Epidemiology of mood disorders

Australians use a number of public and private health service providers for mental healthcare. These include general practitioner and community-based and hospital-based mental health services.

• Community-based services—according to recent statistics from Australia’s Health 2006 (AIHW 2006), clients with a principle diagnosis of either mood disorder (24%) or schizophrenia (49%) accounted for the largest number of contacts with government-operated community mental health services in 2003/04. After mood disorders and schizophrenia, the next largest group of clients were those with neurotic, stress-related or somatoform disorders—these accounted for nearly 10% of all service contacts.

• Hospital-based services—most public and private hospitalisations for mental health are for at least one night. Mood disorders accounted for 32% (22,170 public, 11,870 private) and schizophrenia accounted for 31% (30,450 public, 2400 private) of all overnight private and public mental health hospital admissions for 2003/04 (106,100 in total: 83,200 public, 22,900 private) (AIHW 2006). Neurotic, stress-related and somatoform disorders accounted for 13% of admissions (9780 public, 3820 private).

Mood disorders make up a significant proportion of Australia’s mental health disease burden. Overall, according to recent statistics, mental health disease accounted for 13% of the disease burden in Australia in 2003 (Begg et al 2007). Mental health problems were also associated with increased exposure to health risk factors, poorer physical health and higher rates of death from many causes, including suicide (Begg et al 2007).

Depression

Depressive symptoms may range from mild, such as ‘feeling blue’, to very severe, where there is extraordinary sadness and dejection, and an inability to take pleasure in activities. The illness is described as major depressive disorder if the depressive symptoms are all-pervasive and debilitating in most areas of the client’s existence. If the client describes ‘feeling blue’ for a prolonged period of time and shows symptoms of mild depression, their illness could be characterised as dysthymia.

The important differentiating factors are: number of symptoms, degree of severity and duration of symptoms. It is also important to recognise that, depending on life events, periods of transitory sadness and grief are part of normal human functioning and we should not see these periods as disease states.

Aetiology of depression

Biopsychosocial model of causation

What causes depression? As with many diseases in mental health, researchers have focused on the influence of three main areas: biological, psychosocial and sociocultural factors. Each of these areas has been studied in detail to assess how they contribute to this mood disorder. To accurately assess what causes depression, we need to understand that there is unlikely to be any one factor that is wholly responsible. Rather, it is a combination of factors interacting that causes the illness. This combination of factors is called the biopsychosocial model of causation.

Genetic factors

Sullivan, Neale & Kendler (2000) examined a number of twin studies (more than 21,000 twins studied in total) and found that an identical twin was approximately twice as likely to suffer from major depression as a non-identical twin. Sullivan et al (2000) concluded that genetic factors accounted for 31–42% of the likelihood of developing major depression.

Gene–environment interaction

Much research has been devoted to identifying the specific genes involved in depression. So far there has been limited success, but a number of approaches have shown promise. One of these is the concept of the gene–environment interaction. Researchers have found that, while some people had a genetic predisposition to depression (in the serotonin transporter gene), if they had also had stressful life events in the past five years or had been severely maltreated as children, they were far more likely to develop depression than those with the gene only or stressful life events/maltreatment as children only (Caspi et al 2003; Moffitt, Caspi & Rutter 2005). This suggests that searching for the genes involved in depression would be more fruitful if the gene–environment interaction was also examined.

Neurochemical factors

The idea that depression is a result of a complex interaction between neurotransmitters and other systems in the brain originated in the 1960s and gained influence since. It should be emphasised that depression is not simply a consequence of low levels of serotonin or other neurotransmitters (monoamines) in the brain. This was the ‘monoamine hypothesis’ and originated in 1965, but by the 1980s researchers had concluded that this approach was too simplistic. For example, a number of studies have found that people with severe depression had increased levels of neurotransmitters such as noradrenaline and that only a small proportion had decreased levels of serotonin (Thase, Jindal & Howland 2002). More recently, researchers have suggested that the causes of depression are more complex and probably depend on an interaction between neurotransmitters and disturbances in hormonal, neurophysiological and biological systems in the body (Southwick, Vythilingam & Charney 2005). Although this is a more accurate description, it is not easy to explain it as a single mechanism or process.

Hormone systems and circadian rhythms

It has been suggested that hormonal systems, and specifically the hypothalamic-pituitary-adrenal (HPA)

Nurse’s story: a depressed young man

Branko had been the main support for his family since his father died when Branko was fifteen. He lived with his mother and two younger sisters in an inner-city suburb and worked as a storeman at a local supermarket.

His mother had suffered from depression for as long as Branko could remember. Antidepressants and counselling from their local priest seemed to help his mother, but much of the time Branko worked, paid the bills, cooked the meals and organised his sisters for school each day. His position at the supermarket had some flexibility and so he would pick his sisters up from school and then return to work in the evening when his family was settled.

The eldest daughter, a 14 year old, had called into the local health centre, concerned that her mother had become ‘unwell’ again. She asked if a nurse could come to their house to see her. That’s where I came in.

When I arrived at their house the next day I was surprised to find Branko at home and still in his dressing gown. He told me that his mother had remained in bed for these last two weeks and was eating poorly. He was worried for her. His mother and I talked, I made an assessment and then spent the next half hour organising her admission to an acute mental healthcare ward.

