Explain and evaluate the biological basis of depression with empirical evidence
Depression is classified in the DSM 5 as a mood disorder. According to DSM criteria, symptoms of MDD include feeling sad and helpless every-day for weeks, which is important to distinguish from general feelings of low mood that every individual will at some point experience. Other symptoms include having little energy to carry out every-day tasks, feelings of worthlessness and hopelessness, as if things will never get better. Difficulty sleeping is another symptom, patients with depression often have difficulty falling asleep or find that they sleep too much, they may also express suicidal thoughts. One key symptom of depression is anhedonia, which is the inability to feel pleasure, many people with depression find that activities and hobbies which they used to enjoy no longer provide pleasure or joy. Peters et al, 2003, gave participants a beeper which would alert them at random points in the day and asked them to diarise their mood and events, people with depression in-fact feel the same amount of unpleasant feelings as controls, but experienced far below the average number of pleasant mood and experiences. There are two types of MDD, unipolar depression refers to the tendency to alternate between feelings of low and normal mood, whereas bipolar refers to the switching between moods of severe depression and mania, where people often become impulsive and over-excited, this can be seen through behaviours such as excessive spending, excess energy with little need to sleep and rambling sentences. Psychotic symptoms of both aspects of MDD can sometimes include hallucinations and delusions. People with depression can also experience physical symptoms, such as headaches, vertigo, constipation and often suffer from IBS.
The cause of depression is something which has been studied extensively in psychology, previous explanations from pioneers such as Freud say that depression arises from a conflict between the id and the ego, whereas cognitive psychologists pinpoint a faulty thinking style, such as Beck’s negative triad of the self, the world and the future. However, most researchers are in agreement that a key factor which increases the likelihood of an individual experiencing depression comes from biology.
One biological explanation for depression boils down to genetic differences. Shih et al, 2004, found that there is a moderate degree of heritability for depression. Monozygotic twins have higher concordance rates for the mood disorder than dizygotic twins. People with early onset depression are also likely to have relatives with the disorder, as well as relatives with anxiety disorders, compulsive disorders and alcoholism. Whereas people with late onset are often found to have relatives with circulatory problems – the distinction between early and late onset of depression is critical when trying to identify a ‘depression gene.’ Other research has also indicated a relationship between genetic disposition and the environment, for example, 5-HTT, a serotonin transporter regulates the ability to reabsorb serotonin. It has been found that people with two short alleles of this gene have an increasing likelihood of developing depression combined with a higher number of life stressors, this was significantly less for individuals who have two long forms of 5-HTT (Caspi et al, 2003).
However, since this initial study, many other researchers have failed entirely to replicate these results, whilst others found no relationship between 5-HTT and depression, or 5-HTT and life stressors. This can lead to an interpretation that the first finding by Caspi and colleagues was wrong. Although, it is possible to critique Caspi’s study based on poorly measured variables. It is particularly difficult to gain valid measurements for stress, and what counts as a life stressor, each person individually decides what is stressful to them and this depends heavily on the situation. For example, if one individual gets fired from a job, they may experience a lot of stress, whereas if this individual was planning to leave regardless and had a better job lined up for them, they’re likely to experience much less stress. Wray et al, 2009, also found that the biochemical methods used to measure different forms of the gene may have been inaccurate in many cases.
Also, no paper on depression and the 5-HTT or meta-analyses looked at the impact early life experiences can have on depression when combined with the 5-HTT allele, in-fact Caspi’s study excluded all people with had an onset of depression before 21, they placed importance which was undue on the impact of recent life events, rather than early ones, which may have been mistaken; considering recent studies show early childhood maltreatment is more consistent with depression being brought on by life stressors, it may be that previous research has failed to identify the crux of the interaction between the environment and depression. Instead, most researchers are now considering that depression may be caused by a contribution of entire pathways of genes, and the view that a single gene or allele causes depression is outdated.
