Abnormal Study Pack PDF

1 Abnormal study pack  2 Contents Topic Page Sex: Skovlund 13 Prevalence rates for disorders Cult...

1 Abnormal study pack  2 Contents Topic Page Sex: Skovlund 13 Prevalence rates for disorders Culture: Parker 19 Biological explanations: Genetic Caspi 26 serotonin hypothesis Neale 29 March 34 Biological treatments: Leuchter 36 Antidepressants Neale 29 Cognitive explanations: Beck’s Alloy 43 cognitive model of depression Joiner 44 Psychological treatments: Cognitive Kuyken 51 behavioural therapy March 34 Sociocultural explanations: Brown & Harris 55 vulnerability model Swartz 57 Role of culture in treatments: Ando 61 cultural variations in psychological Zhang 62 treatments Contrasting in the abnormal 65 approach Research methods 73 Ethics 75 Example questions 80  3 Notes  4 What is depression? Depression, otherwise known as major depressive disorder or clinical depression, is a common and serious mood disorder. Those who suffer from depression experience persistent feelings of sadness and hopelessness and lose interest in activities they once enjoyed. Aside from the emotional problems caused by depression, individuals can also present with a physical symptom such as chronic pain or digestive issues. To be diagnosed with depression, symptoms must be present for at least two weeks. Depression DSM-5 Diagnostic Criteria The DSM-5 outlines the following criterion to make a diagnosis of depression. The individual must be experiencing five or more symptoms during the same 2-week period and at least one of the symptoms should be either (1) depressed mood or (2) loss of interest or pleasure. 1. Depressed mood most of the day, nearly every day. 2. Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day. 3. Significant weight loss when not dieting or weight gain, or decrease or increase in appetite nearly every day. 4. A slowing down of thought and a reduction of physical movement (observable by others, not merely subjective feelings of restlessness or being slowed down). 5. Fatigue or loss of energy nearly every day. 6. Feelings of worthlessness or excessive or inappropriate guilt nearly every day. 7. Diminished ability to think or concentrate, or indecisiveness, nearly every day. 8. Recurrent thoughts of death, recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide. To receive a diagnosis of depression, these symptoms must cause the individual clinically significant distress or impairment in social, occupational, or other important areas of functioning. The symptoms must also not be a result of substance abuse or another medical condition. Symptoms can be grouped into affective, behavioural, cognitive and somatic. Cognitive Affective (mood) Behavioural (thoughts) Somatic symptoms symptoms symptoms Difficulty (physical) concentrating, symptoms Prolonged Spending lots of negative thinking sadness, feelings time sleeping, Fatigue, nausea of guilt self-harm  5 Sort the symptoms below according to whether they’re affective, behaviour, cognitive or somatic: 1. Feelings of sadness 2. Sluggishness/disorientation in the morning. 3. Crying spells 4. Insomnia - or hypersomnia 5. A change in eating habits 6. Feeling unattractive or social withdrawal 7. Feelings of sadness 8. A change in eating habits 9. Digestion problems 10. Fatigue How is Depression Different from Sadness? Given that the primary symptom associated with depression is sadness it can be hard to know how to make a distinction between the two psychological states. Depression is more than just sadness, and the difference doesn’t lie in the extent to which a person feels down, but rather in a combination of factors relating to the duration of these negative feelings, other symptoms, bodily impact, and the effect upon the individual’s ability to function in daily life. Sadness is a normal emotion everyone experiences at some point. Be it the loss of a job, the end of a relationship, or the death of a loved one, sadness is usually caused by a specific situation, person, or event. When it comes to depression, however, no such trigger is needed. A person suffering from depression feels sad or hopeless about everything. This person may have every reason in the world to be happy and yet they lose the ability to experience joy or pleasure. With sadness, you might feel down in the dumps for a day or two, but you’re still able to enjoy simple things like your favourite TV show, food, or spending time with friends. This isn’t the case when someone is dealing with depression. Even activities that they once enjoyed are no longer interesting or pleasurable. What’s more, when you experience sadness triggered by a certain something you’re still able to sleep as you usually would, remain motivated to do things, and maintain your desire to eat. Depression, on the other hand, is associated with serious disruption of normal eating and sleeping patterns, as well as not wanting to get out of bed all day. In sadness, you might feel regret or remorse for something you said or did, but you won’t experience any permanent sense of worthlessness or guilt as you might with depression. One of the diagnostic features of depression is this kind of self-diminishing, negative thought patterns. Finally, self-harm and suicidal inclinations don’t arise from non-depressive sadness. Those struggling with severe depression may have thoughts of self-harm, death, or suicide, or have a suicide plan  6 Factors influencing diagnosis notes  7 Help with critical thinking When evaluating research: Use I SCREAM Internal validity: Does the research test what it intended to test? This will be lowered by factors such as researcher bias, demand characteristics, extraneous variables and social desirability bias. Sample: YAVIS – students are often young, affluent, verbal, intelligent and social, which can limit the generalisability of research using students. Also consider the sampling method, sample size, gender and age of the participants. Culture: Lots of research takes place in Europe and the US which may make it difficult to generalise the findings elsewhere. These countries are WEIRD – westernised, educated, industrial, rich, democratic. Reliability: Has the research been replicated to test the reliability of the findings? Is the procedure standardised enough that replication is possible? External validity: Can the findings apply to other contexts. This includes the real world (ecological validity), other people (population validity) and other periods of time (temporal validity). Alternative evidence: Consider what each study brings to the argument, as well as if there has there been any research to offer an alternative perspective. Methodology: Consider the research design, research method and triangulation (data/method/researcher) When evaluating theories: Use U CRAP’ED Unbiased: A good theory does not show bias towards a gender or a culture. Many early theories in psychology were androcentric (research was done on and applied only to men) or ethnocentric (research was very culturally biased and focused on Western culture). Clearly defined variables: A good theory makes sure that its variables are clearly defined so that they can be reliably measured. Reductionist: Does the theory attempt to explain behaviour focusing on a limited number of factors e.g. the role of one neurotransmitter. If so, then it is not holistic as it doesn’t consider the influence of other factors on the same behaviour (therefore it’s reductionist). It is good to suggest alternative factors that might influence the behaviour in question. This is a good opportunity to link to other theories you have learnt in the course. Application: A good theory can be applied to many different situations/behaviours Predictive validity: A good theory does not just describe what is happening, it predicts behaviour. Is a theory simple labels behaviours but does not predict when or why a person might demonstrate that behaviour with any reliability, then the theory has low predictive validity. Empirical support: A good theory has evidence to support it. Good empirical support is not from a highly artificial situation and it is reliable (the evidence can be replicated). Determinist: Does the theory propose that behaviour is influenced by something outside of the individual’s control? If so, it can be argued to be deterministic as it does not consider how free will influences behaviour.  8 Prevalence rates and disorders Prevalence rates are not simply statistical accounts of how many people suffer from a specific disorder. They also provide us with information about the nature of disorders. For example, we sometimes see that there is a difference in the prevalence rates of a disorder in men and women. We also see that different cultures have different levels of a disorder. Key vocabulary Prevalence: the proportion of a population that has a psychological disorder at a specific point in time. For example, over 300 million people are estimated to suffer from depression, equivalent to 4.4% of the world's population. Incidence: the number of new cases diagnosed in a certain period of time within a population. This statistic is often reported over a 12-month period. For example, the NIMH estimates that 16.2 million US adults had at least one major depressive episode in 2016. Lifetime prevalence: the proportion of a population that at some point in life has ever had the disorder. For example, Hasin (2018) found a lifetime prevalence of major depression of 20.6% in US adults. That means, 20.6% of adults experience depression at some time in their lives. Discuss the prevalence of mental health statistics below. Have you heard of any of these before? Do any statements in particular surprise you? Mental health problems affect both men and women, but not in equal measure. 1. In England, in 2014, one in six adults had a common mental health problem: about one in five women and one in eight men. From 2000 to 2014, rates of common mental health problems in England steadily increased in women and remained largely stable in men. 2. In 2018, there were 6,507 suicides registered in the UK, and in 2019, there were 5,691 suicides registered in England and Wales. Of these, three-quarters were among men, which has been the case since the mid-1990s 3. Three times as many men as women die by suicide, and men aged 40 to 49 have the highest suicide rates in the UK. 4. Men are less likely to access psychological therapies than women: only 36% of referrals to NHS talking therapies are for men. 5. Men are nearly three times as likely as women to become dependent on alcohol, and three times as likely to report frequent drug use. 6. Men are more likely to be compulsorily detained (or ‘sectioned’) for treatment than women. 