Motivation and emotion/Book/2015/Major depressive episodes and motivation

Major depressive episodes and motivation:
How do MDEs affect motivation?

Overview

The modern day pandemic of depressive disorders has arrived. Depression, or Major Depressive Disorder (MDD) as the diagnosis was called since the 1960s (Barrot, DiLeone, Eisch, Gold, Monteggia, Nestler, 2002), was predicted by the World Health Organisation (WHO) to account for 5.3% of total deaths worldwide by the year 2030 (Loncar, Mathers, 2005). As a result of the seriousness of this disease, many experiments have been conducted on the effects of depression, its treatment options and severity levels. However the complexity of this disease inhibits the development of a straightforward ‘one-size-fits-all’ approach to treatment. Many factors influence the onset and duration of depressive disorders, (Ball, Manicavasagar, Mitchel, O’Kearney, 2014), and one key factor in of those is motivation. A classic symptom of MDD is a loss of motivation or interest in activities. However, evidence has been discovered that shows the link between depression and motivation is a two-way street (Nolen-Hoeksema, 1991). Therefore, this article has aimed to answer several questions:

Major Depressive Episodes: What are they?
How do we define Motivation?
How does depression effect motivation?
How can motivation hinder or aid the treatment of depression?

Major Depressive Episodes: What are they?

A major depressive disorder, or ‘MDD’, is classified by feelings of sadness, hopelessness, emptiness and/or apathetic attitude towards activities which had previously been enjoyed. In accordance with the current Diagnostic and Statistical Manual of Mental Disorders (DSM-5) classification, the disorder must also cause significant distress or impairment, and must also include at least 4 additional symptoms that occur nearly every day (DSM-5, 2013).

Significant weight loss or gain	Figure 1 – weight fluctuation image (Smart Girl Politics: Where politics and culture collide, 2014)
Insomnia or hypersomnia	Figure 2 - Insomnia Image (Gallery Hip, n.d.)
lethargy	Figure 3 - Homer Simpson image (Walpaperus, n.d.)
Psychomotor agitation or retardation (restlessness vs slowed movements)	Figure 4 - Stress Image (Imgarcade, n.d.)
Difficulty in concentrating or decision making	Figure 5 - Indecision image (Photobucket, n.d.)
Excessive/inappropriate feelings of guilt or worthlessness	Figure 6 - Guilt Trip image (Tut and Groan, 2015)
Recurring thoughts of death, self-harm or suicide	Figure 7 - Death Image (Pixshark, n.d.)

Figure 8 – inclusive list of symptoms (DSM-5, 2013)

Major Depressive disorders differs from other forms of depressive disorders as shown in ‘figure 9’ below[1]:

Disorder	Symptoms	Duration
Persistent Depressive Disorder (PDD)	-Change in appetite -Hypo/hypersomnia -Low energy -Low self –esteem -Difficulty concentrating -Feelings of hopelessness	Chronic (2 years +)
Disruptive Mood Dysregulation disorder	-Severe, recurring outburst (verbal or physical) -Difficulty controlling temper -Outburst disproportionate to stressor/trigger -Outbursts don’t occur exclusively with a Major Depressive Episode (MDE) - must cause clinical distress or impairment in functioning	Chronic (12 months +)
Substance/Medication Induced Depressive Disorder	-diagnosis of depressed mood occurring soon after a) withdrawal from substance or b) consumption of substance -behaviour doesn’t occur exclusively during intoxication (substance use) -must cause clinical distress or impairment to functioning	Acute (4 weeks or less)
Figure 9 - forms of depressive disorders (DSM-5, 2013)
This table represents a general summation of disorders. For full description, see DSM-5 (2013)

With depression currently accounting for 24% of all non-fatal disabilities in Australia (2012, Black Dog Institute ), and being predicted by the World Health Organisation (WHO) as the leading cause of disability by 2030 (Manicavasagar, V., 2015 ), depressive disorders show a significant risk to the functioning of an individual though daily life. Many studies have been conducted to determine the etiology of depressive disorders.