A second factor which has evidential support in causing depression stems from a neurochemical basis. The monoamine hypothesis posits that depression may be due to a chemical inbalance in the brain regarding a group of neurotransmitters in the brain, known as the monoamine group (Noradrenaline, serotonin and dopamine). Serotonin is responsible for regulating mood, sleep cycles and memory/learning, and is the neurotransmitter most extensively researched in this field. Studies using tryptophan depletion, which reduces serotonin synthesis, found that this can lead to the development of depressive symptoms (in a study of healthy subjects). Serotonin inhibition can also cause noradrenaline and norepinephrine to fluctuate, associated with the extremely polar levels of mood associated with bipolar. Charney et al, 2004, found that depressed patients often show fewer norepinephrine transporters, while treatments which aim to alter chemical balances are often effective in treating depression. MAO inhibitors alleviate depression by increasing levels of serotonin and noradrenaline, SSRI’s which inhibit reuptake of serotonin are also linked to improved mood.
The treatments which aim to relieve depression also support the mainly biological basis of the disorder. There are different varieties of anti-depressant medication. Tricyclis work by blocking transporter proteins that reabsorb dopamine and norepinephrine, meaning the chemical stays in the synaptic gap for longer and continues hitting receptors sites. SSRi’s block reuptake of serotonin and are the most widely used form due to their milder side effects. MAOI’s such as Nardil work to metabolise catecholamines and serotonin into inactive forms, this inhibits MAO levels in the brain, but are often only prescribed if other medications prove ineffective. Finally, atypical anti-depressants are also used, which are often available without prescription, such as St John’s Wort, the way in which these work remains unclear.
However, one can argue that having fewer neurotransmitters available is not solely responsible for depression. Some studies show that people with depression have normal levels of neurotransmitter being released, and some even have increased levels of serotonin (Barton, et al, 2008). The decrease in serotonin levels by consuming amino acids does not seem to provoke depressive feelings, (Neumeister et al, 2004). This implies that the link between neurotransmitter levels and depression is not sufficient to explain the disorder. There are individual differences which call into question the role of neurotransmitters in treating depression. Around 30% of depressed patients fail to respond to any given drug or show very small beneficial effects, drug therapy is not effective for all sufferers. In addition to this, it is often the case that anti-depressants can take between 2-6 weeks to lift the mood of users, even though the neurotransmitter increase at the synapse can increase within minutes of taking the drug. The magnitude of benefit of antidepressant medication compared with placebo increases with severity of depression symptoms and may be minimal or non-existent, on average, in patients with mild or moderate symptoms. For patients with very severe depression, the benefit of medications over placebo is substantial, indicating that in mild cases of depression – it may be a change in thinking styles which contribute to subsiding symptoms, it may not always be the increase in NT which cause anti-depressants to work. Some researchers go as far as suggesting that neurotransmitters may be irrelevant, there may be a structure or phenomenon occurring in the brain which acts as a precursor to neurotransmitter imbalance which needs to be identified. Continued and regular anti-depressant usage increases the volume of the hippocampus, leading some to lean toward a neuroanatomical view of depression.
Neuroanatomical differences in depression have been studied producing varied results. Jacobs and Snyder, 1996, have shown a strong relationship between happy mood and increased activity in the left PFC, other research shows an association between decreased activity in the left PFC and depression. It may be the decrease in cortical activity which results in feelings of depression. FmRI studies have also shown that the hippocampus is often smaller in people with depression, by around 9-13% in women in comparison to healthy controls, there is also correlation between frequency of bouts of depression and hippocampus size. The fact that anti-depressants can induce growth in the hippocampus suggests that neuroanatomy may have a more profound impact on the disorder than neurotransmitters. In animal studies, anti-depressants have been shown to enhance the growth and branching of nerve cells in the hippocampus. Whereas drugs which treat bipolar and aim to decrease mania, decrease the number of glutamate receptors in the hippocampus (the main excitatory NT in the brain.) Thus, it may be the case that depression does not have a sole cause, but is instead produced as a complex interaction between atypical neuroanatomical structures and chemical imbalance – which interact with the environment (diathesis-stress model).