Chapter 4
Models of depression
Epidemiological studies of depression give important insights into populations at higher risk of depression. For example, the prevalence of depression is higher in groups living in socially adverse conditions, and is higher in those with a recent experience of bereavement. However, not everyone in these circumstances will develop a clinical depression. Theories about the causes of depressive illnesses can help to clarify the reasons for these individual differences. Here, we highlight some of the best-known biological, psychological, and social models and then discuss attempts to integrate these into a multi-dimensional theory.
Biological models: monoamine and neuro-endocrine hypotheses
The initial chemical imbalance model of depression arose by serendipity. In the mid-20th century, reports began to appear that suggested that a number of medications used to treat medical problems could increase or decrease symptoms of depression. Knowledge of how these drugs affected the amount of different chemical molecules in the brain led to the development of the monoamine hypothesis of depression. To understand this, it is useful to briefly outline how messages are transmitted through the nervous system.
Many brain regions are important in the regulation of emotions. Communication between these regions and with the rest of the body occurs via the nervous system. Each neuron (nerve cell) comprises a cell body with an axon (like a tail) that has many dendrites (branches). Multiple communication pathways are established through the development of connections between networks of dendrites, and some nerve cells increase the activity of neurons in their network, whilst others decrease responses (called inhibitory neurons). Nerve cells are not in direct contact with each other, they are separated by a small gap called a synapse, and information is passed across the synapse by a molecule called a neurotransmitter (chemical messenger). When the electric impulse passes down the axon it leads to the release of the neurotransmitter from a vesicle (storage area). This molecule ‘docks’ with a receptor on the next cell and the message is transferred across the network (see Figure 4). The receptors are deactivated between messages and the neurotransmitter is released from the dock back into the synapse from where it is reabsorbed into the neuron from which it originated (a process referred to as re-uptake). There are at least thirty neurotransmitters, but the subgroup called monoamines that include norepinephrine, dopamine, and serotonin are regarded as particularly important in depression. It is suggested that serotonin regulates many important functions in the body such as sleep, eating, and mood; norepinephrine is implicated in stress reactions and alertness and energy and interest in life, and dopamine levels may influence motivation, pleasure, and ‘reward-seeking’ behaviour. Also, it is suggested that changes in serotonin may promote or reduce norepinephrine activity.
4. A synapse in the nervous system.
In the 1950s, separate observations were reported regarding the effects on mood, energy, and appetite of a new anti-hypertensive drug and a new anti-tuberculosis medication. Reserpine was introduced as a treatment for high blood pressure, but about 15 per cent of individuals receiving it reported experiencing significant levels of depression, sometimes accompanied by thoughts of suicide. In contrast, individuals in a sanatorium on Staten Island in the USA who received iproniazid as a treatment for tuberculosis reported feeling happier, more energized, and their appetite improved. Although these drugs were apparently unconnected, it was established that they acted on the same neurotransmitter systems in the brain and that reserpine reduced the circulating levels of monoamines, whilst iproniazid increased the levels (by preventing the action of monoamine oxidase, an enzyme that reduces the amount of monoamine neurotransmitters available in neurons).
The monoamine theory of depression was very popular in the 1960s and 1970s, and it was suggested that a deficiency in monoamines available in the synapse (either because of underactive production or overactive breakdown of these neurotransmitters) could explain the observed symptoms of depression. There were slight differences in views regarding whether the most important disturbance was in norepinephrine (favoured in the USA) or in serotonin (favoured in Europe), but support for the notion of monoamine ‘imbalances’ was provided by research on animals and humans. The latter included post-mortem studies demonstrating differences in monoamine levels in depressed versus non-depressed individuals and the experimental effects on mood and activity of drugs that alter monoamine levels. In addition, studies of individuals who had died by suicide showed reductions in monoamines in some regions of the brain thought to be associated with emotional regulation. The findings from these studies and enthusiasm for this apparent biological cause of depression led to the introduction of antidepressant medications that increased the availability of monoamines in synapses.
