BIOLOGICAL, PSYCHOLOGICAL, AND SOCIOCULTURAL CAUSES OF DEPRESSION
BIOLOGICAL, PSYCHOLOGICAL, AND SOCIOCULTURAL CAUSES OF DEPRESSION
In depression, as in many other mental disorders, it is very almost impossible to establish simple cause-effect relationships between the contributing factors and thew disorder. It is difficult to distinguish between different factors because they usually interact with each other. The symptoms of depression themselves can sometimes become the factor than further aggravate the cause of illness. Possible causes of depression are often classified into biological, psychological, and soiocultural causes, although the distinction between them is not always clear cut.
Family studies have shown that the first-degree relatives of depressed patients have nine percent risk of becoming depressed, while the rate of depression in the general population has been estimated at three percent (Plomin, De Fries, McClearn, and Rutter, 1997). Plomin et al. (1997) have based these estimates on the results of seven different studies that focused only on the severely depressed patients that needed to be hospitalized. It is possible that the base rate of depression would be larger, and the family risk smaller if less severe cases of depression were taken into account (Plomin et al., 1997).
Twin studies of depression have shown higher concordance rates among monozygotic than among dizygotic twins (Plomin et al., 1997). In less severe forms of depression, however, the concordance rates for monozygotic and dizygotic twins have been found to be almost identical (Kendler, Neale, Kessler, Heath, and Eaves, 1992a; cited in Plomin et al., 1997). Concordance rates for unipolar major depression in monozygotic and dizygotic twins can bee seen in Table 1. A study of twelve pairs of identical twins reared apart showed that 67 percent (eight of twelve pairs) were concordant for major depression (Bertelsen, 1985; cited in Plomin et al., 1997).
Adoption studies found that the risk of developing depression was could be estimated at eight percent for the biological relatives of depressed individuals and five percent among their adoptive relatives (Wender, Ketty, Rosenthal, Schulsinger, Ortmann, and Lunde, 1986; cited in Plomin et al., 1997).
It has been argued that depression might be due to depletion of one or more neurotransmitters at their synapses in the brain (for a drawing of neurotrensmitter action at neuronal synapse see Figure 1). Dopamine, norepinephrine, and serotonin are the neurotransmitters most often implied in neurochemical theories of depression. The depletion of neurotransmitters could be due to impaired synthesis of these neurotransmitters at presynaptic neuron, to their increased degradation in the synaptic cleft, or to dysfunction of the postsynaptic receptors (Zamar, 1999).
Norepinephrine could have influence on one’s mood through acting on limbic system areas which play an important role in emotional regulation (Nemeroff, 1998). Many studies have found that the metabolites of norepinephrine in urine and cerebrospinal fluid, which are indirect marker of norepinephrine levels in the brain, are lower in depressed individuals (Nemeroff, 1998). Postmortem studies of depressed suicide victims have shown an increased number of certain norepinephrine receptors in cerebral cortex of these individuals. Increased number of receptors is often a consequence of “up-regulation” due to lack of norepinephrine concentration in brain synapses (Nemeroff, 1998).
Serotonin depletion could lead to depression by influencing amygdala, hypothalamus, and certain areas of cerebral cortex. Serotonin neurons also project to CNS regions involved in secretion and regulation of norepinephrine, and it is possible that depletion of serotonin may lead to depression indirectly by causing decrease in norepinephrine transmission (Nemeroff, 1998). The class of drugs known as selective serotonin reuptake inhibitors, which block the reuptake of serotonin in presynaptic neurons, are known to decrease the symptoms of depression (Anderton, 1997). There has been some evidence that depressed people have lower than normal levels of a serotonin metabolite, 5-hidroxyinodolaetic (5-HIAA) acid in the cerebrospinal fluid (Ricci and Wellmen, 1990). Post-mortem studies of depressed individuals have also found greater number of serotonin receptors in the brains of depressed suicide victims ( Nemeroff, 1998).
It is now known, however, that depression is not caused by depletion of any single neurotransmitter, but rather by overall imbalance in the chemical functions of the brain (Shelton, Hollen, Prudon, and Loosen, 1991; cited in Carson, Butcher and Mineka, 1999). Furthermore, some studies suggested that the overall activity of norepinephrine in depressed patients was not decreased but increased (Shelton et al., 1991; cited in Carson, Butcher and Mineka, 1999). It has also been argued that antidepressant drugs, which take at least several weeks to show their therapeutic effects, increase the availability of norepinephrine and serotonin only on the short run. Their long-term effect is thought to be the decrease in the number of some of the postsynaptic receptors and increase in the number of others. This lead to conclusion that depression was most probably caused by abnormalities in postsynaptic receptor systems (Shelton et al., cited in Carson, Butcher and Mineka, 1999). Another problem with chemical theories of depression is that one cannot say with any certainty that the changes in neurotransmitter systems are the cause of depression. The changes could easily be the result, rather than cause of the illness (Carson, Butcher and Mineka, 1999).