7. Men are more likely to be victims of violent crime (1.5 more likely than women). 8. Women between the ages of 16 and 24 are almost three times as likely (26%) to experience a common mental health issue as males of the same age (9%). 9. Women are twice as likely to be diagnosed with anxiety as men.  9 Depression over time: When looking at prevalence rates, it is important to consider the environmental factors that may play a role in triggering disorders. Some environmental triggers are obvious. For example, the Rwandan genocide had a significant impact on the mental health of the average Rwandan. However, we cannot assume that negative environmental conditions will always lead to an increase in mental illness. When considering the economic crises that hit such countries as Greece and Spain in the early 2000s, one would expect to see an increase in mental health problems. However, the World Health Organization (2011) published a report that showed that there was no clear link between the economic crises and a change in the prevalence of disorders. According to the report, family support, state programs and an increase in the price of alcohol may have all contributed to the stability of prevalence rates. Twenge (2015) argues that one of the reasons for an increase in the prevalence of depression among young people is a change in social norms that make a diagnosis of depression less of a stigma. The media may play a role in promoting the need to seek help or to take medication. Prevalence rates are based on reported cases - if there are more people coming forward for help, that will result in a higher prevalence rate. Covid-19 Across the UK, rates of depression are still significantly higher than prior to the pandemic. Around 17% of adults in the UK experienced some form of depression in summer 2021, compared to just 10% before the pandemic.  10 Gender/sex Research shows that women are twice as likely to experience depression than men. The Office for National Statistics, reported that in 2021, younger adults and women were more likely to experience some form of depression, with around 1 in 3 (32%) women aged 16 to 29 years experiencing moderate to severe depressive symptoms, compared with 20% of men of the same age. This year, Champion Health revealed the impact and prevalence of depression among UK professionals in the Workplace Health Report: 2022. 61% of employees experiencing depression are female Before we get onto your main research, consider the points below reasons why depression is higher in women than men: Puberty Hormone changes during puberty may increase some girls' risk of developing depression. However, temporary mood swings related to fluctuating hormones during puberty are normal — these changes alone don't cause depression. Puberty is often associated with other experiences that can play a role in depression, such as: Emerging sexuality and identity issues Conflicts with parents Increasing pressure to achieve in school, sports or other areas of life After puberty, depression rates are higher in females than in males. Because girls typically reach puberty before boys do, they're more likely to develop depression at an earlier age than boys are. There is evidence to suggest that this depression gender gap may continue throughout the lifespan.  11 Premenstrual problems For most females with premenstrual syndrome (PMS), symptoms such as abdominal bloating, breast tenderness, headache, anxiety, irritability and experiencing the blues are minor and short-lived. But a small number of females have severe and disabling symptoms that disrupt their studies, jobs, relationships or other areas of their lives. At that point, PMS may cross the line into premenstrual dysphoric disorder (PMDD) — a type of depression that generally requires treatment. The exact interaction between depression and PMS remains unclear. It's possible that cyclical changes in estrogen, progesterone and other hormones can disrupt the function of brain chemicals such as serotonin that control mood. Inherited traits, life experiences and other factors appear to play a role. Pregnancy Dramatic hormonal changes occur during pregnancy, and these can affect mood. Other issues also may increase the risk of developing depression during pregnancy or during attempts to become pregnant, such as: Lifestyle or work changes or other life stressors Relationship problems Previous episodes of depression, postpartum depression or PMDD Lack of social support Unintended or unwanted pregnancy Miscarriage Infertility Stopping use of antidepressant medications Postpartum depression Many new mothers find themselves sad, angry and irritable, and experience crying spells soon after giving birth. These feelings — sometimes called the baby blues — are normal and generally subside within a week or two. But more-serious or long-lasting depressed feelings may indicate postpartum depression, particularly if signs and symptoms include: Crying more often than usual Low self-esteem or feeling like you're a bad mum Anxiety or feeling numb Trouble sleeping, even when your baby is sleeping Problems with daily functioning Inability to care for your baby Thoughts of harming your baby Thoughts of suicide Postpartum depression is a serious medical condition requiring prompt treatment. It occurs in about 10 to 15 percent of women.  12 Perimenopause and menopause Risk of depression may increase during the transition to menopause, a stage called perimenopause, when hormone levels may fluctuate erratically. Depression risk may also rise during early menopause or after menopause — both times when estrogen levels are significantly reduced. Most women who experience bothersome menopausal symptoms don't develop depression. But these factors may increase the risk: Interrupted or poor sleep Anxiety or a history of depression Stressful life events Weight gain or a higher body mass index (BMI) Menopause at a younger age Menopause caused by surgical removal of the ovaries Life circumstances and culture The higher rate of depression in women isn't due to biology alone. Life circumstances and cultural stressors can play a role, too. Although these stressors also occur in men, it's usually at a lower rate. Factors that may increase the risk of depression in women include: Unequal power and status. Women are much more likely than men to live in poverty, causing concerns such as uncertainty about the future and decreased access to community and health care resources. These issues can cause feelings of negativity, low self-esteem and lack of control over life. Work overload. Often women work outside the home and still handle home responsibilities. Many women deal with the challenges of single parenthood, such as working multiple jobs to make ends meet. Also, women may be caring for their children while also caring for sick or older family members. Sexual or physical abuse. Women who were emotionally, physically or sexually abused as children or adults are more likely to experience depression at some point in their lives than those who weren't abused. Women are more likely than men to experience sexual abuse.  13 Key Study: Skovland et al (2016) Prevalence of depression in women As you’ve just read, it is widely believed that hormonal fluctuations strongly affect moods in women. Women are believed to be more prone to depression during the premenstrual period, the postpartum period, and menopause, each of which is characterized by changes in the levels of a number of hormones. The 2 female sex hormones—estrogen and progesterone—have been hypothesized to play a role in the cause of depressive symptoms. Millions of women worldwide use hormonal contraception. Despite the clinical evidence of an influence of hormonal contraception on some women’s mood, associations between the use of hormonal contraception and mood disturbances remain inadequately addressed. In a recent review, Toffoletto et al (2014) found initial evidence that sex steroid hormones have an influence on the cortical and subcortical regions implicated in emotional and cognitive processing. Aim To investigate whether the use of hormonal contraception is positively associated with subsequent use of antidepressants and a diagnosis of depression at a psychiatric hospital. Procedure The Danish Sex Register is an ongoing nationwide cohort study that includes all women living in Denmark. This study combined data from women and adolescents aged 15 to 34 years who were living in Denmark and using different types of hormonal contraception. The databases were available through Statistics Denmark, and approval for their use was obtained from the Danish Data Protection Agency, which also determined that informed consent was not required because the study use deidentified data from large databases. Just over 1 million women were used in the analysis, with a mean age of 24. They were followed up from 2000-2013, to see if they had no prior depression diagnosis and if they redeemed prescriptions for antidepressants, other major psychiatric diagnosis. All women with a prior depression diagnosis or use of antidepressants prior to the study were excluded, as well as women who underwent treatment for infertility or with a diagnosis of cancer. Women immigrated after 1995 were excluded to ensure information on prior depression and other censoring variables for at least 5 years before study entry.  14 Hormone use was defined as current or recent use (cessation within the previous 6 months). Depression was measured in 2 ways. One was by looking at whether an antidepressant was recorded in the National Prescription Register who cover all Danish pharmacies. The second outcome was a first discharge diagnosis of depression from the Psychiatric Central Research Register. This outcome included all inpatients and outpatients in psychiatric departments in Denmark. Results An increased risk for first use of an antidepressant and first diagnosis of depression was found among users of different types of hormonal contraception, with the highest rates among adolescents. The relative risks generally decreased with increasing age. Conclusions Use of hormonal contraception, especially among adolescents, was associated with subsequent use of antidepressants and a first diagnosis of depression, suggesting depression as a potential adverse effect of hormonal contraceptive use. The findings comply with the theory of progesterone involvement in the aetiology of depression and may also indicate that adolescent girls are more vulnerable to risk factors for depression. Evaluation Strengths: The primarily nonselective inclusion of all adolescents and women aged 15 to 34 years living in Denmark and followed up for 14 years with no loss to follow-up and a study population of 1 million women. The information on the use of hormonal contraception and antidepressants was obtained through bar codes, eliminating recall bias. This huge amount of data increases the reliability of the findings, as well as the external validity to the Danish population. 