Published critiques of the monoamine hypothesis frequently highlight the dangers of the selective focus on so few of the neurotransmitters that operate in the brain, as there is limited information on what the other 90 per cent of chemical messengers are doing during this process. Also, in animal studies it is clear that monoamines influence multiple behaviours not just those that might be interpreted as being depression related. Most international researchers are aware of these weaknesses in a model of depression that implicated a single neurotransmitter system and even Schildkraut, who was one of the first American scientists to describe the monoamine theory, was quoted as saying the theory was ‘undoubtedly, at best, a reductionist oversimplification of a very complex biological state’.
The monoamine theory was instrumental in the development of depression-specific medications, but the widespread use of antidepressants has exposed other flaws in the model. The most obvious is that not all medications that alter monoamine levels produced the anticipated mood or behavioural effects. Also, there is a time-lag of about two weeks between increases in monoamine levels and evidence of changes in depressive symptoms that cannot be fully explained by the model and may indicate that the monoamine changes are a secondary or downstream effect of some other primary biological process. Partly in response to this, later revisions of the model shifted away from a focus on the amount of neurotransmitter available in the synapse to the importance of receptor sensitivity, suggesting deficiencies in docking system may be more germane. Also, scientists have highlighted that the neurotransmitter systems have important links with other neural pathways and the neuro-endocrine (hormone) system.
Another key biological model of depression is the neuro-endocrine hypothesis. A range of hormones have been implicated in the causes of depression and individuals with endocrine disorders such as hypothyroidism are at increased risk of depression. Whilst disturbances in several hormones (e.g. thyroid hormones, testosterone, oestrogen, progesterone) have been associated with depression, most research has focused on the regulation of stress responses through the linkages within the hypothalamic-pituitary-adrenal axis (HPA axis), an important system connecting the nervous system and the endocrine system.
The endocrine system consists of a number of organs in the body such as the thyroid and adrenal glands that help regulate many body functions through the release of hormones into the bloodstream. The hormones are produced in response to messages from the brain and the levels of different hormones fluctuate in a predictable way at certain stages of life (e.g. sex hormone levels change at puberty) and also during the course of the day (e.g. varying over the 24-hour sleep–wake cycle). Unlike neurotransmitters, the messengers that control the first link in the chain between the brain and the endocrine glands are molecules (peptides) called releasing factors. Releasing factors are produced in a brain region called the hypothalamus (a key structure for regulating hormone secretion) and send messages to the pituitary gland which in turn prompts the release of hormones from endocrine glands. The increased levels of circulating hormones in the bloodstream regulate a number of processes around the body, but also influence the activity of the neuro-endocrine system and prevent the overproduction of hormones via a feedback loop.
Serotonin, norepinephrine, and dopamine receptors are all present in the hypothalamus, suggesting connections between the activity of the monoamine system and the regulation of hormones. Furthermore, these monoamine pathways link the amygdala and hippocampus (brain structures known to play a critical role in emotional regulation) to the neuro-endocrine system. In day-to-day life, hormone levels change when the body responds to acute stress. For example, higher levels of adrenalin are produced when a person encounters any sort of anxiety provoking event, which can range from public speaking to life threatening situations, etc. In these circumstances a person’s heart rate may increase, they may begin to feel dizzy or nauseous, and they may become hyper-vigilant (the so-called flight or fight response).
Interestingly, the brain responds to chronic adversity or sustained stress by producing a different sequence of hormones. First, corticotrophin releasing factor (CRF) is released from the hypothalamus. This in turn increases the production of adreno-corticotrophic hormone (ACTH) from the pituitary and ACTH regulates the release of cortisol (a stress hormone) from the adrenal gland. Cortisol has wide-ranging effects around the body including significant effects on metabolism (e.g. delivering fuel to muscles) as well as affecting behaviour via its links with numerous brain regions (see Figure 5).