It has been proposed that depression could be caused by hormonal abnormalities due to disorders connected with hypothalamic-pituitary- adrenal (Sheldon et al., 1991; cited in Carson, Butcher and Mineka, 1999) and hypothalamic-pituitary-thyroid axis (Marangell, Ketter, George, Pazzaglia, Callahon, Pareleh, Anderson, Horwitz, Hereschovitch, and Post, 1997).
Holsboer (1992; cited in Carson, Butcher and Mineka, 1999) suggested that could be due to faulty hormone regulation in the hypothalamic-pituitary-adrenal axis, which is responsible for managing body responses to stress. Under elevated levels of stress, hypothalamus increases the production of corticotropin releasing factor (CRF), which stimulates pituitary gland to increase secretion of adrenocortictropic hormone (ACTH). ACTH signals to adrenal glands to increase the release of hormone cortisol (Nemeroff, 1998). It has been found that levels of this hormone can be elevated up to 60 percent depressed patients (Holsboer, 1992; cited in Carson, Butcher and Mineka, 1999). Some postmortem studies have found that depressed people had increased numbers of neurons responsible for the production of corticotropin releasing factor (Nemeroff, 1998).
It has also been suggested that depression could develop due to dysregulation of hypothalamic- pituitary-thyroid axis (Marangell et al., 1997). It is well known that people with low thyroid levels often become depressed. Even depressed people with normal thyroid levels, however, show some dysregulation on the hypothalamic-pituitary- thyroid axis (Marangell et al., 1997). Marangell et al. (1997) used proton emission tomography (PET) to measure the global and regional cerebral blood flow, and cerebral glucose metabolism in depressed people. (See Figure 2 for a PET scan of a depressed person’s brain.) They then examined their relationship to peripheral thyroid measures, such as serum thyrotropin stimulating hormone (THC). High levels of serum THC are associated with lower thyroid hormone availability and lower somatic metabolism of this hormone (Marangell et al., 1997). There was a negative correlation between serum THS and the measures of cerebral blood flow and glucose mechanism. Dysregulation of hypothalamic-pituitary-thyroid axis could, therefore, produce depressed mood through reduction of cerebral blood circulation and glucose metabolism in the brain (Marangell et al., 1997). Marangell, George, Callahon, Ketter, Pazzaglia, Herron, Leverich, and Post (1997) found that administration thyrotropin releasing hormone (potirelin) lead to 50 percent decrease in depressive symptoms in refractory depressed patients.
It had been observed that patients with lesions in the left cerebral hemisphere often experienced symptoms of depression and anxiety (Davidson, 1984; cited in Henriques and Davidson, 1990). Robinson, Kubos, Starr, Rao, and Price (1984; cited in Henriques and Davidson, 1990) found that the severity of poststroke depression was related to the location of damage produced by the stroke. The closer the lesion was to the left frontal pole, the more severe depression was experienced by the stroke victims. Henriques and Davidson (1991) recorded the baseline resting electroencephalogram activity in 15 clinically depressed and 13 nondepressed subjects. The depressed subjects had relatively higher levels of electrical activity in the right midfrontal brain areas, while the control subjects showed relatively higher levels of activity in the left midfrontal areas of their brains. The level of electrical activity in right hemisphere was not different between the two groups, but the level of activity in the left hemisphere was significantly lower in the depressed subjects (Henriques and Davidson, 1991). Different measures of resting brain activity levels in depressed and nondepressed subjects are presented in Figures 3 and 4.
Henriques and Davidson (1990) also found that depressed subjects showed less left-sided anterior and less right-sided posterior activation than did the never depressed subjects. This pattern of activation seemed to be present even among the subjects who had previously been depressed, but no longer met the criteria for clinical depression. This suggested that EEG activity could be one of the permanent biological markers for depression (Henriques and Davidson, 1990). Tomarken, Siemien, and Garber (1994; cited in Carson, Butcher and Mineka, 1999) found that children who are at risk for depression exhibit similar pattern of EEG activity.
Sleep disturbances are very common in depressed patients, insomnia is even one of the criteria for diagnosing major depression (DSM, 1994). It has been suggested that depression is associated with both quantitative and qualitative disturbances in sleep cycles (Shelton et al., 1991; cited in Carson, Butcher and Mineka, 1999). Electroencephalographic sleep measurements have shown that many depressed patients enter the rapid eye movements stage of sleep earlier than do nondepressed people, and that they have greater amounts of REM sleep early at night (Shelton, 1991; cited in Carson, Butcher and Mineka, 1999). Some studies have found that disturbances in REM sleep rhythm are present in previously depressed patients, as well as in people who are at high genetic risk for depression (Lauer, Schreiber, Holsboer, and Krieg, 1995; cited in Carson, Butcher and Mineka, 1999).
