Compare and contrast psychological and biological explanations of major depression

Compare and contrast psychological and biological explanations of major depression

Compare and contrast psychological and biological explanations of EITHER major depression OR schizophrenia

 

 

 

Introduction

This essay compares and contrasts psychological and biological explanations of major depression, the predominant theories used in explaining major depression. Biological theories of major depression refer to genetic and neurochemical level factors used to explain the aetiology of depression while psychological theories of depression look at cognitive and behavioural-level explanations behind clinical depression (Davey 2011). The essay will look at each theory individually before making comparisons in terms of similarities and later contrast them looking at variances, before coming to a conclusion regarding which one offers the best explanation for major depression.

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What is major depression?

This is a clinical disorder characterised by extreme distress to the person, leading to significant diminishment in many areas of life such as occupational effectiveness or social impairment in relating with other people. Persons who are diagnosed with major depression experience long-term maladaptive cognitive patterns lasting beyond 6 months at which point it becomes major depression (Davey 2011). It is characterized by certain physiognomies such as feelings of sadness, apathy, lack of motivation, loss of appetite, irregular sleeping, and general negativity about self or the world (Weissman et al., 1996). 

Psychological explanations of major depression

Psychological explanations of depression refer to those cognitive/mental and behavioural-level causal factors that can be used to explain the aetiology of major depression. Psychological explanations of major depression postulate that the way a person mentally interprets and remembers certain situations can initiate depression. The bulk of theory and empirical research is centred on three major theories; Becks negative cognitive theory (Beck 1967), hopelessness theory (Abramson et al., 1989) and rumination theory (Nolen-Hoeksema 1991).

Negative cognition style

The first theory by Becks (1969) posits that negative cognition/perception or predisposition to negative thinking can precipitate depression.  A person’s perception and appraisal of a major event can make them vulnerable to major depression (Blaney 1977). Experimental studies have for instance shown that depressive states can be induced in participants simply by manipulating their focus of attention or individual beliefs towards the negative, supporting Becks position. Moon et al (1973) requested participants to remember a sad event, focussing their attention on negative and unpleasant thoughts, which influenced their affective state. Other experiments have shown even lowering a person’s belief regarding self-worth and esteem will result in mild depression (Ludwig 1975; Coleman 1975). In other words, negative cognitive bias regarding self, the world and the future, what Becks (1969) refers to as the negative triad, is central to depression. It is also important to remember it is major life events that lead to stress factors precipitating to major depression (Flett and Hewitt 1990; Haaga et al., 1991).

Hopelessness/attribution theory

The second psychological explanation of major depression is the hopelessness theory by Abramson et al (1989) which postulates that onset of depression can be triggered by (a) tendency to negatively attribute the causes of negative events such as an earthquake (b) the tendency to catastrophize the consequences of that negative event, and (c) the tendency to deduce negative characteristics about the self after the negative event (Hankin 2008). 

Rumination theory

The last psychological theory is the rumination response, which represents another cognitive vulnerability factor in major depression. According to Nolen-Hoeksema (2000), people with a ruminative response style in essence “ruminate” repetitively and passively about the negative emotions elicited by negative events, and a number of studies have confirmed this response style predicts depression. For example, a study cited in Nolen-Hoeksema (2000) of college students at the time of the 1989 San Francisco earthquake showed that those possessing a ruminative style before the earthquake experienced elevated depressive symptoms shortly after the earthquake and 7 weeks after it, even controlling for depressive symptoms before the quake (Nolen-Hoeksema & Morrow, 1991). 

Despite significant evidence supporting all three psychological theories in predicting major depression, it is a multifaceted disorder with multiple factors and mechanisms contributing to its ontogeny. Cognitive explanations thus are only a contributory factor, and not a necessary, cause of depression, since persons can become depressed without necessarily showing cognitive vulnerability (Hankin et al., 2009).In the following section, we thus review some of the biological factors that may actually contribute to the emergency and developmental origins of cognitive vulnerabilities that predict depression.

 

Biological explanations of major depression

According to Davey (2011), biological explanations of major depression postulate that the aetiology of major depression can be down to two factors; genetic vulnerability and neurochemical imbalances.

Genetics

According to McGuffin et al (1997), human beings are shaped by genetics and much of what a person is or becomes is inherited, including behaviour, temperament as well as disposition to certain diseases. This was illustrated by a study of MZ and DZ twins to determine their concordance rates when it came to major depression. The study showed that concordance rates for MZ twins was 69% compared to just 29% for DZ twins illustrating the genetic likelihood of inheriting major depression, if one twin also had it. 

Neurochemical factors

The second biological cause for major depression is linked to neurochemical factors specifically low levels of neurotransmitters serotonin and norepinephrine, with resulting symptoms similar to affective states of depression. In comparing psychological and biological explanations of major depression, many studies (e.g. Hayden et al., 2008; Lau et al 2006; Lau and Eley 2008; NolenHoeksema and Simen 2007) have actually found supporting evidence that shows biological origins for cognitive vulnerabilities. 

Lau et al (2006) for instance found considerable genetic heritability of attribution styles and depression in MZ twins. Expanding on this study, Lau and Eley (2008) replicated these results, finding moderate genetic links between attribution style and depressive symptoms among non-depressed MZ twins although the specific genes for cognitive vulnerability couldn’t be identified. Hayden et al., (2008) found a more pronounced biased recall of negative words among children having a certain genotype (two copies of the S allele) when a negative mood was induced. These findings were replicated by Sheikh et al., (2008) who found children with 1 or 2 copies of the of the S or LG allele had a higher tendency to negatively attribute the causes of negative events compared to those possessing long alleles.

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Comparison and variance between the two

In comparing and contrasting cognitive and biological explanations of major depression, we can thus deduce the following comparisons and variances between both explanations. Both psychological and biological explanations of major depression can be associated and linked interchangeably as one mechanism that can predict major depression. This has been shown by the many studies that have established gene-cognitive vulnerability interplay and co-relation that leaves persons with certain gene phenotypes vulnerable to negative attribution styles that induce major depression. This link brings both psychological and biological explanations when comparing their explanations of the aetiology of major depression following major negative events.

However, despite this comparison, both explanations have variances than need to be pointed out. First is the fact biological genetic vulnerabilities are natural occurrences that cannot be changed or influenced, which may explain why drugs such as SSRIs are still regarded as ineffective in treating major depression. On the other hand, research on cognitive or psychological explanations of major depression suggests certain cognitive dysfunctions can be influenced through manipulating beliefs, attitudes and environmental cues. Hankin et al (2009) for instance noted that children who face emotional abuse, maltreatment exhibit increases in depression. Thus eliminating such behaviour from their environment can reduce the development of dysfunctional attitudes that lead to psychological vulnerabilities to depression.

Conclusion

Overall, psychological explanations of major depression have more scope for research and influence with a better degree of control in reducing vulnerability to them compared to biological explanations. The fact that variations in environment and experiences of children and adolescents can alter individual cognitions positively or negatively makes for at least efficacious psychotherapeutic work as opposed to biological mechanisms.

 

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