5. The Hypothalamic-Pituitary-Adrenal Axis and the ‘normal’ negative feedback loop.
The difference between normal and abnormal adaptation to chronic stress is that in the latter scenario the normal feedback loop does not function as expected. This has several implications, for example CRF levels appear to be important in ‘fear conditioning’ and the development of emotional memories of reward and punishment. Most importantly, the HPA system is no longer turned off by high levels of circulating cortisol and the normal daily variation in the amount of cortisol in the bloodstream is lost. Persistently high levels of cortisol are not good for many brain cells, and may speed up the usual rate of death of some neurons and have negative effects on memory and learning. In addition, these high levels of cortisol can be associated with reduced levels of the neurotransmitters linked to mood regulation.
The changes in mood, appetite, and energy seen in these abnormal responses to stress resemble the core features of clinical depression, leading many researchers to propose that disturbed HPA axis functioning was the underlying cause of depression. At one point in the 1980s, it was hoped that a laboratory investigation that measures the functioning of the HPA axis and the feedback system (called the dexamethasone suppression test) might provide a diagnostic test for depression. However, whilst animal and human models of depression demonstrate abnormalities in the HPA axis, not all individuals who experience depression show such abnormalities and some individuals who do demonstrate HPA axis abnormalities do not have depression but have other mental health problems such as anxiety, bipolar, or post-traumatic stress disorders, etc.
Despite the complexity of unravelling the cause and effects of altered HPA axis functioning in depression it remains an important focus for international research. Many ongoing studies are exploring whether targeting the functioning of this axis might enable the development of new medications that can reduce the risk of depression or treat its symptoms.
Psychological models: Beck’s cognitive model
Although several cognitive and behavioural theories of depression have been described, we focus mainly on Aaron Beck’s model. Beck, who qualified in medicine at Brown University in the USA, is usually regarded as the founding father of Cognitive Behaviour Therapy (CBT). Beck developed an interest in psychotherapy at a time when there was a shift towards behavioural models of emotional disorders, partly driven by the failure to demonstrate a scientific basis for psychoanalysis. Beck attempted to find evidence in support of psychoanalytic theories, but his research on thinking and cognition in patients with depression undermined the notion of unconscious motivations. Beck found that the content of an individual’s conscious thoughts and the ways in which they processed information offered a far more powerful explanation of the experiences described by depressed patients and during the 1960s Beck wrote his seminal papers on depression detailing a cognitive model of emotional disorders (see Figure 6).
6. Beck’s Cognitive Model of Depression.
Beck’s model offers a continuity hypothesis, which is to say that the model suggests that disorders such as depression are exaggerated forms of normal emotional responses such as sadness. It also views emotional and behavioural responses to events or experiences as being largely determined by the cognitive appraisal made by the individual, for example, social avoidance may arise if a person experiences negative thoughts such as ‘other people will find me boring’. The model includes two critical elements related to information-processing—cognitive structures (thoughts and beliefs) and cognitive mechanisms (called systematic errors in reasoning).
In Beck’s model, it is proposed that an individual’s interpretations of events or experiences are encapsulated in automatic thoughts, which arise immediately following the event or even at the same time. The difference from a Freudian model is that Beck suggested that these automatic thoughts occur at a conscious level and can be accessible to the individual, although they may not be actively aware of them because they are not concentrating on them. The appraisals that occur in specific situations largely determine the person’s emotional and behavioural responses, and this sequence is referred to as the Event-Thought-Feeling-Behaviour link. Furthermore, in depression, the content of a person’s thinking is dominated by negative views of themselves, their world, and their future (the so-called negative cognitive triad).