It has further been suggested that depressed people have disturbances in circadian rhythms including not only REM and sleep-awake cycles, but also the secretion of hormones such as cortisol, thyroid-stimulation hormone, and melatonin (Shelton et al., 1991; cited in Carson, Butcher and Mineka, 1999). Healy and Williams (1988) have suggested that the primary disturbance in circadian cycles causes the alterations in neurotransmitter balance as a secondary consequence, and provides a framework for interactions between biological and psychological factors responsible for development of depression.
Certain prescription drugs such as antihypertensive medications, anti-Parkinsonian drugs, and medications prescribed for artritis, ulcers, and seizures can lead to development of depressive symptoms (Turkington and Kaplan, 1997). Some cholesterol lowering drugs, and even some acne medications can be responsible for depression (Bender, 1998). If one notices the onset of depression symptoms shortly after starting a new medication, one should contact the doctor immediately, and change the medication type or modify its dosage (Bender, 1998). For a list of medications associated with the development of depressive symptoms see Table 2.
Brown and Harris (1979; cited in Carson, Butcher and Mineka, 1999) found that depression often followed one or more stressful events, usually involving the loss of self-esteem, disruption of an important goal, or fall from one’s social sphere. Billings, Cronkite, and Moos (1983) compared 409 depressed and 409 nondepressed subjects on different measures of environmental stress and found that the depressed subjects experienced significantly higher number of stressful events than did the controls. The most pronounced difference between the groups was found with respect to personal and children’s health problems (Billings, Cronkite, and Moos, 1983).
Monroe and Simons (1991) argued that not all stressors should be viewed as equally important contributors to a development of depression. The stress usually differs in its form, strength, and duration, and different types of stress can interact with each other to influence the development of the depressed mood. Researchers should, therefore, be more specific in identifying a particular stressor or a specific interaction between different forms of stress that would lead to increased vulnerability to depression (Monroe and Simons, 1991). Each person’s perception of a stressor is important in the evaluation of its severity as different people often perceive identical events in different ways. Only if one carefully defines the type and intensity of stress can the problem of subjective interpretation be overcome (Monroe and Simons, 1991).
Kessler (1997) reviewed
a large body of literature on stress and depression and concluded that
the majority of studies had found a link between the two. Kessler (1997)
pointed out at some methodological problems, found in most of the studies,
that could prevent us from making causal inferences about the effects of
stress on development of depression.
Many studies were retrospective in nature. Depressed people may
not be very accurate in reporting the number of stressful events and the
amount of stress they experienced because their perception and memories
of the events are affected by the illness (Kessler, 1997). Even the prospective
studies may be flawed, however, because they assume that exposure to negative
life events and depression are the variables independent of each other.
This is often not the case, since the same factors that increase one’s
vulnerability to depression may lead to a greater number of negative events
and the greater amount of stress in one’s life (Kessler, 1997).
According to diathesis-stress models of depression, stress alone is not sufficient for someone to develop depression, the person also needs to be predisposed to develop this illness (Monroe and Simons, 1991). Genetic vulnerability, personality traits, cognitive schemas, attributional styles, hopelessness, and early childhood trauma are only some of the factors suggested to predispose people for depression.
Monroe and Simons (1991) argued that the way in which the diathesis-stress interaction is portrayed in these models is often ambiguous. The nature of interaction is often not carefully specified. The stress is usually portrayed as rather nonspecific and continuous, varying only in degree but not in kind. Diathesis, on the other hand, is portrayed as discontinuous and categorical (people either have it or not). The researchers should bear in mind that diathesis can often become continuous once certain threshold has been reached, and that the interactions between diathesis and stress can be rather complex since diathesis and stress are rarely independent of each other (Monroe and Simons, 1991).
Since it has been shown that there is a moderate hereditary component in depression, it is easy to see how diathesis for this disorder could be genetic in nature. Kendler, Kessler, Walters, MacLean, Neale, Heath, and Evans (1995) found that stressful events and genetic liability both had a significant impact on development of depression. Genetic factors acted as control mechanisms through which the impact of stressful life events was mediated. However, although the main effects of genetic and stress factors were highly significant, the interaction between stress and genetic liability failed to reach statistical significance (Kendler et al., 1995).
This indicated that the risk of developing depression was influenced by genetic factors even in the absence of stressful events, and that stressful events alone could increase the risk of depression (Kendler et al., 1995). The findings suggested that the simple additive genetic diathesis-stress models of depression could not hold and that one should look at more dynamic nature of genetic influence on the experience of stress (Kendler et al., 1995).
People with high levels of sensitivity to negative stimuli, high negative affectivity and neuroticism, and low levels of extraversion and positive affectivity could be more predisposed to develop depression (Clark, Watson, and Mineka, 1994). Adaptive personality traits such as self-confidence and easy going disposition could also protect people from developing depression (Holohan and Moos, 1991).