80% of the female population in Denmark has used hormonal contraception sometime during their reproductive life, which explains why women using hormonal contraceptives represent the general population of women in Denmark and not a selected subpopulation. There were lots of controls in the inclusion of participants in this study. Women who used an antidepressant or had a diagnosis of depression before study entry were excluded. Next, women were temporarily censored during pregnancy and 6 months after delivery to reduce the influence of postpartum depression. Information on hormonal contraceptive use was updated daily. This ensures that the internal validity of the findings remains high, as extraneous variables are kept to a minimum. Finally, researchers used alternative analysis strategies with 2 different outcomes and conducted a number of sensitivity analyses, all with consistent results. This increases the reliability of the findings.  15 Limitations: Depression is mentioned in the hormonal contraception leaflet was a possible adverse effect. So, could it be that prescribing physicians are more observant of the onset of depressive symptoms among patients to whom they have described hormonal contraceptives? Although consent was not deemed necessary, some women may not be happy to learn that their data has been used in this study, especially as some girls are 15, which is under the usual age to consent by themselves. There are also ethical implications with the results of this study. Could it lead to a self-fulfilling prophecy, where if women discover the negative implications of antidepressants, it could lead them to develop depressive symptoms? Critical thinking depression being higher in women: The income effect: Earlier on it was mentioned that women’s socioeconomic status is lower than men’s, and this could account for the difference in depression rates. However…. Ensel (1982) tested for this possibility by comparing men's and women's mean scores on a depression scale, controlling for income level, education level, and occupation. In both of these studies, women still had more depressed mean scores than men after all these socioeconomic indicators were taken into account. These results suggest that observed sex differences in depression are not simply the result of differences in income. Biological factors: Kessler (2001) found that although the gender difference first emerges in puberty, other experiences related to changes in sex hormones (pregnancy, menopause, use of oral contraceptives, and use of hormone replacement therapy) do not significantly influence major depression. This direct goes against Skovlund’s findings, although bear in mind that Skovlund’s findings are more recent, so perhaps Kessler’s view is now outdated.  16 Culture Depression affects about 1 in 15 adults in any given year, and 1 in 6 people will experience depression at some time in their life. An Our World In Data study estimates about 3.4% of the global population has depression. This is about 264 million people worldwide. According to WHO estimates, the ten countries with the highest prevalence of depression are:  17 Depression rates are rising around the world, but it's likely that this rise is due at least in part to a good thing: More patients than ever before are seeking and receiving treatment for mental illness rather than going undiagnosed. In many countries, including the United States, the stigma surrounding mental illnesses is gradually decreasing. This enables a more open discussion of mental illness and makes people more likely to seek help when they need it. Yet research shows a rather interesting pattern: depression is far more prevalent in Western cultures, such as the US, Canada, France, Germany and New Zealand, than in Eastern cultures, such as Taiwan, Korea, Japan and China. This shows that depression is a modern health epidemic that is also culture- specific A nation’s culture can also have a significant impact on both the mental health of its population and the availability of mental health treatment services. Additionally, certain symptoms of depression are more common in some societies than others due to cultural factors. For example, while depression is relatively uncommon in Japan, suicide rates are high for children and teens ages 10-19. This is most likely due to pressure to do well in school and work and conform to group norms.  18 Prevalence rates are also problematic because a diagnosis is not always reliable across cultures. Symptoms may be different for the same disorder in different cultures. When applying an etic approach, we may see that another culture exhibits a lower prevalence of a disorder because the symptoms do not align with a standardized checklist. On the other hand, if we use an emic approach and then attribute a set of symptoms within a culture to a disorder in another culture, this could also be problematic. For example, if we assume that somatic symptoms are actually signs of depression, this may raise the prevalence rate. However, is this truly the same disorder that we are seeing in Western psychiatry?  19 Key Study: Parker (2001) Prevalence of depression in British Asians Background information One of the questions of psychology is whether psychological disorders are universal. Early clinicians argued that since certain symptoms were not observed in different cultures, that disorders were not universal. More modern research argues that the disorders may be universal, but that their symptoms may not be. As early as 1986, Kleinman found that depressed Chinese people do not report feeling sad, but rather express boredom, discomfort, feelings of inner pressure, and symptoms of pain, dizziness, and fatigue. When attempting to diagnose these patients, Western psychiatrists may fail to attribute these symptoms to depression. Researchers have argued that this may be due to cultural dimensions; in collectivistic societies it is less appropriate to reveal one's emotions, so perhaps the somatization is the way that they communicate mental distress. Others argue that it may be because of the stigma associated with mental illness in Chinese society that leads people to express "appropriate symptoms." The study by Parker et al was carried out almost 20 years later and found similar results to Kleinman's original study. Aim To compare the extent to which depressed Chinese patients in Malaysia and Caucasian patients in Australia identified both cognitive aspects of depression and a range of somatic symptoms as a sign of their depression and the reason that they sought professional help. Procedure The sample was made up of 50 Malaysian participants of Chinese heritage and 50 Australian participants of Caucasian, Western heritage. Whereas the Australians all had English as their first language, the Chinese were a mix of Chinese (80%) and English (20%) as their first language. All participants were out-patients who had been diagnosed with Major Depressive Disorder, but who did not have other diagnoses as well, such as drug addiction or schizophrenia. The questionnaire was based on two sets of symptoms. First, a set of mood and cognitive items common in Western diagnostic tools for depression. Secondly, a set of somatic symptoms commonly observed by Singaporean psychiatrists. The questionnaire was translated into Malay and Mandarin Chinese. It was back-translated to establish credibility. The patients were asked to judge the extent to which they had experienced each of the 39 symptoms in the last week. They had only four options: all the time, most of the time, some of the time and not at all. They were also asked to rank the symptoms that they experienced in order of how distressing they were. Through the assistance of their psychiatrists, it was also noted what the primary symptom was that led to them seeking help. Results  20 When looking at which symptom led them to actually seek help, 60% of the Chinese participants identified a somatic symptom, compared to only 13% of the Australian sample. Below you can see how each culture ranked the various symptoms in terms of the amount of distress they cause. However, when comparing the lists of which symptoms each group acknowledged experiencing, something rather interesting happened. There was no significant difference in the number of somatic symptoms indicated by each group as being linked to their depression. However, the Chinese participants were significantly less likely to identify cognitive or emotional symptoms as part of their problem. They were less likely to rate feeling helpless and hopeless, a depressed mood, having poor concentration, or having thoughts of death than the Australian participants. Conclusion: The role of culture is evident here; in Western culture it is more appropriate to discuss one's emotions and depression is seen as linked to a lack of emotional well-being; whereas in Chinese culture, it is less appropriate and even stigmatized if one speaks about a lack of emotional health. Evaluation The study attempted to develop a questionnaire based on cultural evidence relevant to the participants. They did not simply use a standardized Western questionnaire that may have influenced the results. Creating a questionnaire that incorporated the somatic symptoms identified by Singaporean psychiatrists is an example of an emic approach. They did choose participants based on the DSM-IV criteria for diagnosing Major Depressive Disorder. In this sense, the study demonstrates an imposed etic approach to research. It may have eliminated people from the sample who may have a form of depression that does not meet the Western criteria for diagnosis; this may account for the similarities in the two samples.  