Beck’s theory suggests that the themes included in the automatic thoughts are generated via the activation of underlying cognitive structures, called dysfunctional beliefs (or cognitive schemata). All individuals develop a set of rules or ‘silent assumptions’ derived from early learning experiences. Whilst automatic thoughts are momentary, event-specific cognitions, the underlying beliefs operate across a variety of situations and are more permanent. Most of the underlying beliefs held by the average individual are quite adaptive and guide our attempts to act and react in a considered way. Individuals at risk of depression are hypothesized to hold beliefs that are maladaptive and can have an unhelpful influence on them. Such beliefs may be dormant for long periods but become reactivated by a so-called critical incident, namely an event that carries a specific meaning for that person (and has parallels to the events or experiences that led to the initial development of the belief). For example, an individual who experienced emotional neglect as a child may develop a negative belief that they are unlovable and this belief may be reactivated by an experience of personal rejection.
In depression, the automatic thoughts represent biased appraisals of external events or internal stimuli (arising from within the body), and the conviction that these thoughts are accurate reflections of reality is maintained by systematic errors in reasoning. This means that an individual may selectively focus on or screen out information from their environment that either supports or refutes their view of themselves and their world. For example, in someone who is depressed, the failure of a friend to return a telephone call may lead to ‘jumping to conclusions’ and focusing on the thought that the person no longer values the friendship (rather than considering other plausible explanations such as their friend was very busy or is notoriously forgetful). Importantly, this faulty information processing contributes to further deterioration in a person’s mood, which sets up a vicious cycle with more negative mood increasing the risk of negative interpretations of day-to-day life experiences and these negative cognitions worsening the depressed mood.
Beck suggested that the underlying beliefs that render an individual vulnerable to depression may be broadly categorized into beliefs about being helpless or unlovable. Thus events that are deemed uncontrollable or involve relationship difficulties may be important in the genesis of depressive symptoms. Beliefs about ‘the self’ seem especially important in the maintenance of depression, particularly when connected with low or variable self-esteem.
A common criticism of Beck’s model is that the automatic thoughts and reasoning errors might not precede the development of the depressive episode but may actually be a consequence of a negative mood shift. This has long been acknowledged by Beck, who stated that whilst the vicious cycle of negative thinking leading to low mood and then to further negative thinking may represent a causal theory in some cases, it can be a perpetuating factor in other forms of depression. A further unresolved issue is whether maladaptive underlying belief patterns are separate vulnerability factors for depression, or represent the individual’s temperament or personality style. Furthermore, dysfunctional beliefs are reported in a range of mental health problems and, as with the biological models, key elements of the model may not specifically predict depression.
Over the last forty years, there have been a number of developments and revisions of the cognitive model, with increasing attention to cognitive-emotional regulation. For example, one ‘response coping style’ that can amplify negative mood states is called rumination. A ruminative response style that includes reflection and distancing oneself from a situation to gain sufficient perspective and reduce the negative effect on oneself is not necessarily problematic. However, in some individuals rumination takes the form of toxic brooding on issues, with the individual constantly asking the question ‘why does this happen to me?’, becoming preoccupied with their own negative feelings and being unable to escape the negative cognitive-emotional loop. This response, sometimes described by the phrase ‘getting depressed about being depressed’, also tends to reduce the likelihood that a person can actively engage in solving their problems and this response style is closely linked to the onset and maintenance of depression. As such, rumination offers an important potential target for the new models of CBT that are being developed and is also relevant to models used in mindfulness.
Social models: Brown and Harris’s studies of depression in women
A moment of reflection about some of the social factors that may increase the risk of developing a depressive disorder leads to the conclusion that many of them are interrelated and likely to occur at the same time. This is particularly true with regard to issues such as unemployment, low socio-economic status, and poor housing, which can be interlinked in a variety of ways. As such, researchers initially found it difficult to disentangle these macro-level phenomena and it was hard to gain a clear understanding of the unique aspects of any individual’s experience of their social circumstances; the quality of their core social roles; and the differences in the personal meanings of the life events they reported. A British psychologist called George Brown and a sociologist called Tyrell Harris undertook a series of studies during the 1970s and 1980s that began to link social and psychological perspectives and to understand how these could increase a person’s susceptibility to depression. A key element of the studies was the implementation of new types of research interviews that examined the unique individual meaning of any life events and the social difficulties described.