Beck (1967; cited in Carson, Butcher and Mineka, 1999) suggested that cognitive symptoms always precede and often cause the mood symptoms of depression. According to Beck (1967; cited in Carson, Butcher and Mineka, 1999) the diathesis for depression consists of depressogenic schemas and beliefs that people develop in childhood. These beliefs and schemas are activated by daily stressors. Once activated, they trigger a pattern of automatic negative thoughts that occur outside one’s awareness and include the negative thoughts about self, one’s environment, and the future (Beck, 1967; cited in Carson, Butcher and Mineka, 1999). Back (1967; cited in Carson, Butcher and Mineka, 1999) called this pattern of thoughts the negative cognitive triad and saw it as one of the major causes of depression.
Abramson, Seligman, and Tessadale (1978; cited in Metalsky, Abramson, Seligman, Semmel, and Peterson, 1982) suggested that different attributional styles could act as causal factors for depression. People are able to attribute different events to ether internal or external, stable of unstable, and global or specific causes (Abramson, Seligman, and Tessadale, 1978; cited in Metalsky et al., 1982). Abramson, Seligman, and Tessadale (1978; cited in Metalsky et al., 1982) argued that people with internal, global, and stable attributional styles had increased vulnerability for depression. However, the internal, global, and stable attributional styles themselves, in the absence of negative life events, would not be enough to trigger a depressive reaction.
Metalsky et al. (1982) tested the above mentioned theory of depression on 27 university students by examining whether their attributional styles could predict the severity of depressed mood upon the reception of low grades on a midterm examination. The students were administered the Attributional Style Questionnaire, a questionnaire that measured their aspiration for the midterm exam, and the Multiple Affect Adjective Checklist that measured their transient levels of depressed mood. The presence of transient depressive moods was examined both before and after the exam. Students were considered to have received low grades if their grades were lower or equal to the grades they said that they would be unhappy with (Metalsky et al., 1982). Neither attributions nor the low grades alone could predict the extent of depressive moods students experienced after receiving their exam grades. Students who had a tendency to make external and specific attributions seemed rather invulnerable to depressive reactions after receiving low grades. Students who made internal and global attributions, on the other hand, experienced more depressive moods after receiving low grades. The stability of students’ attributions, however, did not predict the intensity of the depressive reactions to low grades (Metalsky et al., 1982). For the correlations between students’ attributional styles and the change in their moods after receiving the midterm grades see Table 3.
Abramson, Metalsky and Alloy (1989) proposed a theory of depression according to which all other proposed causes contributed to depression through invoking hopelessness. Hopelessness expectancy was defined as a perception that the bad outcome was going to occur, while the desirable one was not going to happen, and that one could not do anything to change this (Abramson, Metalsky, and Alloy, 1989). Metalsky, Joiner, Hardin, and Abramson (1993) offered some support for this theory when they found that students’ initial depressive reactions to bad grades would continue after a period of four days only if they saw their condition as hopeless and if they had low self-esteem. Alloy and Abramson (1997; cited in Carson, Butcher and Mineka, 1999) also found that students who were hypothesized to be at high risk for developing depression were seven times more likely than the students in a low-risk group to actually develop depressive disorder in the two following years.
Brown and Harris (1979; cited in) found that women who lost their mother before the age of 11 were more likely to develop depression. The women who lost the mother by death were more likely to develop severe psychotic depression, while women who lost mother by separation were more likely to experience less severe forms of depressive disorders (Brown and Harris, 1979; cited in Carson, Butcher and Mineka, 1999).
Ray (1985) compared 300 depressed patients with 300 matched control subjects on the variety of factors including the experience of permanent separation from parent, not due to death, in the period of childhood and adolescence. Significantly higher number of the depressed patients experienced parental loss before the age of 17. The effect of separation was much stronger if it occurred before the participant was 11 years old. Loss of father was more strongly related to depression than the loss of mother, and the separation had stronger effect on the working class than on the middle class participants (Ray, 1985). It is worth noting, however, that the majority of the depressed patients had not experienced parental loss before the age of 17. For the percentages of depressed and nondepressed participants who experienced parental in childhood and adolescence see Figures 5 and 6.
Amato and Keith (1991) argued that children of divorced parents showed lower levels of psychological well being in adulthood. Their analysis, based on 23 independent samples of participants tested in different studies, found that parental divorce had a significant negative effect (mean effect size = -.32) on psychological adjustment measures that included the measures of depression, anxiety, life satisfaction, and emotional adjustment.
Feather and Baker (1983) tested
116 unemployed male and female subjects on the measures of expectations
of success, internal and external attributions, perceived uncontrollability
and employment importance, and the measures of self-esteem and depression.
The means and standard deviations of each of the measured variables can
be seen in Table 4.
