Etiology is the study of the cause of a disease or abnormal behaviors in a scientific context. Depression is defined as a serious medical condition in which a person feels very sad, hopeless, and unimportant and often is unable to live in a normal way. Depression disorder is not caused by one thing, depression occurs when more than one factors are combined. These factors are grouped into 4 categories and the essay will explained the interaction between biological, psychological, social and cultural factors of the depression.

There is a theory of genetic predisposition is based on the assumption that disorders have a genetic origin. The most fascinated researches under the subject of etiology of depression are the relationship between genes and depression. The mapping of the human genome gives clear explanation how genes influence the formation of depression. According to findings of research based on sex of DZ and MZ twins, depression rates were similar in male and female twins with an average of 39% (Kendler et al., 1999). Historically, the influence of genes on depression has been revealed in researches conducted on twins. Results of the twins studies show that, DZ twins have lower concordance rates than MZ twins for depression disorder. According to family studies show that,
individual with no family is more likely to experience depression than individual with relatives. Direct comparison of genes has become a popular method to demonstrate the link between genes and mood. While the results of twin and family studies cannot explain the effect of learning on the development of depression, DNA is unlikely to be influenced by personal experience. In DNA studies, it is able to compare characteristic of the certain genes that associate with neurotransmitters, which is related to depression disorder. Dikeos and his colleagues (1999), compared the differences of genetic location of D3 dopamine receptor in depressed and control group. According to the research, genotypes bearing alleles associated with D3 polymorphism were found in 50% in the control group and in 75% in the depressive individuals, and these results prove genetic effects of depression (Hersen et al., 2011).

According to data of FMRI, the researches have been conducted on individuals with brain damage and PET showed that, the four brain regions are associated with depression. Amygdala is the one of the region that is responsible for memory of emotional reaction to stimuli. Orbitofrontal cortex is the other region, which is responsible for cognitive processing such as putting logical meaning to the stimuli, and responsible from decision making (what should be done about the stimuli), while dorsolateral prefrontal cortex responsible for social judgment, planning, intentionality and decision making. Finally, last region of the brain associated with depression is anterior cingulate cortex, which is responsible for modulation of emotional responses, error detection anticipation of tasks and motivation (Koenigs et al., 2009). These regions of the brain help individual to manage their emotional reaction to the problem stimuli; if they work well together we are able to manage our problems. Any of these regions in our brain can cause depression as results of brain damage, learned behavior patterns and congenital anomalies. For instance, As a consequence of the damage to the dorsolateral cortex, the individual cannot control the emotional response to the problem
(Koenigs & Grafman, 2009).

According to sources, lack of two neurotransmitters such as serotonin and norepinephrine can be cause of depression. There are antidepressants that regulate the secretion and distribution of norepinephrine and serotonin. These drugs are more effective in producing the neurotransmitters rather than increasing the receptor use. According to sources, any abnormality in neurotransmitters is not always lead to depressed mood (Moore & Bona, 2001). Neuroendocrinology studies provide a clear explanation for biological causes of depression.

The most important research in this area was made between the hypothalamic- pituitary-adrenal axis functioning and age of 40 or older participants (Lopez-Duran, Kovacs, & George, 2012). The most important part of the neuroendocrine system is the hypothalamic- pituitary-adrenal axis, which regulates the bodily process including stress responses. Any abnormalities in thyroid functions can be cases of depression’s symptoms. According to neuroendocrine studies, abnormal baseline level of
prolactin, sharper prolactin and cortisol responses to serotonergic challenges associated with depression. In addition, these abnormalities provide explanation for complete understanding of causation and also help for development of effective drug treatment for depression (Pariante& Lighman, 2008). Researchers have been conducted lot of studies to support social, behavioral and environmental causes of depression. According to a literature review, there are three psychological variables including cognitive attributions, coping skills and learned helplessness, and additionally there is a learning theory related to depression. Individuals with negative expectation and cognitive vulnerabilities are more likely to develop depression when they faced the stress or problem. Thus, individuals with high level of negative expectations about themselves and their environment are
increased developing of depression (Seligman et al., 1984).The ability to cope with our problems is also linked to depression, for instance, individuals who use passive form of copping skills when they faced to problem stimuli more likely to develop depression than individuals with active coping skills. The interaction between cognitive style and coping skills contribute has greater impact on
developing depression. This interaction in learned helplessness is supported by most studies. This theory has been tested on animal models. In the test, unsolved questions were presented to the animal models and the animals met with unpleasant consequences such as electroshock when they attempt to solve the problems. The experiment of Altenor and colleagues showed that group
of rats which were shocked with an unescapable pattern were then unlikely to solve the shock problem through using the lever-press mechanism but the rats which were not given any unescapable pattern of shock were more likely to use the lever-press to solve the electroshock (Altenor, Volpicelli, & Seligman, 1979). The accumulating scientific evidences then underlied the association of depression and learned helplessness. In addition, it was observed that the individuals with high risk of attribution were significantly prone to depression while facing stressful events (Hersen et al., 2011).

On the other hand there is a person’s learning history can also play an important role for developing depression. According to Ferster (1973), depressed people are avoid engaging with the activities. The decreased level of attending activites may result fewer opportunities to learn and eventually fewer fundamental solutions while coping lifetime problems.(contingencies of reinforcement). According to Lewinsohn’s (1974) approach to depression, depression is associated with environmental factors and personal skills of following right routes to have positive reinforcements. Individual who gain positive reinforcements will repeat sort of actions to be positively reinforced again. Individual who is far to this type of behavoir pattern may be predisposed to have depression. According to Jacopson and colleagues’ theory of depression, the withdrawal of individual from surrounding world may disrupt basic everyday routines which may in turn heighten the depressive state and hampers the capability of solving the problems.