While we waited for the ambulance I sat down with Branko. He seemed very flat. There was little animation in his voice. I asked him why he wasn’t at work and he replied rather vaguely that he just wasn’t feeling very well. It was obvious that he didn’t want to talk and so we sat for a little while in silence. The ambulance eventually came and before I left I made an appointment to catch up with him a week later.

I had known Branko superficially for a number of years in the context of providing care for his mother. I suspected that he was under strain but had hoped that he was coping. I had never seen him so flat before and sensed he was in some distress. My first priority was to visit him regularly to try to develop a therapeutic relationship. This was partly in the context of planning for his mother’s discharge from hospital but also because I wanted to engage with him and develop a sense of trust between us. I hoped that he would open up and talk about how he felt. This happened very slowly. Much of the time we would sit quietly together each time I visited. At all times I tried to be as genuine and honest with him as I could. As a consequence he gradually opened up to me.

Branko described how he had lost his appetite and felt constant fatigue. He was also irritable much of the time with the long hours at work and burdens at home. He recognised his irritability and hated himself for it. He didn’t like being irritable with his family. He’d had a girlfriend for a couple of months the year before, but there was little time in his life to devote to another relationship and it soon ended. He then found himself lacking energy and more irritable than before. At times during our interactions Branko was angry with himself. At other times he turned his anger on me. I realised he wasn’t targeting me personally and that it was a symptom of his illness. He would always apologise after the anger had passed and we would be relaxed with each other again.

All the time I was with him I expressed hope to him that his spirits would lift. I focused on what a good, caring son and brother he was. He regularly visited his mother in hospital. I also praised him on how his sisters were turning out with his help. They were well respected at the school and getting good marks in their studies.

Finally his mother did return from hospital. This seemed to be a turning point for him. Branko had missed his mother keenly. She was brighter and able to help more around the house and with the two girls. Branko himself seemed to be coping better and was taking less time off from work. He agreed to trial some antidepressant medication. He had also mentioned during my last visit that he was thinking of getting in touch with his ex-girlfriend to see if she wanted to spend some time with him.

On my final visit a couple of weeks later it was obvious that he was better. He’d recently gained a promotion at work and his girlfriend was coming around that night for dinner with his family. He thanked me for my efforts over the past couple of months and spoke in positive terms about his future. I was glad.

axis and the cortisol and thyroid hormones, are implicated in depression (Marangell et al 1997; Thase et al 2002). Also implicated are low levels of brain activity in key regions of the brain (Davidson et al 2002), the qualities of REM sleep, and disturbances in circadian rhythms (24-hour body cycles) (Thase et al 2002).

It has been argued that psychosocial factors play as strong a part in the development of depression as biological factors. However, it is likely that it is the impact of stressful life events on the biochemical hormonal and circadian systems that causes depression (Hammen 2005; Howland & Thase 1999).

Sex differences

It has long been established that women are more than twice as likely to develop depression as men (Nolan-Hoeksema 2002). The theories that have been proposed to explain this range from biological (hormonal and genetic factors) to social and psychological (Helgeson 2002; Nolan-Hoeksema 2002).

One approach suggests that depression is largely a consequence of women’s roles in society. These researchers argue that women regularly experience a lack of control over negative life events and that this contributes to the development of depression. These events include poverty, discrimination in the workplace, unemployment, imbalance of power in relationships with men, high rates of abuse (sexual and physical) and overload in role expectation (e.g. wife, work, children) (Ben Hamida, Mineka & Bailey 1998; Heim, Graham & Miller 2000; Nolan-Hoeksema 2002). Again, it is likely that these life events affect hormonal and neurophysiological systems to produce depression.

Table 16.1 Nursing interventions for clients with depression

Intervention	Rationale
Be genuine and honest with patients. Accept them for who they are (both negative and positive aspects).	• Depressed people have chronically low self-esteem. • Genuine acceptance by others is a first step to recovery.
Treat anger and negative thinking as symptoms of the illness, not as personally targeted at the nurse.	• Depressed people are often negative and angry. • By identifying that negativity and anger are aspects of the illness, the nurse can encourage the client to move on from these issues to express more appropriate emotions.
Never reinforce hallucinations, delusions or irrational beliefs.	• It is not appropriate to agree with the client’s perceptual abnormalities. Equally, arguing that they do not exist serves little purpose. • The nurse should state their perception of the situation. • The nurse should state that there is a discrepancy between what is perceived by the client and what is perceived by the nurse. • The nurse should then steer the conversation to discussing real people and real events.
Spend time with withdrawn clients, even if no words are spoken.	• Withdrawn people are still very aware of where they are and who they are with. • Simply by spending time with withdrawn clients, nurses can help the clients emerge from their isolation by providing a non-threatening one-on-one relationship, practising assertive interactions and providing positive regard.
Make positive decisions for clients if they are unwilling to make decisions for themselves, e.g. it is time to get out of bed.	• Depressed people can have difficulties making even the simplest of decisions. • By using problem-solving techniques—i.e. identifying options, the advantages and disadvantages of each option available, and exploring the consequences of taking these actions—the nurse can guide the client to appropriate decisions.
Express hope that they will get better. Focus on their strengths, however small these seem.	• By identifying their strengths and giving them hope and positive regard, we encourage them to regain a sense of self-worth.
Identify and involve clients in activities where they can enjoy success.	• It is important for clients to feel good about themselves. • By involving clients in activities that they can accomplish, they may begin to improve their sense of self-worth.