Depression was positively related to perceived importance of having
a job and to the perceived uncontrollability of unemployment, and negatively
correlated with self-esteem. Attributional styles, however, seemed to contribute
to only a small portion of variance in depressed feelings experienced by
unemployed subjects. The results obtained by a multiple regression
analysis showed that unemployment may be contributing to development of
depression bought through the perceived lack of success in achieving a
valued goal and through self-blame and lowering of self-esteem (Feather
and Baker, 1983).
Dew, Penkower, and Bromet (1991) conducted a literature review in the effects of involuntary unemployment on mental health of men and women. They found that unemployment contributed to experience of depressed feelings not only by the unemployed person, but also by their spouses and children. Although unemployment was found to have significant negative effects on the mental health of men, the women seemed even more affected (Dew, Penkower, and Bromet, 1991). Table 5 gives a summary of findings obtained in some of the studies included in their review.
Billings, Cronkite, and Moos (1983) found that depressed participants had smaller number of friends, network contacts, and close relationships than nondepressed controls. The perceived quality of social support contacts was also smaller among the depressed participants. Mean ratings of number and quality of social contacts for depressed participants and nondepressed control subjects are presented in Table 6.
Siegal and Kuykendall (1990) examined psychological responses to a recent loss of a family member (not marital partner) in elderly men and women. They found that the severity of psychological response to the experienced loss was modified by the availability of social support, such as the presence of the spouse, or the membership in a church or temple. Familial loss was related to elevated rates of depressive symptoms only among the male participants. Siegal and Kuykendall (1990) argued that this could be because the men often have smaller reference groups and fewer people, other than their marital partner, who they could confide in. The lack of a supportive marital partner would, therefore, have more negative effects on men than on women (Siegal and Kuykendall , 1990). Widowed men experienced more depressive symptoms than did those whose marital partners were still alive. Widowed men who did not belong to a church or a temple suffered more depression than those who did (Siegal and Kuykendall, 1990).
Holohan and Moos (1991) found that positive family support could act prospectively to reduce depressive symptoms in the following four years. In people who experienced high levels of stress, social support reduced the risk of depression indirectly, through increasing the incidence of people involving in adaptive stress-coping strategies. In people who experienced low levels of stress social resources had direct influence on the reduction of risk (Holohan and Moos, 1991
Marsella (1980; cited in Carson, Butcher and Mineka, 1999) reviewed cross-cultural literature on depression and found that, although people suffered from depression all over the world, the symptoms of depression were not identical everywhere. In China, for example, people experienced the somatic, but not psychological symptoms of depression. People in other non-western cultures also experienced somewhat different symptoms. The feelings of guilt and self-recrimination, which are among the major characteristics of depression in Western world, seemed to be absent in other cultures (Marsella, 1980; cited in Carson, Butcher and Mineka, 1999). This suggests that cultural values can influence the ways in which depression manifests itself and the ways in which it is experienced by people.
It has already been noted that most of the above mentioned factors are only contributory causes of depression. Presence of more than one factor is often necessary if depression is to develop. All of the factors can interact with each other, and one factor can become the cause of another. Most people do not find it hard to see how different psychological and social factors could interact with each other to cause depression. There is often more confusion, however, when one takes into consideration the biological factors of depression.
It is usually assumed that biological dysfunctions arise only from within the individual and, while they can have influence on psychological wellbeing and one’s experience, they cannot in turn be influenced by them. Studies have found, however, that environmental stress can change the balance of neurotransmitters in the brain (Yahoda, Southwick, and Giller, 1992; cited in Carson, Butcher, and Mineka, 1999). Meaney, Diarrio, Francis, Widdowson, LaPlante, Cladji, Shama, Sechel, and Platsky (1986; cited in Nemeroff, 1998) have shown that maternally deprived rats develop permanent increase in CRF and ACTH levels in the brain. When the biological markers for a certain disorder are found we cannot immediately assume that its cause is biological because a whole range of psychological and social factors can lead to biological changes within an organism (Gorwnstein, 1992; cited in Carson, Butcher, and Mineka, 1999).
Abramson, L. Y., Metalsky, G., & Alloy, L. B. (1989). Hopelessness depression: A theory-based subtype of depression. Psychological Review, 96, 358-372.
Amato, P. R., & Keith, B. (1991). Parental divorce and adult well being: A meta-analysis. Journal of Marriage and Family, 53, 43-58.
Anderton, S. M. (1997). Major depression and the neurotransmitter serotonin. http://ww2.lafayette.edu/~loerc/ander.html
Bender, K. J. (1998). New warning of depression with Accutane could apply to other medications. Psychiatric Times, 15, http://www.mhsource.com/pt/p980501b.html
Billings, A. G., Cronkite, R. C., & Moss, R. M. (1983). Social-environmental factors in unipolar depression: Comparison of depressed patients with nondepressed controls. Journal of Abnormal Psychology, 92, 119-133.