According to literatures, stressful life events increase for individual to develop depressive episodes. It has been proven that, individuals who have been under psychosocial stress for a very long time show signs of depression (Hammen et al. 2009). Kendler et al., (2010) found depressive symptoms in people who have face difficulties for more than 6 months or who are under severe stress. Kapci and Cramer (2000) found many depressive symptoms in people who faced often with negative life events that they think they are not able to solve these problems with their abilities. The multiple factors regarding coping skills, attribution of coping skills and negative experiences may influence risk of having depression. Depression is a multifactorial disorder and the specific influence of life events on depression is difficult to clearly differentiate from other parameters (Hersen et al., 2011). Many researchers have compared individuals’ depression symptoms based on their gender and racial-ethnic lines and try to give clear explanation if the symptoms show difference across gender and/or racial-ethnic lines. Some researchers have found differences when they compared the depression symptoms they expected with the symptoms Caucasian population presented (Escalante et
al., 2000; Ryder et al., 2008). According WHO, the symptoms and the treatments of the depression are similar across to cultures. Alexopoulo, (2005) hypothesized that the different rate of depression in ethnic groups associated with the stressful events in the country, such as financial or urban stress. According to Hersen et al., (2011), when depression rates are compared between the
middle class and rich minorities and the middle class and the rich Caucasus, similarities are observed in international rates of depression. Differences in the causes of depression between men and women are still a complex finding. The low rate of men depression was attributed to men’s low level of admiting problems, men’s tendency to overcome stress through substance abuse and increased prevalence of depression in women due to being under higher risk of exposure to sexual abuse and therefore higher level of stressor than men. According to some authors, a universal male to female difference of depression prevalence may be related to hormonal and biological factors (Hersen et al., 2011).

If any conclusion may be draw, depression is a disease that affects your mood, your words, your behavior, and your mental health. According to research have been made, depression disorder is not caused by one thing, depression occurs when more than one factors are combined. The essay was explained the etiology of four main factors including, biological, psychological, social and
cultural and how theses factors interact with each other.

Clinical Psychologist Beyhan Perim Secmen


Alexopoulos, G. S. (2005). Depression in the elderly. The lancet, 365(9475), 1961-1970. Altenor,
A., Volpicelli, J. R., & Seligman, M. E. (1979). Debilitated shock escape is produced by both
short-and long-duration inescapable shock: Learned helplessness vs. learned inactivity. Bulletin of
the Psychonomic Society, 14(5), 337-339.

Dikeos, D. G., Papadimitriou, G. N., Avramopoulos, D., Karadima, G., Daskalopoulou, E.

G., Souery, D., … & Stefanis, C. N. (1999). Association between the dopamine D3 receptor
gene locus (DRD3) and unipolar affective disorder. Psychiatric genetics, 9(4), 189-196.

Escalante, A., del Rincón, I., & Mulrow, C. D. (2000). Symptoms of depression and psychological
distress among Hispanics with rheumatoid arthritis. Arthritis Care & Research, 13(3), 156-167.

Ferster, C. (1973). A functional analysis of depression. American psychologist, 28(10), 857.

Hammen, C. (2009). Adolescent depression stressful interpersonal contexts and risk for recurrence.
Current Directions in Psychological Science, 18(4), 200-204.

Hersen, M., Turner, S. M., & Beidel, D. C. (Eds.). (2011). Adult psychopathology and diagnosis.
John Wiley & Sons.

Kapçi, E. G., & Cramer, D. (2000). The mediation component of the hopelessness depression in
relation to negative life events. Counselling Psychology Quarterly, 13(4), 413-423.

Kendler, K. S., Karkowski, L. M., & Prescott, C. A. (1999). Causal relationship between stressful
life events and the onset of major depression. American Journal of Psychiatry.

Kendler, K. S., Kessler, R. C., Walters, E. E., MacLean, C., Neale, M. C., Heath, A. C., & Eaves,
L. J. (2010). Stressful life events, genetic liability, and onset of an episode of major depression
in women. Focus, 8(3), 459-470.

Koenigs, M., & Grafman, J. (2009). The functional neuroanatomy of depression: distinct roles for
ventromedial and dorsolateral prefrontal cortex. Behavioural brain research, 201(2), 239-243.

Lopez‐Duran, N. L., Nusslock, R., George, C., & Kovacs, M. (2012). Frontal EEG asymmetry moderates
the effects of stressful life events on internalizing symptoms in children at familial risk for
depression. Psychophysiology, 49(4), 510-521.

MacPhillamy, D. J., & Lewinsohn, P. M. (1974). Depression as a function of levels of desired and
obtained pleasure. Journal of Abnormal Psychology, 83(6), 651.

Moore, J.D., & Bona, J.R. (2001). Depression and dysthymia. Medical Clinics of North America, 85,

Pariante, C.M., & Lightman, S.L. (2008). The HPA axis in major depression: Classical theories and
new developments. Trends in Neurosciences, 31(9), 464-468.
Peterson, C., & Seligman, M. E. (1984). Causal explanations as a risk factor for depression: theory
and evidence. Psychological review, 91(3), 347.

Ryder, A. G., Yang, J., Zhu, X., Yao, S., Yi, J., Heine, S. J., & Bagby, R. M. (2008). The cultural
shaping of depression: somatic symptoms in China, psychological symptoms in
North America?. Journal of abnormal psychology, 117(2), 300.