Modern medical research has contributed much to our understanding of depression. However scientists do not know the exact mechanism that triggers depressive illnesses. Doctors believed that depression was the result of thoughts and emotions that were troubling a person. Most recently, experts realized that there can be several factors working together that will lead a person to become depressed.
Many brain chemicals and hormones have been linked to the development of depression, meaning a person is depressed because of a biochemical imbalance, usually involved with the functioning of neurotransmitters that help different parts of the brain communicate with each other. There are many neurotransmitters each serving different purposes, but the three important ones that affect a persons mood is serotonin, noradrenalin and dopamine. Low levels of these chemicals have not been proven to cause depression, however, it is believed that elevation of these chemicals can improve the mood of a depressed person. Suffers of depression were given a treatment in the form of an antidepressant drug that would boost serotonin and noradrenalin levels giving a 60% reduction in depressive symptoms. This shows brain chemicals and hormones are a strong factor, but as it is not proven in every case of depression there must also be other factors to take into consideration, which triggered theorists to conduct studies to try and determine what other factors could be associated with the causes of depression.
McGuffin et al (1996) conducted a study to see if it was possible that genetics was a component for depression. They studied identical (monozygotic, MZ) twins, which share 100% of their genes, with non-identical (dizygotic, DZ) twins who, like normal siblings, share around 50% of their genes. Out of the total of 109 pairs of twins he found that when a MZ twin was diagnosed with depression, there was a 46% chance that the other twin would receive the same diagnoses, whereas the figure for DZ twins was only 20%. The study supports the idea that a higher proportion of identical twins share the disorder, but as the percentage is no where near 100% it shows genetics can play a part but it can not be totally down to genetics.
Bierut et al (1999) conducted a twin study using a significant amount of twin pairs to determine the genetic factor. They used 2662 pairs and found a heritability factor of between 36% and 44%, but claimed environmental factors played a larger role. They also found that gender differences indicating lifetime prevalence of 31% for females and 19% for males, indicating females are more likely to suffer from the disorder.
Hendler & Prescott (1999) conducted the same study using 3790 twin pairs and found a heritability factor of 39% with the remaining 61% down to environmental factors. Unlike Bierut et al he found no difference between males and females.
It should be noted, however, that there have been criticisms of the underlying assumptions of twin studies. One of the most common criticisms is what effects the environment has on the study. Twins usually share the same environment as they develop through time, but the factor is dismissed as a component. Reiss and Neiderhiser (2000) suggested that “it needs to be subjected to continuing criticisms as we learn more about the nuances of sibling relationship and how they evolve overtime. It may well be that subtle differences in the social worlds of identical twins in comparison to fraternal twins are still masquerading as genetic influence” They do not suggest ignoring the studies altogether but suggest integration with observations about the social environment in developmental theories.
Some psychologists thought that research from twin studies were limited due to the fact stated that they usually shared the same environments. Wender et al (1986) conducted studies to compare people, who have been adopted at an early age, with their biological and adoptive parents. Since they had been raised apart from their biological parents, similarities with those parents would indicate genetic influences. The studies showed adopted children who later develop depression are more likely to have a biological parent who has had depression, or another psychological disorder or had committed suicide.
Harrington et al (1993) found that most studies with adoptees that had been diagnosed with depression show that there is a 20% chance that their biological relatives have similar diagnoses, compared to the 5% - 10% chance of there adoptive relatives, which is the rate for the general population. This shows that there is a slightly stronger link between biological relatives that adoptive, but again the percentage is no where near 100%, in fact it is less than a quarter of 100% showing genetics can only play a very small part in a small minority of people. Most of the children and adolescents in this study had other disorders such as dysthymia, an anxiety disorder, disruptive or antisocial disorder or a substance abuse disorder. This suggests that in some cases depression may have arose in response to the other disorders and not all due to genetics.
Birmaher et al (1996) conducted a study to see if depression was passed on through family history. They found that between 20 and 50% of children and adolescents who suffer depression have a family history of the disorder. They stated that children of a depressed parent are three times more likely, than that of children of non depressive parents to experience a depressive disorder and they are also more vulnerable to other mental and somatic disorders. Hammen et al (1990) found that parents with a depressed child or adolescent vary from approximately 1 in 6 to just under half.
These studies of children and adolescents were conducted with those who attended mental health clinics with patients who tend to suffer from more severe or recurrent depression, thus they may not be representative of all the children and adolescents that suffer from the disorder. It is also not clear in family studies whether it is genetics playing a part or whether it is the depressed parents that create an environment that increases that likelihood of a mental disorder developing in their children.
Psychologists agree that stressful life events can trigger depression in people who are predisposed to the illness. Freud related depression with early relationships with parents. He suggests that a child who was either under or over gratified in their infant lives were more likely to suffer depression. If a child received too much love from their parents, they would want the experience to last their lifetime, yet the love they received as a child is not fourth coming as they grow older. If the child, on the other hand, does not get enough love as a child, they would feel unworthy and consequently have low self esteem. Both experiences involve loss, and they will seek to compensate for the loss and become overly dependant on others for love, attention and self esteem. Freud thought that these feelings are repressed into the unconscious mind and a loss in adulthood could re-emerge their feelings of unworthiness and rejection they experienced as a child, and trigger depression. Freud also suggested that depression involves guilt and self – criticism, which can be related to a loss in childhood. The child could feel anger and hostility towards their parent if they do not receive enough love and warmth that is needed for healthy development. However these feelings are turned inwards and the child blames itself for the loss and feels guilt and leads to self – criticism. The loss of a loved one in adulthood may bring back these feeling and would feel anger towards the loved one for dying and leaving them. This anger then could be internalised, leading to guilt, which would then lead to depression.
Freud received a lot a criticism for this theory as he suggests that loss in adulthood triggers depression caused by early life experiences, but what about people who suffer from depression, who have not lost a loved one? From his theory he did not consider other factors and stated that a depressed person must have experienced a loss in their lives to be a sufferer of the disorder.
Parker et al (1998) devised a ‘lock and key’ hypothesis to establish the way depression is triggered off. Early adverse experiences, such as parents dying and being taken into care, which is the lock, is triggered off by later experiences, such as loss of your job, which is the key. They interviewed 270 severely disturbed patients and found that the ‘lock and key’ hypothesis in one third of the cases. This, again like the other theories, show that there are only a small number of people, from the sample used that have the ‘lock and key’ hypothesis, meaning the hypothesis is not a strong factor that causes depression.
It is clear form all the studies undertaken that there is no black and white answer to reveal how and why people suffer from depression. In reviewing a multitude of twins, adoption and family studies, it is clear to see that the foundation for each human is diverse in structure. For some cases genetics seems dominant, in some environment explains all, and in others it is the two factors combined together making people who and what they are. This is a strong indicator that the causes of depression will never be put down to one factor and the reason will have to be rationalised on a case by case basis.
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Classroom notes and handouts, 2006, N Warmsley