Carson, R. C., Butcher, J. H., and Mineka, S. (1999). Abnormal psychology and modern life. Ally and Bacon: Boston.
Calrk, L. A., Watson, D. & Mineka, S. (1994). Temperament, personality, and the mood and anxiety disorders. Journal of Abnormal Psychology, 103, 103-116.
Dew, H. A., Penkower, L., & Bromet, E. J. (1991). Effects of unemployment on mental health in contemporary family. Behavioral Modification, 15, 501-544.
Diagnostic and statistical manual of mental disoders IV. (1994). American Psychological association.
George, M. (1993). Depression PET scan. http://www.nimh.nih.gov/hotsci/scandep.htm
Feather, N. T., & Baker, J. G. (1983). Depressive reactions and unemployment. Journal of Abnormal Psychology, 92, 185-195.
Healy, D., & Williams, J. M. G. (1988). dysrhytmia, dysphoria, and depression: The reaction of learned helplessness and circadian dysrhytmia in the pathogenesis of depression. Psychological Bulletin, 103, 163-178.
Henriques, J. B., & Davidson, R. J. (1990). Regional brain electrical asymmetries discriminate between previously depressed and healthy control subjects. Journal of Abnormal Psychology, 99, 22-31.
Henriques, J. B., & Davidson, R. J. (1991). Left frontal hypoactivation in depression. Journal of Abnormal Psychology, 100, 535-545.
Holohan, G. J., & Moss, R. H. (1991). Life stressors, personal and social resources, and depression: A 4-year structural model. Journal of Abnormal Psychology, 100, 31-38.
ITP Mood Disorders Answers. Psychological Causes of Depressive Symptoms. http://www.med.nyu.edu/Psych/ITPNYU/itp.moodA24Tab.html
Kendler, K. S., Kessler, R. D., Walters, E. E., & MacLean, C. (1995). Stressful life events, genetic liability, and outset of an episode of major depression in women. American Journal of Psychiatry, 152, 833-842.
Kessler, R. C. (1997). The effects of stressful life events on depression. Annual Review of Psychology,48, 191-214.
Marangell, L. B., Ketter, T. A., George, M. S., Pazzaglia, P. J., Callahon, A. M., Pareleh, P., Anderson, P. J., Horwitz, B., Herschovitch, P., & Post, R. (1997). Inverse relationship of peripheral thyropin-stimulatory hormone levels to brain activity in mood disorder. American Journal of Psychiatry, 145, 224-230.
Marangell, L. B., George, M. S., Callaman, A. M., Ketter, L. A., Pazzagila, P. J., Herron, T. A., Leverich, G. S., & Post, R. M. (1997). Effects of intracheal thyrotropin-releasing hormone in refractory depressed patients. Archives of General Psychiatry, 54, 214-221.
Metalsky, G. I., Abramson, L. Y., Seligman, M. E. P., Semmel, A., & Peterson, C. R. (1982). Attributional styles and life events in the classroom: Vulnerability and invulnerability to depressive mood reactions. Journal of Personality and Social Psychology, 43, 621-617.
Metalsky, G. I., Joiner, T. E., Hardin, T. S., & Abramson, L. Y. (1993). Depressive reactions to failure in a naturalistic setting: A test of the hopelessness and self-esteem theory of depression. Journal of Abnormal Psychology, 102, 101-109.
Monroe, S. M., & Simons, A. D. (1991). Diathesis-stress theories in the context of life stress research: Implications for depressive disorder. Psychological Bulletin, 110, 406-425.
Nemeroff, C. B. (1998). The neurobiology of depression. Scientific American, 42-49. http://www.sciam.com/1998/0698issue/0698nemeroff.html
Plomin, R., De Fries, J., McClearn, G. E., & Rutter, M. (1997). Behavioral genetics (3rd ed.). New York: W. M. Freeman.
Ray, A. (1985). Early parental separation and adult depression. Archives of General Psychiatry, 42, 987-991.
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Siegal, L. M., & Kuykendall, D. H. (1990). Loss, widowhood, and psychological distress among the elderly. Journal of Consulting and Clinical Psychology, 58, 519-524.
Turkington, C., & Kaplan, E. (1997). Causes of depression. http://health.excite.com/topics_content/dmk/dmk_article_5963103
Zamar, A. C. (1999). Neurotransmitters
and depression. http://www.depression.org.uk/usad/depression/depressionneur.html
Concordance Rates for Unipolar Major Depression in Monozygotic and Dizygotic
Twins
| Study |
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| Allen |
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| Bertelsen, Harvald, & Hauge |
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| Kendler, Neale, Kessler, Heath, & Eaves |
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| McGuffin, Katz, & Rutherford |
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| Torgerson |
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Adopted from Plomin et al. (1997).