Etiology of depression: Theories

[Provide more detail]

Beck’s theory of depression

A prominent theory of the epidemiology of depression was Beck’s theory on depressive cognitions. It was developed throughout the late 1960s to mid-1970s (Leahy (ed), 2004), and retained much recognition in the years after it was first released. However the simplicity of Beck’s theory was one of its major criticisms, and lead to its eventual decline in popularity (Blaney, 1977).

Beck’s theory stated that, although external variables impacted on the situation, the leading cause of depression was internal negative cognitions or schemas (Leahy (ed), 2004), (Beck, 1964). He argued that these cognitions were continually ruminated upon by the individual, leading to prolonged and more severe cases of depression. Beck hypothesised that these cognitions first develop through childhood experiences. Thus, years later, these negative experiences lead the adult to view their[grammar?] own life experiences through a negative light, focusing their memories on a) events that were negative or b) neutral events in a negative light. This, he theorised, was the main cause of depression.

However, if this was the case, the treatment options for depression could be found primarily in the use of cognitive behavioural therapies (CBT) or mindfulness sessions, to change these maladaptive cognitions. Unfortunately, the treatment options for depression are not a one-size-fits-all design.

Nevertheless, this tendency for depressed individual’s[grammar?] to ruminate on maladaptive cognitions is a core feature of MDD, and altering these cognitions is a difficult task. To first alter these patterns, the motivation behind continual rumination must be addressed. The answer for this could be found in Seligman’s theory of learned helplessness.

Seligman’s learned helplessness model

Another theory on the development of depression stemmed from Seligman and Maier’s experiment in 1967: the theory of learned helplessness (Powell, Honey, Symbaluk, 2005). The experiment administered electric shocks to dogs while they were restrained and unable to escape the shocks. While the dogs initially fought their restraints in an attempt to escape the negative stimuli, they eventually realized they could not escape and stopped trying to do so. The final stage of the experiment found that even when the dogs’ restraints were removed, they did not attempt to escape despite being free to do so. The dogs had learned to become helpless, and were unable to contemplate escaping the unpleasant stimuli.

This pattern of behaviour is seen often in domestic violence relationships, where the abused partner displays a high rate of passivity, and is unable to leave their volatile and abusive relationship (Launis, Lindquist, 1988). This apathetic acceptance of an individual’s situation is a symptom, and sometimes a cause, of major depressive disorder. Seligman’s theory of learned helplessness has shown a causal relationship between a) the development of depressive disorders and b) the motivation to escape versus ruminate on the situation (Powell et al, 2005). This shows another example of how aversive life events can trigger an individual to become passive and dejected and, as Powell (2005) said:

“Like animals exposed to inescapable shock, they show little interest [or motivation] in improving their lot in life.” (Powell et al, 2005).

This theory displayed a unique insight into how situational circumstances effect our motivation and, in this case, how it can lead to dire consequences.

MDD doesn’t only represent a change in learning; it also creates a change of brain structure. During a major depressive episode (MDE) the brain experiences a variety of physical changes. The hippocampus, the area of the brain responsible for learning and memory, undergoes a process of shrinkage during a major depressive episode (MDE) (Weiten, 2013). But this is not the only biologically significant variable involved with depression. Research has been conducted on the biological causes of depression as well as the effects depression has on the body. This is the theory of what causes a predisposition, or vulnerability, to developing the disease.

Predisposition:

The biological aspect of depression, including what genetic makeup an individual has, is an important factor in predicting the development of the disorder.

Genetic vulnerability:

Evidence of the ‘depression gene’ is difficult to empirically prove as a genetic vulnerability. However, the isolation of a specific abnormal gene has been linked with a susceptibility to the development of depressive disorders. This is known as the serotonin transporter gene (SETG), or 5-HHTLPR (McCord, n.d.), (Eaves, et al, 2009). As the name suggests, this gene is responsible for the delivery and reuptake of serotonin, one of the chemicals responsible for the regulation of sleep and emotion through the brain’s pathways. The gene is made up of either a short or a long version, making three possible groups (SS, SL, LL) (Eaves, et al, 2009).The hypothesis proposed that two short genes (SS) would indicate the highest chance of developing depression, one of each length (SL) would yield similar results, but the likelihood and severity would not be as much as two short gene lengths. Finally, two long genes (LL) would show no pre-disposition to developing a depressive disorder (Eaves, et al, 2009). Unfortunately, the study found that there was no correlation between a) the difference in the length of this gene, and b) the pairing of a stressful life event with the gene to influence depression.