21 Asking patients to recall their "first symptoms" is open to memory distortion and to demand characteristics. If in the West we believe that depression is an emotional disorder, patients may expect that this is the correct response. Malaysia is a very modern and Westernized society. The effects of globalization may account for the relatively small difference in the data. Research on more cultures would be necessary to test the reliability of the findings. Critical thinking of depression being higher in the West: Interpreting the data on depression While prevalence data across cultures are valuable and vital, it is important to keep in mind that the true rates are likely much higher, especially in less developed countries. Depression is much more likely to be diagnosed in highly developed countries, whose more robust health care infrastructures are far better equipped to identify and treat mental illnesses. Therefore, less developed countries do not necessarily have less depression—rather, their treatment of mental illnesses often takes a back seat to broader concerns such as hunger, disease, and sanitation. In fact, the World Health Organization estimates that 76–85% of people suffering from mental disorders in low- and middle-income countries lack access to the necessary treatment. Even in developed nations, many cases of mental illness go undiagnosed and unreported because the patients are either ashamed of their illness or unaware that it's a medically treatable condition. Stigma: It could be possible that depression is actually as common in collectivist cultures, but it’s under reported due to the stigma associated with depression. Reporting bias – low hospital admission rates for particular ethnic groups may not reflect true prevalence, but instead cultural beliefs about mental health. In India, mentally ill are cursed, and China carries big stigma for mental illnesses, so are careful to label people Cultural norms: Neurasthenia was popularised by the American neurologist George Miller Beard, who described it as an “exhaustion of the nervous system”. At the time, the Industrial Revolution was leading a massive upheaval of everyday life, and he believed that neurasthenia – a syndrome of headaches, fatigue and anxiety, among other things – was the result. They commonly have symptoms of depression and anxiety, but fatigue is predominant. Eventually neurasthenia spread to European colonies around the world, but as the years passed, neurasthenia gradually lost its appeal in the West, as it became associated with more serious psychiatric problems. Now it’s been forgotten about altogether. But elsewhere, the opposite  22 happened: it was adopted as a diagnosis that didn’t come with stigma of mental illness and remains in use to this day. In some parts of Asia, people are more likely to say they have neurasthenia than depression. A study by Hall et al (2018) of a random sample of adults from Guangzhou, China, found that 15.4% identified as having the former versus 5.3% who said they had the latter. The role of globalisation A concern about globalization is the marketing of pharmaceuticals. As individuals are exposed to the marketing of drugs that are alleged to improve one's mental health, this may lead to more people seeking out medical advice. This may also increase the reported prevalence of a disorder. An example of this is the prevalence of Major Depressive Disorder in Japan. Traditionally, depression was seen as a need for spiritual guidance and/or time with family. The Japanese did not see depression as a "disorder," but rather as a sign that one had to get back to their "moral compass." Transnational pharmaceutical companies eventually came to Japan and began advertising SSRIs. Prozac came up with a slogan that had cultural resonance, "depression is like a cold of the soul." This avoided having a social stigma attached to the disorder. It also indicated that depression was common and nothing exceptional. The advertisements also pushed the economic argument that there was a huge cost to untreated depression, which counted in lost man-hours and decreased production. Thus, the drug was seen as a way to make people more competitive in the job market. Finally, the crown princess Masako suffered from depression. When it was revealed that she was taking SSRIs as part of her treatment, this was a huge boost for sales in the country.  23 Prevalence catch up page  24 Biological explanations for depression: genetic serotonin hypothesis Neurotransmitters are the brain chemicals that communicate information throughout our brain and body. They relay signals between neurons at the synapse. The brain uses neurotransmitters to control movement and physiology, but they can also affect mood, sleep and other behaviours, and can cause adverse symptoms when they are out of balance. Neurotransmitters, are released from one neuron at the presynaptic membrane and then cross the synaptic gap where they may be accepted by the next neuron at a specialized site called a receptor on the post-synaptic membrane when they contribute to triggering a new impulse The monoamine hypothesis Abbreviations MA = a family of monoamines such as serotonin, noradrenaline and dopamine MAO = monoamine oxidase (obviously oxidases destroy the monoamines such as serotonin) MAOH = monoamine oxidase hypothesis=monoamine hypothesis MAOI = monoamine oxidase inhibitors (obviously encourage the monoamines to hang around in the synapse) The theory essentially hypothesises that depression involves a reduction in the levels of the monoamine neurotransmitters serotonin and noradrenaline in synapses. The theory is supported by the facts that depleted monoamine neurotransmitters produce symptoms of depression, and also that high levels of monoamines result in mania (abnormally elevated or irritable mood). According to this hypothesis, depression should be alleviated by drugs that increase the availability of noradrenaline and serotonin in these synapses. One such method of increasing monoamines would be to block the action of MAO (monoamine oxidase which breaks down monoamines such as serotonin) which would therefore lead to an increased availability of these monoamine neurotransmitters. Serotonin is a neurotransmitter produced by specific neurons in the brain that are called serotonergic neurons because they produce serotonin. In the central nervous  25 system (CNS), serotonin is almost exclusively produced in neurons originating in the raphe nuclei located in the midline of the brainstem. These serotonin-producing neurons form the largest and most complex efferent system in the human brain. Serotonin has been shown to be involved in the symptoms of major depressive disorder, and serotonin in the brain is thought to regulate anxiety, happiness, and mood. Antidepressant treatment should therefore aim to regulate serotonin levels. When serotonin attaches to receptors on the post-synaptic neuron it can help to stabilise mood. Low levels of serotonin in the brain are thought to play a causal role in developing depression. This is because before serotonin gets a chance to attach to the receptors on the post synaptic neuron, it gets reabsorbed back into the pre-synaptic neuron. Recently, depression has been linked to a particular gene – the serotonin transporter gene 5-HTT – and it was shown that this gene determines one’s vulnerability to developing depression in response to stressful life events. The 5HTT gene is the gene which transports serotonin effectively around the body. Research proposes that if you have 2 short alleles on this gene, then serotonin transportation is less effective. This can make you more What is an allele? vulnerable to depression. A variant form of a gene It was shown that this gene determines a person’s vulnerability to developing depression in response to stressful life events. This is in line with the diathesis stress theory that predicts that an individual's reaction to stressful events Genetic depends on their genetic make-up. If an individual has a makeup specific genotype, then interaction with the environment may cause these genes to be expressed. Depressive reaction The risk of depression after a stressful event is elevated among people who are at high genetic risk and diminished Environmental among those at low genetic risk. However, it is not known if stressors specific genes lower the risk of depression as a response to environmental stress or if it is others that raise the risk.  26 Key Study: Caspi (2001) Biological factors influencing depression Background information Diathesis-stress theories of depression predict that an individual's reaction to stressful events depends on their genetic make-up. If an individual has a specific genotype, then interaction with the environment may cause these genes to be expressed. Aim The aim of this study was to determine whether there is evidence for a gene-environment interaction (G x E) for a mutation of the serotonin transporter gene - 5-HTT. The serotonin transporter is involved in the reuptake of serotonin in brain synapses. Procedure Caspi and his team looked at a sample of 847 New Zealand 26-year-olds. All were members of a cohort that had been assessed for mental health on an every-other-year basis until they were 21. They were divided into three groups based on their 5-HTT alleles: 1. Group 1 had two short alleles; 2. Group 2 had one short and one long allele; 3. Group 3 had two long alleles. The mutation of the 5-HTT gene has the shorter alleles. Roughly 43% of people have the shorter alleles. The participants were asked to fill in a "Stressful life events" questionnaire which asked them about the frequency of 14 different events - including financial, employment, health, and relationship stressors - between the ages of 21 and 26. They were also assessed for depression. Past-year depression was assessed using the Diagnostic Interview Schedule. A correlation was tested for between stressful life events and depression, between the length of the alleles and depression and an interaction between perceived stress and the length of the alleles. A further test was done to see if life events could predict an increase in depression over time among individuals with one or two short alleles. Results People who had inherited one or more short versions of the allele demonstrated more symptoms of depression and suicidal ideation in response to stressful life events. The effect was strongest for those with three or more stressful life events. Conclusion: Simply inheriting the gene was not enough to lead to depression, but the genes' interaction with stressful life events increased one's likelihood of developing depression.  