Drugs That May Cause Depression
| Analgestics and anti-inflamatory drugs | Antibiotics and antifungials | Antihypertensives and cardiac drugs | Antineoplastics | Neurological and psychiatric drugs | Steroids and hormones | Miscellaneous |
| Ibuprofen | Amplicillin | Alphamethyldopa | C-Asparaginase | Amantadine | Corticosteroids | Acetazolamide |
| Indomethacin | Cycloserine | Bethadine | Azathioprine | Antypsychotics | Danazol | Choline |
| Opiates | Ethinoamide | Beta-Blockers | 6-Azauridine | Baclofen | Oral contraceptives | Cimetidine |
| Phenacetin | Griseofulvin | Clonidine | Bleomycin | Bromocriptine | Prednisone | Cyproheptadine |
| Metronidazole | Digitalis | Trimethprim | Carbamazepine | Triamcinolone | Diphenoxylate | |
| Nalidix acid | Guanabenzacetate | Vincristine | Levodopa | Disulfiram | ||
| Nitrofurantoin | Guanethidine | Phenytoin | Methysergide | |||
| Streptomyclin | Hydralzine | Sedatives | Stimulants | |||
| Sulfametethoxazole | Lidocaine | |||||
| Sulfonamides | Prazosin | |||||
| Tetracycline | Procainamide | |||||
| Rescinnamine | ||||||
| Reseprine | ||||||
| Veratrum |
ITP Mood Disorders Answers. http://www.med.nyu.edu/Psych/ITPNYU/itp.moodA24Tab.html
Correlations of Attributional Style Subscales for Negative Outcomes
and Standardized Residual Changes in Multiple Affect Adjective Chacklist
Depression
| High grade students (n = 28) | Low grade students (n = 53) | |||
| r | p | r | p | |
| Attributional subscale | ||||
| Internality | .12 | ns | .34 | .01 |
| Stability | .36 | .06 | .04 | ns |
| Globality | .22 | ns | .32 | .05 |
Metalsky, Abramson, Seligman, Semmel, and Peterson (1982).
Means and Standard Deviations of Major Variables and Correlations With
Depressive Affect, BDI Depresson, Number of Weeks Out of Work, and Number
of Unsuccessful Job Applications
|
|
|
|
|
|
|
|
|
| Expectation of success | |||||||
| Initial confidence |
|
|
|
-.12 | -.17 | -.08 | .08 |
| Present confidence |
|
|
|
-.07 | -.08 | -.03 | .04 |
| Employment importance |
|
|
|
.44*** | .19 | -.02 | .17 |
| Perceived uncontrollability |
|
|
|
-.12 | .31*** | .23* | .01 |
| Attribution measures | |||||||
| Internal causes |
|
|
|
.05 | .28** | .32*** | .20* |
| External causes |
|
|
|
.19* | .03 | .12 | -.07 |
| Self-esteem score |
|
|
|
-.13 | -.46*** | -.12 | -.11 |
| Depressive affect |
|
|
|
.13 | -.05 | -.01 | |
| BDI depression |
|
|
|
.13 | .11 | .26* |
Feather and Barber (1983).
Studies Comparing the Relationship of Job Loss to Depression in Men
and Women
| Cross-sectional studies | |||||
| Study | Sample | Employment Measure | Depression Measure | Findings | |
| Warren (1980) | Community sample of 348 men, 361women in Detroit area. Response rate not given. | Unemployed = laid off.Compared to employed workers and housewives. | Checklist of psychosomatic and depressive symptoms. | All women reported more stress than men. Unemployed women had higher symptom levels than both employed women and housewives. No differences among men. | |
| Oliver & Pomicter (1981) | 145 ssembly-line workers in St. Louis, predominantly men. 9 % response rate. | Unemployed = layed off during prior year. Compaired laid-off, reemployed, and continuously employed groups. | Beck Depression Inventory. | Unemployed workers were more depressed than reemployed workers; no gender differences | |
| Shamir (1985) | 191 men, 240 women aged 27-47, college graduates, registered woth Israeli national employment office. 39% response rate. | Unemployed = jobless and looking for work. Compared currently to reemployed workers. | Depression Adjective Checklist; five-item anxiety scale. | Unemployed workers were more distressed than reemployed workers. Unemployed men were more distressed than reemployed men; unemployed women were more anxious but not more depressed than reemployed women. | |
| Kessler, Turner, & House (1987) | Community sample from 14 census tracts in Michigan. 297 men, 195 women. 81% response rate. | Unemployed = laid off or looking for work or both. Compared to reemployed and always employed workers. | Symptom Checklist-90 anxiety, depression, somatic items. | Unemployed were more distressed regardless of gender. | |
| Perrucci, Targ, Perrucci, & Targ (1987) | 148 men, 180 women from cabinet-making plant in Indiana. Comparison group from roller bearings plant. 48% response rate. | Unemployed = laid off during plant closing. Compared to continously employed workers. | 9-item depression scale. | All unemployed had higher symptom levels. Unemployed women and men were equally depressed. For men, but not for women, job loss was associated with increased symptoms. | |