In contrast, Blair et al (2006) found that although the gene wasn’t an outright indicator of depression, when paired with a stressful life event the gene was found to be a “significant predictor of…major depression” (Blair et al, 2006). While this research is a substantial leap forward in the treatment of depression, the mixed results indicate that the field still has a long way to go before a conclusive result is found.

Heritability & environmental factors:

The argument of nature versus nurture has been widely debated by psychologists throughout history, with the modern day consensus generally agreeing that both are important factors of behaviour (Weiten, 2013). The issue of developing MDD in the context of families, addresses just this combination of environmental and genetic factors.

The research of Fava and Kendler (2000) presented an American study which found the likelihood of an MDD sufferer’s children developing the disease was three times more likely than a child who came from a non MDD family. However, from this original study, they could not empirically determine if this was a result of genetic factors, such as the serotonin transmitter gene, or environmental factors such as home life. In contrast, the comparative work of Barrot, DiLeone, Eisch, Gold, Monteggia and Nestler (2002) showed that genetic factors account for approximately 40 to 50% of risk in developing depression. This astonishing statistic predicts dire consequences for future generations in the same condition. However, the use of motivation as a tool can be seen as form of treatment. So how does major depressive disorder tie in with the process of motivation?

2. What is Motivation?

Definition:

According to Huitt (2011), motivation is defined as an internal state that stimulates, guides and drives both the direction and force of a particular behaviour. The cause of how behaviour is exerted is based whether the incentive to perform behaviour comes from an external (extrinsic) or internal (intrinsic) source.

Intrinsic vs Extrinsic motivation:

As specified by Reeve (2009), motivation is made up of two components: intrinsic and extrinsic motivation. Intrinsic motivation is the desire to perform a task, purely because individual finds it enjoyable to do so, for example listening to music (Cherry, n.d[1].). Extrinsic motivation on the other hand is the motivation to perform a task based on some form of external reward, e.g. going to work to earn the reward of a pay check (Cherry , n.d.). Extrinsically motivated tasks are often used as form of motivation in environments such as the workplace, offering employees bonuses for working harder. However, research has shown that while initially successful, if extrinsic motivation is over used it leads to a decrease in intrinsic motivation, and overall effort, altogether (Cherry, n.d.), (Reeve, 2009). In the course of their research, Bénabou and Tirole (2003) found that in an IQ test, extrinsically motivated children performed significantly poorer than their intrinsically motivated counterparts. This aspect of motivation is an important tool to use when understanding the dual-process model.

Dual process model:

The duel-process model is the term granted to the existing ‘push-pull’ force between the instant gratification motivation of the subcortical brain, and the cognitive control exerted by the cortical brain ((Reeve, 2009). Essentially, this model represents the regulation of intrinsic versus extrinsic motivational actions, or the self-control aspect of the brain. For the depressed brain, the instant gratification motivation is important in the sense of giving the individual a short 'break' from their symptoms, by granting a quick, positive achievement. However, if the instant gratification is used for primarily maladaptive or negative actions, such as avoiding friends and family, this can actually increase the severity and longevity of the disorder.

3. How does depression effect motivation?

So how does depression affect motivation? The image below contains a picture of two brains: one depressed and one not.

