, C.L., 2016. The role of inflammation in depression: from evolutionary imperative to modern treatment target. Nature Reviews Immunology, 16(1), p.22.
• Penninx, B.W., 2017. Depression and cardiovascular disease: epidemiological evidence on their linking mechanisms. Neuroscience & Biobehavioral Reviews, 74, pp.277-286.
• Price, R.B., Rosen, D., Siegle, G.J., Ladouceur, C.D., Tang, K., Allen, K.B., Ryan, N.D., Dahl, R.E., Forbes, E.E. and Silk, J.S., 2016. From anxious youth to depressed adolescents: Prospective prediction of 2-year depression symptoms via attentional bias measures. Journal of abnormal psychology, 125(2), p.267.
• Proudfit, G.H., 2015. The reward positivity: From basic research on reward to a biomarker for depression. Psychophysiology, 52(4), pp.449-459.
• Spinelli, M.G., Endicott, J., Goetz, R.R. and Segre, L.S., 2016. Reanalysis of efficacy of interpersonal psychotherapy for antepartum depression versus parenting education program: initial severity of depression as a predictor of treatment outcome. The Journal of clinical psychiatry, 77(4), pp.535-540.
• Temin, P., 2016. Great Depression. In Banking Crises (pp. 144-153). Palgrave Macmillan, London.
• Wakefield, J.C., Horwitz, A.V. and Lorenzo-Luaces, L., 2017. 8 CHAPTER Uncomplicated Depression as Normal Sadness: Rethinking the Boundary Between Normal and Disordered Depression. The Oxford handbook of mood disorders, p.83.
• Wang, M.J., Song, L.P., Song, B.L., Du, Q.R., He, X.X. and Bai, X.J., 2017. Correlation Analysis of Resilience, Defense Mechanism and Depression in Patient with Depression. China J. Health Psychol, 25, pp.165-168.
• Williams, L.M., Debattista, C., Duchemin, A.M., Schatzberg, A.F. and Nemeroff, C.B., 2016. Childhood trauma predicts antidepressant response in adults with major depression: data from the randomized international study to predict optimized treatment for depression. Translational psychiatry, 6(5), p.e799.