In the initial study, the research team interviewed women in South London, and found that nearly 10 per cent had developed a depressive disorder during the previous year and that nine out of ten of those who became depressed reported serious adversity (negative life events such as domestic violence or ongoing difficulties such as caring for a parent with dementia). In contrast, serious adversity was reported by only a small proportion of the women who had not become depressed. The researchers also found that although there was a much higher rate of depression among working-class women, this only occurred among those with children at home. The women in Brown and Harris’s study, who lacked social support from an intimate relationship in their life, were four times more likely to become depressed in the face of these negative experiences (see Box 6). The researchers proposed that the women who experienced depression in the face of these life events were more likely to report a set of specific vulnerability factors; findings which were published in a seminal book called Social origins of depression: a study of psychiatric disorder in women.
Box 6 George Brown’s vulnerability factors in women
The second study concentrated on working-class women with a child living at home. Over 400 mothers living in Islington, an inner-city area in north London, were interviewed and anyone who was currently depressed was excluded from the study. One year later over 300 women were interviewed again and the researchers explored social and psychological experiences associated with new onsets of depression. The findings concerning life events were particularly thought-provoking as the researchers uncovered some important caveats that may explain different reactions to similar events and the nature of events linked to onset of depression and also to recovery. For example, the study confirmed that severe threatening events, especially those concerning loss, were important precipitants of depression in women with one or more of the identified vulnerability factors (listed in Box 6).
Interestingly, the use of more refined assessment procedures allowed the researchers to uncover that life events that could be categorized as ‘humiliation’ or ‘entrapment’ experiences were particularly associated with the onset of a depressive episode. Loss events which did not involve humiliation were more than 50 per cent less likely to be followed by the onset of depression. The match between such events and the shame felt by some women seemed to be explained by underlying low self-esteem. Also, the researchers reported that even in depressed women who were experiencing difficulties in one area of their life (such as marital difficulties), a ‘fresh start event’ in another life domain (such as starting a college course) often seemed to help to set them on the pathway to recovery. Taken together, these findings offered important insights into differences in the predisposition to develop depression, the risk factors that may precipitate a specific depressive episode, but also social events that might modify the course of illness and be associated with recovery.
Biopsychosocial models
Whilst media pronouncements on theories about depression take polarized views of the literature, researchers are more inclined to acknowledge that there are important overlaps between elements of psychological, social, and biological models. For example, the concept of matching events in women at risk of depression described in Brown and Harris’s work is very similar to Beck’s notion that it is the life events with a specific personal meaning for an individual that activate underlying beliefs and set off the cycle of depression.
The neuro-endocrine and monoamine models highlight that these two biological systems are connected and therefore affect the regulation of neurotransmitter and stress hormones. They also emphasize the importance of the level of stress in an individual’s social and family environment, recognizing that life events or chronic adversity are potent causes of changes in the nervous and neuro-endocrine systems.
The four theories described highlight the interaction between stress and vulnerability factors, but in order to integrate these approaches more fully it is useful to consider the origins of the vulnerabilities. For example, why are some individuals more likely to manifest monoamine dysfunctions or to have an HPA axis that is more sensitive to stressors, and why do some people develop dysfunctional and unhelpful underlying beliefs?
Figure 7 offers a simple representation of the stress-vulnerability model. This simple schematic identifies that under extreme stress anyone might experience a depressive episode, but it does not differentiate the different elements of vulnerability. To provide a snapshot of some of the ongoing difficulties of differentiating ‘nature versus nurture’, we will briefly highlight current ideas on gene-environment interactions and how the many different systems in the body may interact. We begin by examining research on families, then genes and the environment.
