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This overview explores the biological level of analysis in depression, focusing on two primary hypotheses: the serotonin and catecholamine theories, as proposed by Joseph Schildkraut in 1965. It discusses how low levels of noradrenaline and the impact of neurotransmitters like serotonin contribute to depressive symptoms. The cortisol hypothesis highlights the hormone's role in stress and depression, showing how high cortisol levels correlate with depressive states. Additionally, genetic factors influencing mood and behavior are addressed, emphasizing the complexity of depression's etiology.
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Biological Level of Analysis In Depression
Catecholamine Hypothesis • Suggested by Joseph Schildkraut in 1965 • Depression is associated with low levels of noradrenaline • Serotonin Hypothesis – depression
Janowsky et al. (1972) • Participants given drug called ‘physostigmine’ • Within minutes, profoundly depressed, self-hate, and suicidal wishes • Mood change artificially, disturbance in neurotransmission? • Drugs increasing noradrenaline reduce depression symptoms
Arguments • Delgano and Moreno (2000) – depression may influence the production of neurotransmitters • Rampello et al. (2000) – MDD patients imbalance of noradrenaline, serotonin, dopamine, acetylcholine – contradicted by Burns (2003) • Lacasse and Leo (2005) – the brain is too complex to consider only one reason behind depression
So far.. • Only one of the theories • Research is less on the neurotransmitter, more on the process as a whole
Cortisol: hormone responsible for the stress system • Belongs to stress hormones called glucocorticoids (plays role in fear and anxiety reactions) • Patients with MDP have high levels of cortisol, indicating possible link
Over-secretion of cortisol may be linked to other neurotransmitters High levels of cortisol may: • lower serotonin receptors • Lowers dopamine levels • Weaken the function of receptors for noradrenaline
Relationship between stress and depression • It cannot be concluded that there is a causational or correlational relationship • However high levels of cortisol are associated with depressive symptoms • Drugs that normalizes cortisol levels help decrease depression symptoms
Effects of Depression Long term depression may lead to structural changes • Decrease of glucorticoid receptors in the hippocampus and prefrontal cortex of suicidal victims • Cushing’s syndrome results in excessive production of cortisol
Genetics • Genetic predisposition/ vulnerability may explain depression Nurnberger and Gershon (1982): • 7 twin studies • Average concordance rate for MZ twins: 65% • DZ twins: 14%
Duenwald (2003): 5-HTT gene: serotonin pathways responsible for controlling mood, emotions, aggression, sleep and anxiety Caspi et al (2003): • Correlation between gene and depression does not indicate causation • Genetic factors moderate responses to environmental factors