27 In a later study by Wilhelm et al (2006), the researchers looked at DNA samples from 127 people who are part of a longitudinal prospective study looking at mental health. The sample had been monitored for over 25 years. At five-year intervals, scientists recorded any major life events and signs of depression. They found that 80 percent of those with two short 5-HTT genes became depressed after three or more negative life events in a year, whereas those with two long genes appeared resilient - only 30 percent developed the illness in similar situations. They also found that childhood maltreatment predicted adult depression only among individuals carrying a short allele and not among those carrying the longer allele. However, much more research is needed before a clear relationship between a gene and a depression can be established. Evaluation The study is correlational, so no cause-and-effect relationship can be determined. The study makes the assumption that serotonin causes depression, but we cannot say that it does with any more certainty. Gene action is highly complex, and actions of other genes could not be controlled. While the stressful life events were standardised as employment, financial, housing, health and relationship, whether or not a participant experienced a certain event as stressful is highly personal and subjective. Information about life-events was self-reported. It may be the salience of the negative life events which plays a role in depression - that is, those that recalled them more easily may have a tendency towards depression. Those who are more resilient, may not recall negative life events as easily. The theory acknowledges the interaction between both biological and environmental factors in depression. This is a more holistic approach, not reductionist. Later studies have not been able to show similar results. Risch et al (2009) carried out a meta- analysis of attempted replications and found that the results were not able to be replicated. It appears that the study has low reliability. There were some participants who did not carry the gene mutation who became depressed; therefore, we cannot say that gene expression alone can cause depression.  28 Backwards reasoning: Success of antidepressant drugs supporting the theory In the early 1950s, researchers noticed that drugs that decreased monoamines resulted in depression, and drugs that increased monoamines relieved depression. e.g. Tricyclics and MAOI’s lower depression All drug treatments effectively raise levels of monoamine neurotransmitters, or increase the activity of monoamine receptors, both of which effectively increase synaptic transmission. Specifically, drug treatments work by: Preventing reuptake of monoamines: Another way to increase monoamines involves blocking the process of reuptake. Blocking reuptake (using drugs) prevents the presynaptic neurone from reclaiming neurotransmitter, which increases the amount of neurotransmitter in the synaptic cleft. Drugs were developed in the 1950s that blocked reuptake in just this way. Antidepressants in the form of selective serotonin reuptake inhibitors (SSRI) block the reuptake process for serotonin. Examples of SSRI’s include Fluoxetine (Prozac), Citalopram and Sertraline. These drugs result in an increased amount of the serotonin in the synaptic gap (see figure 1). The theory is that this increases serotonergic nerve activity leading to an improvement in mood. Essentially, the only evidence that exists in favour of the serotonin hypothesis is the alleged efficacy of SSRIs – if they make your serotonin more potent and this improves your condition, the problem must have been in your serotonin levels to begin with, or so the logic goes. According to Lacoste & Leo (2005) this is an example of backward reasoning. Assumptions about the causes of depression are based on how people respond to a treatment and this is logically problematic. For example, the symptoms of headaches can be treated by aspirin, but this is definitely not to say that the cause of headaches is a deficiency of aspirin.  29 Key Study: Neale et al (2011) Biological factors influencing depression Aim Neale et al. (2011) conducted a meta-analysis of published studies to see the outcome of antidepressants versus a placebo on depression. Procedure They ensured that all studies included in the analysis were randomized, double-blind and placebo- controlled. They also had to meet several other design criteria, such as: Patients must have had a primary diagnosis of depression and a variety of diagnostic methods were allowed. Most published studies excluded depressed patients who had a diagnosis of bipolar disorder or concurrent alcohol or substance abuse. The researchers therefore excluded studies specifically focusing on these special populations. The researchers did not exclude studies in which patients were diagnosed with other comorbid conditions, such as anxiety disorder or diabetes, provided they met all other criteria. They also excluded any study in which patients also received psychotherapy, because it has been shown to influence relapse rates after discontinuation. The study focussed on: (i) patients who started with antidepressants and then changed to placebo, (ii) patients who only received placebo, and (iii) patients who only took antidepressants. Results The study found that patients who do not take antidepressants have a 25% risk of relapse, compared to 42% or higher for those who have been on medication and then stopped it. Conclusion: According to the researchers, antidepressants may interfere with the brain’s self-regulation. They argue that drugs affecting serotonin or other neurotransmitters may increase the risk of relapse. The drugs reduce symptoms in the short-term but, when people stop taking the drug, depression may return because the brain’s natural self-regulation is disturbed.  30 Evaluation The inclusion criteria for studies were very strict. This reduces the chance of extraneous variables influencing the validity of the conclusions. Meta-analysis provides a more precise estimate of the effect size and increases the generalizability of the results of individual studies We may be committing the etiology-treatment fallacy. This is where we assume that the treatment worked because the cause is biological. However, this doesn’t consider extraneous variables which may have been influencing the results e.g. social support at home from family and friends. Meta-analyses can be poorly executed. Carelessness in abstracting and summarizing appropriate studies, failure to consider biases in the methodologies can all contribute to invalid conclusions. Evaluation of biological factors explaining depression How many UCRAP’ED points can you apply to the theory that there is a biological basis to depression involving serotonin? Support for the theory Rausch et al (1985) 18 subjects were either administered physostigmine (a serotonin antagonist) or a placebo in a double-blind study. In comparison to placebo, the drug caused a significant depression in mood, as measured by self- and observer-rated depression scores. Altering serotonin levels by diet (neurotransmission depletion studies) led to depressive symptoms in formerly depressed patients (Moreno and Delgado 2000) Some patients respond positively to SSRIs which increase the level of serotonin in synapses – see the Neale et al (2011) study. There is substantial evidence from drug trials and from post-mortem studies that depression is associated with biochemical abnormalities. Limitations of the theory There have been mixed results with neurotransmitter depletion studies in non-depressed individuals. Since it is not possible to directly measure brain serotonin levels in living humans, there is no way to test the theory. This is supported by Lacasse and Leo (2005) who argue that  31 contemporary neuroscience research has failed to provide evidence that depression is caused by a simple neurotransmitter deficiency. Not all people with depression are successfully treated with SSRIs. The generally accepted success rate is between 20 and 30% of all patients. It's known that all the main antidepressants have an immediate effect on the levels of serotonin and noradrenaline in the brain. But it sometimes takes up to 7-14 days for them to have any noticeable effect on patients' symptoms. It seems that by the time the drugs begin to ‘work’, the neurotransmitter levels have returned to their previous state. So, a simple increase in neurotransmitter levels isn't a sufficient explanation for why the drugs alleviate depression (Davison & Neale, 2001). Abnormal levels of these neurotransmitters might not actually cause the depression, but may indicate that depression can influence the production of neurotransmitters. Current research suggests that mood is controlled by a balance of noradrenaline and serotonin, not by absolute levels of these neurotransmitters or their receptors. According to Kety, serotonin plays a role in limiting noradrenaline levels. When serotonin levels are normal, so are noradrenaline levels, and only normal highs and lows are experienced. However, when serotonin is deficient, it cannot play its limiting role and so noradrenaline levels fluctuate beyond normal high and low levels, leading to mania and depression. Mood disorders result from the removal of the serotonin damper. According to this hypothesis, antidepressant drugs are effective to the degree that they reinstate the ability of serotonin to control noradrenaline, thus restoring the critical balance that controls emotional behaviour. The role of neurotransmitters in mood disorders is further complicated by the fact that antidepressant drugs are not always effective in the reduction of depression, that not everyone suffering from depression shows reduced levels of the neurotransmitters, and that not everyone displaying mania shows increased levels of monoamines. Whilst it seems likely that neurotransmitters do play a role in mood disorders, their exact role remains to be determined. Cognitive symptoms of depression cannot be explained by low levels of serotonin There appears to be a correlation between depression and hippocampal atrophication (Videbech, 2004). This is better explained by the cortisol hypothesis. Cortisol hypothesis: Cortisol belongs to a group of stress hormones that play a role in fear and anxiety reactions, and high levels of cortisol are associated with depressive symptoms. This indicates a possible link between long-term stress and depression. Research seems to indicate that the over-secretion of cortisol during prolonged stress may lower the density of serotonin receptors and impair the function of receptors for noradrenaline, and that this in turn can cause depression. This is consistent with the MAOH hypothesis. Patients with Cushing's syndrome (symptoms include weight gain as well as depression), a disease which results in excessive production of cortisol, are frequently depressed. When given a drug that normalises cortisol levels, these people's depression disappears. This is seen as evidence of a link between cortisol and depression.  