7. A simple representation of a stress–vulnerability model.
Family research
Depression runs in families, and research from around the world robustly and repeatedly shows that the children of a parent who has a history of depression have a two- to fourfold increase in their risk for developing a depressive episode, and a family history in more than one generation (e.g. in parents and grandparents) not only increases the risk of depression, it increases the likelihood that the depression may start earlier in life. However, these findings do not prove that depression is inherited. For example, living with a depressed parent may adversely affect family interactions and might increase the likelihood that other family members would also become depressed. Having several generations affected within a family may mean each generation has developed certain patterns of behaviour or so-called coping styles that affect the family environment in such a way as to increase the likelihood that the next generation may also be at risk of depression.
Genetic vulnerability
To clarify genetic vulnerability to depression it is helpful to examine the genetic makeup of a group of relatives and one of the best methods for doing this is to consider twin studies. Twins can be identical (monozygotic) sharing 100 per cent of their genes in common or non-identical (dizygotic) sharing 50 per cent of their genes in common, and therefore being no more genetically alike than brothers and sisters. Using this knowledge, researchers ascertain the rates of depression in one member of the twin pair, and then investigate how frequently the second twin also reports a depressive episode. The frequency of depression in both twins in one pair is termed the concordance rate. If genetic factors are relevant then the concordance rates in the identical twins should be higher than those in non-identical twins, and the rates of depression in the latter group should be about the same as seen in other family members who share 50 per cent of their genes in common, such as siblings and parents.
One such study of over 100 twin pairs that was undertaken at the Maudsley Hospital in London showed that identical twins had concordance rates of about 46 per cent for depression compared with about 20 per cent in non-identical twins. Similar findings have been shown in other twin studies and they highlight two very significant issues with regard to genetic vulnerability or inheritance. First, they show that genetic factors are important in the risk of developing depression and second, that even if an individual shares 100 per cent of their genes in common with someone who has developed depression, that does not mean they will experience a depressive episode. The latter is worth emphasizing as it means that genetic factors alone cannot explain the occurrence of depression, but that social, psychological, and environmental factors are also important in determining which individuals with genetic vulnerability to depression actually experience a clinical episode.
To help people understand this information, it is useful to briefly consider what ‘genetic risk’ actually means. The genes inherited via our parents are important in determining many of our physical characteristics or traits such as hair colour, and genes can also influence our personality characteristics. However, at a basic level, genes control biological processes, and in reality many genes, often interacting in complex ways, influence the expression of a particular trait. There is not a single gene linked to a specific behaviour or a particular emotional state. As such we will never find a gene that dictates that one person is an introvert or another is an extrovert. By the same token, there will never be a ‘gene for depression’ or a ‘gene for schizophrenia’. A more plausible model is that: (a) some mental processes and behaviours are more strongly inherited than others, but that (b) even when genetic factors are involved, there are likely to be many genes that play a part and that (c) each individual gene only has a small influence on the final picture. Also, just to make matters even more complicated, the activities of many genes can be turned on or turned off in different environments.
Despite the complexities of genetic coding, some interesting findings have emerged, including evidence from the Human Genome project that genes on certain chromosomes (e.g. on genes 12, 15q, etc.) may be more strongly linked to depression than expected by chance alone. Furthermore, some researchers have reported associations between genes that influence serotonin receptors and those that influence monoamine oxidase (the enzyme that influences the breakdown of monoamines and can be associated with depression). However, these findings should be viewed with caution as it is often the case that initially promising linkages are not replicated in later studies.