| Harris, Heller, & Braddock (1988) | 115 men, 333 women employed by a public-sector mental health residential care facility in central Illionois. 46% response rate. | All workers faced job loss. Combined workers still employed with those already layed off or terminated. | Caplan, Cobb, French, Harrison, & Pinneau (1975) scale fro anxiety, depression, and irritation. | Women reported poorer well-being than men, even when demographic and job characteristics were controled. | |
| Prospective studies | |||||
| Study | Sample | Duration of study | Mental Health Measure | Findings | |
| Kasl & Cobb (1979) | 100 married, blue-collar men laid off during closures of one U.S. urban and one rural factory. 70 controls continuously employed at two other factories. 78 % response rate; attrition rate not given. | From 4-7 weeks before to 24 months after factory closures. | Five- to six-item scales for depression, anxiety, anomie, somatic complaints. | Transient elevations in depression, anxiety, somatic complaints during anticipation and immediately followin job loss. Otherwise, no pronaunced mental health effects. | |
| Linn, Sandifer, & Stein (1985) | 30 men laid off or dismissed from jobs. 30 controls matched for age and race. Veterans, aged 30-60, Miami, FL. 92% response rate, attrition rate not given. | Men were seen semianually for 5 years. Data selected from last visit preceding job loss and first visit following job loss. | Hopkins Symptom Checklist Depression, Anxiety and Somatic Complaints subscales. | Groups reported to have similar baseline symptoms levels. Controling for baseline levels, men who lost jobs had elevated depression, anxiety, and somatic symptoms at follow up. |
Dew, Penkower, and Bromet (1991).
Comparisons Between Depressed Patients and Nondepressed Controls on
Social Resources
| Men | Women | |||||
| Item | Patients | Controls | Patients | Controls | Patient-control comparison | % of variance accounted for |
| Number of friends | ||||||
| M | 10.89 | 21.34** | 11.32 | 20.08** | 7.06** | .06 |
| SD | 16.64 | 23.76 | 15.37 | 20.28 | ||
| Number of network contacts | ||||||
| M | 12.43 | 18.04** | 14.21 | 17.88** | 4.68** | .03 |
| SD | 13.22 | 17.56 | 12.48 | 12.06 | ||
| Number of close relationships | ||||||
| M | 3.82 | 6.62** | 4.42 | 6.86** | 7.32** | .06 |
| SD | 4.31 | 5.18 | 3.90 | 6.30 | ||
| Quality of significant relationships (0-24 scale) | ||||||
| M | 13.80 | 16.38** | 14.64 | 17.34** | 9.36** | .10 |
| SD | 4.51 | 3.37 | 4.49 | 3.39 | ||
| Family support (1-9 scale) | ||||||
| M | 5.36 | 6.47** | 5.20 | 6.74** | 9.52** | .14 |
| SD | 1.84 | 1.56 | 1.94 | 1.37 | ||
| Work support (1-9 scale) | ||||||
| M | 5.00 | 6.02** | 5.61 | 6.06** | 3.70** | .03 |
| SD | 2.25 | 2.20 | 2.12 | 1.82 |
Billings, Cronkite, and Moss (1983).
Figure 1. Neurotransmitter action at neuronal synapse.
Schraudolph and Cummins.
http://www.idsia.ch/NNcourse/brain.html
Figure 2. PET scan of a depressed patient's
brain before and after recovery.
George (1993). http://www.nimh.nih.gov/hotsci/scandep.htm
Figure 3. Mean log-transformed alpha (8-13
Hz) power for Cz-referenced electroencephalograms (averaged across eyes-open
and eyes-closed baselines), split by group and hemisphere, for the midfrontal
region. (Decreases in alpha power are indicative of increased activation.
Henrique and Davidson (1991).
Figure 4. Mean log-transformed alpha (8-13
Hz) power for average-referenced electroencephalograms (across eyes-open
and eyes-closed baselines), split by group and hemisphere, for midfrontal
region.
Henriques and Davidson (1991).
Figure 5. The percentages of depressed and
nondepressed subjects who lost mother and father before age of 17.
Ray (1985).
Figure 6. The percentages of depressed and
nondepressed subjects who lost mother and father before age of 11.
Ray (1985).
Ntional Institute of Mental Health: Depression research. http://www.nimh.nih.gov/publicat/depressionmenu.cfm
Causes (etiology) of mood disorders. http://www.psycom.net/depression.central.etiology.html
Caues of depression. http:/www.allaboutdepression.com/cau_01.html
28/11/2000
Bishop's University; PCS 212A: Computers and Databases in Psychology
Maja Dumisic, maja_dum@hotmail.com