32 Biological explanations for depression catch up page  33 Biological treatment for depression: antidepressants Doctors - and in particular psychiatrists who are specialized in the field of mental disorders - need to be able to diagnose and treat mental disorders. They need to be able to distinguish between just feeling sad and clinical depression. The purpose of diagnosis is to implement a treatment. Treatments for psychological disorders are mostly linked to theories about the causes of the psychological disorders, even though our current understanding of causes of psychological disorders is still imperfect. Until the discovery of modern medicine, psychiatrists were working within the psychoanalytic tradition started by Sigmund Freud, suggesting that psychological disorders were rooted in the mind and could be treated through 'talk therapy' conducted by a psychoanalyst. The rise of a more biomedical approach to psychological disorders has been influenced by advances in neuroscience and brain imaging technologies. Biomedical approaches to treatment are based on the assumption that if the problem is based on biological malfunctioning, drugs should be used to restore the biological system. For example, since depression is assumed to involve an imbalance in neurotransmission, antidepressant medications are used to restore an appropriate chemical balance in the brain. However, although chemicals are involved in depression it is not a simple matter of one chemical being too low and another too high. It is probably more correct to say that many chemicals are involved in a dynamic system responsible for mood regulation. Although researchers know more than ever about how the brain regulates mood, their understanding of the biology of depression is far from complete. For example, there are no simple biological markers that can be used from blood or urine testing to help diagnose someone with depression. Psychoactive drugs account for a large proportion of prescriptions. The number of prescriptions for antidepressants in England has almost doubled in the past decade, new figures have shown. Data from NHS Digita show that 70.9 million prescriptions for antidepressants were given out in 2018, compared with 36 million in 2008. As of 2020 in the UK, 7.3 million people take antidepressants (17% of the adult population) The goal of treatment for major depression with antidepressant medication is generally to provide symptom relief. A positive response to drug treatment is defined as a clear improvement, and remission is defined by the near absence of symptoms. However, even when remission is achieved, an individual may have a risk of relapse, that is, the symptoms return after the medication is discontinued. Drugs typically work by affecting neurotransmitters such as dopamine, serotonin or noradrenaline. For example, since serotonin is believed to play a key role in mood regulation, specific drugs can target the level of serotonin. Anti-depressants aim to increase or decrease the levels of available neurotransmitters in the synaptic gap.  34 Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants. One of the most commonly used SSRIs is Prozac. They can ease symptoms of moderate to severe depression, are relatively safe and typically cause fewer side effects than other types of antidepressants do. SSRIs work via neurotransmission, and affect by reuptake pumps. After serotonin is released and binds to the serotonin receptor site on the postsynaptic membrane, serotonin is reabsorbed into the terminal buttons. SSRIs – or Selective Serotonin Reuptake Inhibitors - block this process of reuptake and thus allow there to be higher levels of serotonin in the synapse. Key Study: March et al (2007) Biological treatment for depression If depression is supposedly caused by low levels of serotonin, then increasing serotonin should reduce depressive symptoms. This can be tested by looking at studies which administer anti-depressants. If these reduce depression, then we might be able to say that low serotonin is the cause. Aim To investigate the effectiveness of anti-depressants with regards to the short and long-term effects, in comparison to other treatments. Procedure This was a study conducted funded by the National Institute of Mental Health (NIMH). The participants were adolescents aged between 12-17. The study involved 13 clinics in the USA and the whole project costs $17 million. The sample included 439 participants from all over country, diagnosed with Major Depressive Disorder. Participants were randomly assigned to one of 4 groups a) Fluoxetine alone b) Placebo and clinical management. Clinical management is where they are still allowed to talk to the clinicians, but no specific therapeutic intervention was used. c) Cognitive Behavioural Therapy alone (CBT) d) Combination of CBT and Fluoxetine At the end of the 12-week period, the improvement rate was measured (this is shown in the table in the results below). After this point, the participants on the placebo could choose another treatment, as it would be unethical to withhold treatment from them for any longer. After this, treatment continued for more weeks and improvement was measured at 18 weeks and 36 weeks. Improvement was measured by scores on the Hamilton Depression Scale, a reduction of symptoms, and relapse rate.  35 Results Response rates 12 weeks 18 weeks 36 weeks Placebo 35% discontinued discontinued Fluoxetine 61% 69% 81% CBT 44% 65% 81% CBT and Fluoxetine 71% 85% 86% The results show that after 12 weeks, Fluoxetine is the most effective individual drug. At 18 weeks, it is still the highest individual treatment. At 36 weeks, 81% of participants in the fluoxetine group demonstrated an improvement in their depression. Conclusion: More than ¾ of participants in this very large sample, improved with an SSRI. This could suggest that their depression could have been caused by low levels of serotonin. Evaluation Reductionism: While this study does show that SSRI’s improve depression, the CBT group improved equally as well at 81% too. If they can improve the same amount without any changes to their serotonin levels because of an SSRI, then this suggests that the cause of depression cannot be solely biological. It would be reductionist to assume so, and researchers need to consider other explanations, such as cognitive or sociocultural. We may be committing the etiology-treatment fallacy. This is where we assume that the treatment worked because the cause is biological. However, this doesn’t consider extraneous variables which may have been influencing the results e.g. social support at home from family and friends. Individual differences: No therapy is effective for 100% for patients, which suggests that it’s not as simple as assuming there’s one explanation for everyone. It’s important to think about individual differences. People response differently to treatments, even within one treatment e.g. some people respond better to certain SSRI’s than others. Triangulation: This study was conducted in America, and therefore one might question whether the results generalise to other societies. It would be inappropriate to generalise the findings from this study to cultures which experience different lifestyles, as there is a chance that the successful results are in part due to sociocultural experiences that come from living in America. To improve this, data triangulation could be conducted by testing the effect of SSRIs in other cultures to see whether the results are reliable. Neale et al (2011): use the box below to explain how Neale’s research on page 29 suggests antidepressants may be effective for depression  36 Key Study: Leuchter et al (2002) Biological treatment for depression Background information: An electroencephalogram (EEG) is a recording of brain activity. During this painless test, small sensors are attached to the scalp to pick up the electrical signals produced by the brain. These signals are recorded by a machine and are looked at by a doctor. Aim It has been proposed that 50%-75% of the efficacy of antidepressant medication represents the placebo effect, since many depressed patients improve when treated with either medication or placebo. This study examined brain function in depressed subjects receiving either active medication or placebo and sought to determine whether an electroencephalogram could detect differences in brain function between medication and placebo responders. Procedure Fifty-one subjects with major depression were enrolled in one of two independent, 9-week double-blind, placebo-controlled studies in which either fluoxetine (N=24) or venlafaxine (N=27) was the active medication. Subjects were recruited both from community advertisement and from the outpatient clinics of the UCLA Neuropsychiatric Hospital. The UCLA institutional review board approved all experimental procedures, and written informed consent was obtained after experimental procedures were explained fully to the subjects. All subjects were adults who met DSM-IV criteria for a major depressive episode, as diagnosed with the Structured Clinical Interview for DSM-IV. All subjects had Hamilton Depression Rating Scale scores ≥16, and subjects were excluded if they previously had failed treatment with the antidepressant being studied, if they had a history of suicidal ideation, or if they suffered from any medical illness or received any medication known to significantly affect brain function. Subjects returned for monitoring sessions 2 days after random assignment to study groups and then at weekly intervals. Sessions consisted of symptom evaluation (with the Hamilton depression scale) as well as brief sessions of supportive psychotherapy with a research nurse. These sessions consisted of 15–25 minutes of unstructured counselling and assistance in problem solving. The sessions were mandated by the institutional review board to address safety concerns about dispensing placebo alone to patients with significant depression. Electroencephalogram recordings were performed during the course of treatment. After 9 weeks, the blind was broken and subjects were classified as medication responders, placebo responders, medication nonresponders, or placebo nonresponders. Results No significant pre-treatment differences in clinical or electroencephalogram measures were found among the four outcome groups. Placebo responders, however, showed a significant increase in prefrontal activity starting early in treatment that was not seen in medication responders (who showed decreased activity) or  37 in medication nonresponders or placebo nonresponders (who showed no significant change). This means placebo patients improved just as well as antidepressant