An example of replicating research findings comes from a study by a group of researchers led by a psychiatrist called Caspi. In 2003, they reported that they had identified a connection between a gene that regulates serotonin and an individual’s ability to bounce back from a significant traumatic experience such as childhood abuse or neglect (i.e. their resilience). The researchers undertook a long-term community study that assessed individuals prospectively for many years from the age of about 3 years until around 25 years of age and found that individuals who had one variant of a serotonin transporter gene (without getting too technical, it is called 5HTTLPR-S) developed more depression or were more likely to express suicidal ideas in response to stressful life events than individuals who had another variant (called 5HTTLPR-L). Further research showed that individuals who had the ‘S’ variant also showed increased activity in a brain region called the amygdala (known to be involved in emotional regulation) when exposed to ‘threatening stimuli’ under laboratory conditions. These findings seemed to offer evidence of a gene-by-environment interaction, in which an individual’s response to environmental events is moderated by their genetic makeup, and that the genes were acting on their neurotransmitters (and indirectly on the HPA axis) in areas of the brain that regulate emotional responses.
Psychiatry researchers took notice and the journal Science declared that it was one of the most important discoveries in the field of mental health. However, not all subsequent research has replicated these findings and so it is unclear how robust the links are between the serotonin transporter genes and the development of depression following environmental stress. The important take home message is that any research that tries to uncover the links between depression, genes, and the environment will need to explain not just which gene might be important but how that gene mediates the relationship between causes and effects. In that respect, the association between a gene that regulates a monoamine that is implicated in emotional regulation and the finding that the stress (HPA axis) response is exaggerated in the carriers of that gene at least provides a template for future research.
Environmental effects
Unique environmental effects that may increase the risk of depression are not limited to the offspring of depressed parents and can operate in a number of ways in a range of social contexts.
For example, the development of an individual’s personality will be influenced by their early parent–child interactions such as the development of secure attachments, experiences of separation, and the ‘emotional temperature’ of their environment (such as levels of parental affection or control) as well as by their genetic makeup. Some examples are given to illustrate the potential impact of early social experiences.
In Chapter 3 we commented that post-natal depression is sometimes a misnomer, as many of these women are shown to have symptoms of depression that commence in the antenatal period. Several studies suggest that stress during pregnancy can have a negative impact on the offspring, for example they may be more at risk of premature birth. Also, there may be a direct effect on the development of the HPA axis of the child; a hypothesis known as the set point theory. In utero, foetal development is influenced by the intrauterine environment and high levels of maternal stress hormones (which can pass across the placenta into the foetal bloodstream) may influence the development of systems in the baby such as the HPA axis. This can mean that the child develops a more sensitive HPA system that produces more cortisol in response to stress and other adverse experiences than other individuals.
A number of adverse events in childhood increase the risk of depression in adulthood. These can be related to several deprivations some of which may be linked to social circumstances such as poor nutrition, but also to social and emotional neglect. There is emerging evidence that these experiences can influence the development of the serotonergic system and also the sensitivity of the HPA axis (as many of these systems continue to develop throughout childhood). For example, it has been shown that adult women with a history of childhood abuse who were currently depressed exhibited increased cortisol levels in response to stress, as compared with abused women without depression, or with healthy controls (i.e. women who did not report abuse or depression). Also, there was a positive correlation between the ACTH and cortisol responses to stress, the magnitude of abuse, and the severity of depression. The researchers interpreted the findings as demonstrating that the depressed women with a history of abuse had a chronically overactive HPA system, suggesting it then took less stress to ‘tip them over the edge’ than might be the case for other individuals.
In summary, this chapter aims to demonstrate that unidimensional models, such as the monoamine hypothesis or the social origins of depression model, are important building blocks for understanding depression. However, in reality there is no one cause and no single pathway to depression and, as shown in Figure 8, multiple factors increase vulnerability to depression. Whether or not someone at risk of depression actually develops the disorder is partly dictated by whether they are exposed to certain types of life events, the perceived level of threat or distress associated with those events (which in turn is influenced by cognitive and emotional reactions and temperament), their ability to cope with these experiences (their resilience or adaptability under stress), and the functioning of their biological stress-sensitivity systems (including the thresholds for switching on their body’s stress responses).
8. Diagram showing some of the potential factors involved in the development of depression.