As figure 10 demonstrates, the amount of cerebral activity in a depressed individual is severely decreased in comparison with that of a healthy brain. As such, it is important to note the areas of the brain that are responsible for our emotions and feelings of motivation, and how MDD affects these. As demonstrated by Reeve (2009), Barrot, DiLeone, Eisch, Gold, Monteggia and Nestler (2002), and Wlassof (2014) some of the most important areas of the brain responsible for humankind’s ability to respond to stimuli are as follows:

Brain structure or neurotransmitter	Function	Relationship with motivation and depressive disorders
Basal Ganglia -subcortical (extrinsic)	Responsible for the motivational regulation of movement	MDE inhibit motivational structures. Other symptoms (such as lethargy or insomnia), act as a further deterrent or obstacle to motivation or vigorous movement
Serotonin -neurotransmitter	Responsible for the regulation of a number of things, including appetite, mood and cognition	Decreased levels of serotonin have been linked with mood disorders. Many anti-depressants such as SSRIs inhibit the reuptake of serotonin too quickly
Ventral Striatum Nucleus Accumbens -subcortical (extrinsic)	Regulates motivation, eating and sleeping levels	MDD disrupts all of these
Amygdala -subcortical (extrinsic)	Involved in regulation of emotion and aggression	MDEs disrupt emotional balance and well-being
Prefrontal cortex -cortical (intrinsic)	Our planning area of the brain. It is responsible for formulating plans, goals and intentions. Right hemispheric activity associated with negative (no-go) avoidance motivation, left associated with positive (you go girl) approach to motivation	Depressive episodes leach motivation and the individual’s ability to plan, make goals or stick to them. During an MDE, right hemispheric activation common.
Ventromedial prefrontal cortex -cortical (intrinsic)	Responsible for emotional control.	Emotional control is often limited in the form of outbreaks of intense sadness, temper and/or suicidal ideation.
Dorsolateral prefrontal cortex -cortical (intrinsic)	Responsible for control over urges & risks during the pursuit of long-term goals	Risky behaviour, such as suicide attempts, self-harming or excessive drinking/substance abuse are all symptoms of depressive disorders, difficulty with impulse control can increase risk of these
Anterior cingulate cortex -cortical (intrinsic)	Monitors motivational conflicts. Recruiting other cortical brain structures for executive or cognitive control over basic urges and emotions	Basic urges and emotions often unregulated during a MDE. Motivational conflict exists between urge to get well, and the motivationally draining effect of MDD.
Figure 11 – brain structures (Reeve, 2009), (Barrot et al., 2002), (Wlassof, 2014)

Brain activity is diminished during major depression, as figure 10 shows, including the aspects of the brain that promote motivation.

3. How can motivation hinder or aid in the treatment of depression?

Nolen-Hoeksema (1991) proposed a theory that the duration and severity of depressive episodes were significantly influenced by the individual’s motivation to ruminate on a) their symptoms, and b) the cause of their depression. The study looked at the concept of motivation and depression in a different light to how it was traditionally seen. Rather than seeing how depression affected motivation, this study showed that motivation can significantly affect the duration, and severity of depressive disorders. The results of this study were confirmed by a joint research experiment conducted by McLaughlin, Michl, Nolen-Hoeksema and Shepherd in 2013. They discovered that not only does the motivation to ruminate on or escape depressive symptoms affect depression, but stressful life events or emotions can trigger the desire to ruminate. The overall conclusion drawn from both studies was that understanding our own motivation and emotional states can significantly aid our mental health and well-being in daily life. It also showed that doing the opposite, i.e. not ruminating, would not bring about the severe cosequences[spelling?] of doing so. Some therapies which can aid in this process include mindfulness and Cognitive Behavioural Therapy (CBT). Mindfulness therapy is based on the idea of noticing one’s maladaptive cognitions, and altering them. However, as is often the case with MDD, psychotherapies alone are not enough psychological assistance. This is why pharmacological treatment options are often used in these severe cases.

Treatment options:

Generation	Name	Effect	Side-effects
First	Monoamine oxidase inhibitors (MAOIs)	Inhibits reabsorption of monoamine oxidase from happening too quickly.	Interactions between MOAIs and a type of amino acid (tyramine) -found in various foods, alcoholic beverages and other medications - can cause rapid acceleration of blood pressure. Other side effects include: low blood pressure, dry mouth, insomnia or lethargy, blurred vision, sexual problems, rapid heartbeat and dizziness
First	Tricyclic Antidepressants (TCAs)	Inhibit the absorption of Serotonin and norepinephrine from happening too quickly.	Abnormal heart rhythm, Drowsiness/lethargy, sexual issues, Dizziness, Dry mouth and eyes, Urinary hesitancy and constipation Has a high rate of lethality/overdose
Second	Serotonin-noradrenaline reuptake inhibitors (SNRIs)	Inhibits reabsorption of norepinephrine from happening too quickly.	Nausea, dry mouth, dizziness, excessive sweating
Second	Selective Serotonin Reuptake Inhibitors (SSRIs)	Inhibits reabsorption of serotonin from happening too quickly.	Feeling agitated, shaky or anxious, feeling or being sick, indigestion, diarrhoea or constipation, loss of appetite and weight loss, dizziness, blurred vision, dry mouth, excessive sweating, not sleeping well (insomnia) or drowsiness, headaches, low sex drive
Figure 12 – antidepressant list (NHS, n.d.), (Mayo Clinic, 2015), (NPS Medicine-Wise, 2012), (Mayo Clinic, 2015)

These methods seem a simple enough step to take to improve psychological wellbeing, but a significant percentage of the population don’t seek help for psychological issues (Black Dog Institute, 2012).

Motivation to seek help:

Motivation to seek treatment for mental health issues is significantly stunted in 72% of all males in Australia (Black Dog Institute, 2012). This shocking statistic reflects several variables, but the two most significant were the stigma that surrounds mental health, and gender stereotype expectations.

Stigma

In a case study conducted by Reavley and Jorn (2012), researchers looked at how the Australian public perceived mental illnesses during 2011, in comparison with earlier years (1995, 2003, 2004 and 2006, Reavley, Jorn , 2012). This was done using a group of 6019 participants who were assigned a case study and asked to determine the cause of the illness. They found that approximately 40% of participants designated the cause of a depressive or anxiety related disorder the patient’s “weakness of character”. This stigma of mental health ties in with widespread prejudice surrounding gender expectations.

Traditionally, the stereotypical traits associated with gender followed the hunter-gatherer path. While women were seen as having more nurturing, vulnerable traits, men were seen to be more aggressive and power-oriented (Myers, 2014). This stereotype is one possible factor influencing men’s motivation to seek treatment. The idea that men are ‘tough’ and that to seek help is ‘weak’ is an untrue and pervasive stigma that nevertheless influences male perceptions of mental health issues, and their motivation to seek help. This poses a significant threat to the individual's safety in hindering their motivation t seek treatment. However, the research on, and publications about the facts of mental health are gradually being made clearer. As more is understood about the causes of this disorder, the fewer people in the general population hold onto these beliefs (Reavley, Jorn, 2012).

Conclusion:

Depression, or major depressive disorder as its diagnosed, affects motivation in many ways. Motivation is an internal state that stimulates, guides and drives both the direction and force of a particular behaviour (Huitt, 2011). As well as the well-known symptoms of apathy and hopelessness, MDD affects the parts of the brain that are responsible for regulating emotional control, dopamine based rewards and motivational impulses. Whether it is intrinsic or extrinsic motivation, depression depletes the body’s reserves. Theories that have been developed on the reasons why this happens include Beck’s theory of depressed cognitions, which stated that maladaptive cognitions cause, or at least contribute to, depressive episodes. Seligman’s theory of learned helplessness aided in explaining one reason behind the motivation of continued rumination, and why the individual can’t ‘escape’ their depressed situation. Nolen-Hoeksema’s 1991 study found that not only does depression affect our motivation levels, but motivation can also affect our depression levels. This in turn can act to shorten both the severity of the depressive episode, and its longevity.

Another factor that can contribute to the development of major depression included an individual’s genes and their environmental exposure to the disorder and stressful life events. When a MDE occurs, the treatments which are offered include psychotherapies and pharmacological options. Unfortunately, despite the decrease in stigmatisation of mental health every year, the stigma that surrounds the disorder, and gender stereotypes, are both significant deterrents of a person’s motivation to seek treatment, particularly in males.

This chapter has explained depression and motivation, and how these two concepts work together. Essentially, motivation and depression are irrevocably linked in the sense that one cannot change one of them without affecting the other. This notion is key in understanding and improving our motivational and emotional lives using psychological science.

Quiz:

References

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