patients. Conclusion: Conclusions: Both placebos and antidepressants can lead to similar improvements in depression symptoms, however the two treatments are not physiologically equivalent. In treatment responders, they both affect prefrontal brain function but have distinct effects. "Effective" placebo treatment induces changes in brain function that are distinct from those associated with antidepressant medication. If depression symptoms improve just as well on a placebo, this suggests there are other ways to improve symptoms other than antidepressants (and placebos have less side effects!). If these results are confirmed, activity may be useful for differentiating between medication and placebo responders. Evaluation One of the first studies that has compared subjects treated with placebo and antidepressant medication and documented brain functional changes during treatment in both groups. Self-reported depression symptoms may suffer from problems with bias, but using brain technologies as well, is a form of triangulation. If the results align, which in this study they do, it makes the findings more reliable. One of the biggest studies done to date by Cipriani (2018) challenges the idea that antidepressants are no more effective than a placebo. The study took 6 years and included all the published and unpublished data the scientists could find, including more than 522 trials, consisting of 116, 477 participants, over the age of 18 and of both sexes. In terms of efficacy, all antidepressants were more effective than placebo. The most famous antidepressant of, Prozac – (fluoxetine) – was one of the least effective but best tolerated, measured by a low drop-out rate in the trials or fewer side- effects reported. The most effective of the drugs was amitriptyline, which was the sixth best tolerated, but might be good for those with severe depression. This suggests that antidepressants can be effective in the treatment of depression. Strengths and limitations of biomedical treatments ☺ Use of drug therapies has increased the amount of out-patient care and decreased institutionalization. ☺ Drug therapy shows results more quickly than psychological therapies. Often drug therapy is necessary so that the patient is able to engage in psychological therapy. ☺ The key strength of drug therapy is that for many people who suffer from depression, it alleviates the symptoms that make day-to-day living difficult. Many psychiatrists agree that antidepressants are more effective than placebos for severe mood disorders, and may help to prevent suicide in depressive patients. Geddes et al (2003) carried out a systematic review of 31 randomized trials with 4410 patients and concluded that antidepressant drugs are an effective way to treat depression and prevent relapse. Drugs have been effective in reducing the number of hospital in-patients who are being treated for psychological disorders. ☺ Statistically, men are less likely to access psychological therapies than women: only 36% of referrals to NHS talking therapies are for men. This may be for a variety of reasons including stigma, so they may feel more comfortable taking a treatment that is more discrete, like an antidepressant.  38  A limitation of drug therapy is that clinicians are still not sure how these drugs alleviate symptoms of depression and why the treatment is not effective for all patients. Even though they boost levels of neurotransmitters in the brain within days or even hours of use, it usually takes several weeks of treatment before a therapeutic benefit results. And not all patients respond to them. For example, the serotonin hypothesis has been challenged as an etiology to explain the origins of depression. So, although some may people may benefit from the increased level of serotonin, it may be that drugs like Prozac are simply alleviating a symptom of depression, but not actually addressing the root of the disorder.  There are negative side-effects of using the drug itself. For example, anti-depressants are known to have the following side effects in some patients: nausea, increased weight gain, loss of sexual desire, insomnia, blurred vision, constipation, dizziness, and anxiety. Interestingly, you can see that some of these side effects could actually contribute to lowering one’s self-esteem or sense of autonomy – two characteristics of people living with chronic depression. Sometimes these side effects can also be misinterpreted as a symptom of the disorder e.g. sleeping problems - what is known as an iatrogenic effect.  Drug therapies may lead to addiction and to withdrawal symptoms when the use of the drug is discontinued. In addition, drug therapy may result in negative effects when used in combinations with other drugs or certain foods.  Relying too heavily on drug treatments may lead to the neglect of important psychological or social factors that may play a significant role in the disorder. It can be argued that simply using a drug to treat depression is a reductionist approach. A drug may alleviate symptoms, but if the cause of depression is the stress of poverty or unemployment, then the actual cause of the depression is not addressed. The drug then only provides temporary relief from the symptoms and the chance of relapse is high. An interactionist approach argues that a combination of biological and psychological approaches to understanding a disorder and its treatments should be considered  Another limitation of drug treatment is the problem of developing a dependence on the drug. Anti- depressants and anti-anxiety drugs may lead to discontinuation syndrome – often known as “withdrawal symptoms.” In addition, if drug treatment is discontinued, the chance of relapse is high. Hollon et al (2005) compared the discontinuation of anti-depressants after 16 weeks of treatment to discontinuation of Cognitive Behavioural Therapy. 76% of the patients who had received drug treatment relapsed following medication withdrawal, compared with only 31% of the patients who had been treated with therapy.  There are ethical concerns - unless treatment is regarded as an emergency e.g. the client is suicidal - it cannot be given without the client’s consent, except in cases where the client may not be capable of giving consent. This consent should be given on the basis of full information about the potential benefits and drawbacks of the drugs concerned, in which case it fulfils the ethical criterion of informed consent.  There is a major concern about the rise in prescriptions of drugs such as antidepressants because they can cause harm if they are not prescribed appropriately. There is an ongoing debate among clinicians about possible medical and psychological risks in prescribing so many antidepressants as well as whether they are effective long-term since most clinical trials only last around 6 or 8 weeks and only address whether patients report a reduction in symptoms.  Seeing the potential limitations of drug treatment, it becomes even more apparent that there is a sincere ethical concern about the way that diagnoses are made. When drug treatment is seen as necessary in spite of the potential limitations, it is important the diagnosis has been made in a way that increases its validity. Ideally, every client that is diagnosed as needing drug treatment would have had more than one series of tests carried out by more than one psychiatrist. However, this is rarely the case. Often these drugs are prescribed by a family doctor, not a psychiatrist.  39 Biological treatments for depression catch up page  40 Cognitive explanations for depression: Cognitive model of depression Cognitive theories are based on the recognition that humans are not only social and biological organisms but they are also thinking organisms i.e. there must be a cognitive component to depression. Cognitive models assume that the ways in which people think about, and perceive their world have an important influence on the way that they feel (i.e. thoughts>feelings). Two people may react very differently to the same event, in large part because they may interpret the event (e.g. failing an exam) differently. One may become depressed and the other not. It has long been recognized that people who feel depressed tend to think depressed thoughts. It is commonly assumed that a depressed mood somehow leads to cognitive symptoms. Cognitive theories of depression aim to explain why some people are more vulnerable to depression when confronted with negative events, whereas others suffer only mild short-term distress. Seen from the cognitive approach, the interpretation people give to their life experiences influences their vulnerability to depression, meaning that depressed cognition, cognitive distortions, and irrational beliefs produce the disturbances of mood characteristic of depression. The American psychiatrist Aaron Beck is seen as the founder of cognitive therapy. He argues that depression is rooted in what he called a patient's "automatic thoughts"- that is, negative self-schemas organized around themes of failure inadequacy, loss, and worthlessness. All these personalized thoughts are triggered by particular stimuli that lead to emotional responses and they are seen as potential vulnerabilities for the onset of depression. Beck's theory of depression has three components: 1. The Negative cognitive triad: depressed patients have negative views of the self, the world, and the future. 2. They have negative schemas triggered by negative life events (dysfunctional beliefs). 3. They engage in cognitive biases - also referred to as "irrational thinking."  41 He defined the "depressive triad"—which involve negative, demeaning (self-critical) views of the self, the world, and the future, as being central to our understanding of depression: 1. The self (i.e. self is worthless) 2. The world/environment (i.e. world is unfair) 3. The future (i.e. future is hopeless). Beck called these ‘automatic thoughts’ because they occur spontaneously. It is clearly discouraging, and disabling (e.g. don’t apply for jobs), to be plagued with hopeless and self- critical thoughts. According to Beck's theory, these “pervasive and persistent negative cognitions play a central role in the aetiology of depression.” Beck argues that negative schemas can develop because of family problems, social rejection by peers, poor school experiences or by having depressed members of the family or close social circle. These schema are activated in depressed people whenever they are in a situation which in any way resembles the situations in which the schema were created. Beck describes three typical schema that are characteristic of depressed people: an ineptness schema - that is, I always fail; a self-blame schema - that is, it is my fault for anything that doesn't work out; a negative self-evaluation schema - that is, I am worthless. Beck also argues that there are several patterns of faulty thinking or cognitive biases that are typical in depressed patients. These patterns are explained in the chart below.  42 According to Beck the depressed person is: overly sensitive to obstacles to goal-directed activity (i.e. perceive major barriers to personals objectives) harmless statements by others are interpreted as criticism devalues themselves will selectively recall events which had negative consequences, therefore overestimate the problems and difficulties of a situation (e.g. forming a relationship, exams) will discount the significance of positive events ^ (these are all linked with cognition) Beck suggests that the origins of distorted thinking and depressogenic premises are in childhood. Schemas are packets of information in which our knowledge of each aspect of the world is contained, and self-schemas contain a network of all the information and beliefs concerning ourselves. Beck suggested that in childhood we can acquire a negative set of beliefs (self-schema) about ourselves through experiences with negative or critical parents (e.g. I am useless, I am stupid etc). They can also be formed through various unfavourable life experiences such as loss of a parent, divorce or chronic rejection by peers (e.g. bullying) all affecting self-schema. We then interpret new information based on these existing negative self-schema. According to Beck, existing negative schemas are activated by stressful events (such as exams or illness) or reactivated when the person experiences a similar event to when they were formed.  43 Key Study: Alloy et al (1999) Cognitive factors influencing depression Aim To see if one’s thinking patterns could be used to predict the onset of depression. Procedure In order to do this, they carried out a longitudinal study in which they followed a randomly selected sample of young Americans for six years. As this was a prospective study, their thinking style was tested at the very beginning of the study. They were placed in either the “positive cognitive group” (low risk) or “the negative cognitive group” (high risk) based on a number of tests such as the Cognitive Style Questionnaire. Results After six years, the researchers found that only 1 percent of those in the positive thinking group had developed depression compared to 17 percent in the negative thinking group. Conclusion: The results indicate that there may be a link between negative cognitive style and the development of depression. Evaluation Use of a questionnaire: does this accurately measure cognitive style? Could there be social desirability bias on this questionnaire? All of these factors could lower the validity of the theory that thinking patterns influence depression. Therefore, method triangulation could be used. Think about which method might obtain better quality data. Longitudinal research means we can study the manifestation of depressive symptoms over time, which gives a more realistic picture of the relationship between thinking patterns and depression. This improves the validity and reliability of the findings, because it allows us to test the behaviour over time and obtain richer data on it. However, the temporal validity of this study is low. With the surge in technology use over the last decade, this could have some influence on the role that cognition plays in depression. For example, does social media influence these negative thoughts, which in turn leads to depression?  44 Key Study: Joiner et al (1999) Cognitive factors influencing depression Background information Aaron Beck argues that dysfunctional patterns of thinking may lead to depression. Beck noticed these patterns in his own clients and there are several correlational studies that link this type of thinking to depression. However, correlational studies lead to the question of bidirectional ambiguity. Do dysfunctional patterns of thinking lead to depression, or does depression lead to dysfunctional patterns of thinking. Beck posited that dysfunctional thinking is a vulnerability factor for depression. Joiner et al postulated that dysfunctional thinking should be associated with the development of depressive symptoms in the presence, but not the absence, of negative life events. In other words, they argued that the cognitive approach to depression is based on the diathesis-stress model – when one has negative thinking patterns and then is exposed to a life stressor, there is a higher probability to develop depression. However, negative thinking alone does not lead to depression. In order to test this hypothesis, Joiner carried out a prospective study of the role of exam stress in university students. Aim To determine the role of depressive and anxious thinking patterns on the development of depressive symptoms. They hypothesized that negative thinking patterns, but not anxious cognitions, would play a role in the onset of symptoms related to depression. Procedure The sample was made of 119 American university students, all taking an abnormal psychology course. The mean age of the students was 19 years old. The stressor that the researchers would observe was mid-term examinations. The students were assessed two weeks before and two weeks after their mid-term examinations. As the administration of the exams was naturally occurring in the university setting, this study was a natural experiment. To assess the students, there were three tests that were given. 1. The Dysfunctional Attitudes Scale [DAS] This test measures thinking patterns such as vulnerability, need for approval, perfectionism and the need to impress. This was taken only before the mid-term exams. 2. The Cognitive Checklist [CCL]. Half of the questions determine automatic thoughts linked to depression; the other half, linked to anxiety. This test was taken both before and after the exams. 3. The Beck Depression Inventory [BDI]. A standardized assessment to measure levels of symptoms linked to depression. This test was also taken both before and after the exams.  45 Results The researchers found an increase in the scores on the BDI only in students who had higher scores on the DAS and who had failed an exam. Students who had a higher score on the DAS but did well on the exams showed no significant increase in their BDI score. For the students who had lower scores on the DAS, even if they received low grades, they did not experience depressive reactions. When looking at the scores for the CCL, there was a correlational between having higher scores on the depressive thinking patterns questions and the increase in the BDI scores if a student failed an exam. There was no significant correlation between the anxiety scores and an increase in BDI scores. Conclusion This shows that patterns of cognition alone are not enough to lead to depression, but they must also be in response to environmental stimuli. Evaluation The study was prospective, allowing the researchers to see change over time. This allows researchers to control for bidirectional ambiguity. The study was naturalistic, meaning that there was limited control over extraneous variables. Although there was an increase in depressive symptoms, this is not the same as a clinical diagnosis of Major Depressive Disorder. The experiment's results may not indicate what may happen in clinical depression. There was a sampling bias. The study was carried out on American undergraduates who were studying psychology. The age, culture and education of the sample may all have played a role in the results of the study. The students were all students in an abnormal psychology class, so they must have had some understanding of what the tests they were taking were measuring. This could lead to a self-fulfilling prophecy, but then again, the study did not look at clinical depression, simply "depressive symptoms." Overall, it is not clear if depression is caused by negative thinking patterns or if these patterns are merely the consequence of having depression. If a negative cognitive style causes depression, then replacing negative cognitions with positive thinking patterns could improve the patient’s condition. This is exactly what CBT (cognitive-behavioural therapy) tries to do.  46 Evaluation of cognition explanations of depression Strengths Longitudinal, prospective research has been used to support the role of cognitive factors in depression. Practical application of the theories has led to successful treatments. If a negative cognitive style causes depression, then it suggests that replacing negative cognitions with positive thinking patterns could improve the patient's condition and this is exactly what CBT (cognitive- behavioural therapy) tries to do, and it has improved people’s lives. Limitations Correlational research means that causation cannot be established and bidirectional ambiguity cannot be resolved. It is unclear whether the thinking patterns are the cause or the result of depression, or whether a third variable such as a biochemical imbalance, is involved. The Treatment Aetiology Fallacy – that is, the mistaken notion that the success of a treatment reveals the cause of the disorder. Just because CBT has been very successful in treating depression, it doesn’t mean the cause is necessarily cognitive. The perception and recall of information in more negative terms might be the result of depression rather than the cause of it. Cognitive distortions are generally not unique to depressed patients so although cognitive fac- tors may play an important role in mood disorders, they are only one piece of the aetiological puzzle.  47 Cognitive explanations for depression catch up page  48 Psychological treatment for depression: cognitive behavioural therapy (CBT) Psychological approaches to the treatment of depression come in many forms. These approaches are called psychotherapies; they involve face- to-face interactions with a therapist. Psychotherapy is seen as more personal than drug therapy and can be highly individualized to meet the need of the client. Generally, psychotherapy is more focused on addressing a person's life situation and subjective understanding of his or her psychological problems. Psychotherapy helps people identify unhealthy thought patterns and behaviours as well as suggesting strategies to manage stress and symptoms. A therapist often works with an individual alone, but may also include family members in therapy sessions. Sometimes psychotherapy alone is enough to help an individ