With
regard to the causes that lead to depression, today there are basically two
opposing currents of thought, one that gives more emphasis to biological
causes, the other which gives greater importance to psychological causes. For
example:
·
Genetic
factors. 70% of monozygotic and dizygotic twins show in
conjunction depressive disorder.[1]
Although this figure is used as proof of the genetic origin of depression, the
fact that over 70% of these depressed children have a parent with a major
depression has been used to support the opposite hypothesis, namely that the
environmental may increase the likelihood of developing a depressive disorder.[2],[3]
However, some studies report that children of depressed biological parents,
raised in adoptive families with no depressed parents, have a incidence of
depression 8 times higher than normal. This data is used to support the genetic
origin of depression. But even in this case alternative explanations can be
used, such as the fact that adoption still involves a load of emotional stress,
which may be the real cause behind the onset of depressive disorders.
·
Biological
factors. In the 50s it was found that reserpine, a drug
used to control blood pressure, leads to the onset of depression in 20% of
patients[4]
whereas isoniazid, a drug used to treat tuberculosis, reduces the symptoms of
depression. Both of these drugs regulate the levels of monoamine
neurotransmitters: serotonin and norepinephrine. Resperpine decreases, whereas
isoniazid enhances them. These observations gave birth to the monoamine
hypothesis, according to which depression is caused by an imbalance of these
neurotransmitters. However, it has never been possible to diagnose depression
on the basis of laboratory measurements of these neurotransmitters and this casts
doubt on the hypothesis of a biological cause of depression. Other
neurobiological factors play a role in depression, such as the
hypothalamus-pituitary-adrenal axis, which connects the limbic structures,
hypothalamus, and pituitary, the adrenal gland, and regulates long-term
response to stress, inducing the release of adrenal glucocorticoid hormones and
cortisol. In depressed patients there is a hyperactivity of the
hypothalamic-pituitary-adrenal axis and, consequently, high doses of cortisol
in the blood. High levels of cortisol cause harmful effects throughout the
body, including: insomnia, decreased appetite, diabetes mellitus, osteoporosis,
decreased sexual interest, increased expression of anxiety behavior,
immunosuppression, damage to cerebral vessels and heart disorders. Stressful
events, especially if prolonged, can reduce the rate of some neurotransmitters
such as serotonin and noradrenaline and the hyperactivity of the
hypothalamic-pituitary-adrenal axis with consequent increase of cortisol in the
blood. This is evident in depressed adults, while in children this association
has not been confirmed. Further studies have also revealed a metabolic
impairment that includes the orbitofrontal cortex, paralimbic cortex, the
anterior cingulate gyrus and the anterior temporal cortex, basal ganglia,
amygdala and thalamus. The use of neuroimaging techniques has also revealed a
reduction in the size of the frontal lobes and temporal lobes and has shown not
only changes in neurochemical systems, but also the in the neuroanatomical
structure of the person.
·
Environmental
factors. Several studies have shown a strong correlation
between depression in adulthood and negative life experiences. Depression
arises for example after bereavement, a great sorrow, the departure of a loved
one, but even after a big win. In general, any major change can trigger
depression. It has also been noted that sexual abuse and neglect in childhood
are factors strongly correlated with depression in adulthood.[5]
·
Psychological
factors, such as:
cognitive behavioral approaches emphasize that depression is usually
related to stressful events and that coping, i.e. the ability to accept and
deal with stressful situations and their meaning, may therefore play an
important role in the prevention and treatment of depression; psychoanalysis attributes the cause of
depression to traumatic emotional experiences or to a persecutory superego; the
psychoanalyst René Árpád Spitz points
to the occurrence of depression in orphans who were hospitalized at an early
age. When the hospitalization was protracted, children acquired a more
pronounced form of depression.
The Vital Needs Theory - page 28
[1] Galeazzi A (2004) e
Meazzini P, Mente e comportamento.
Trattato italiano di psicoterapia cognitivo-comportamentale, pag. 281.
[2] Wickramaratne PJ (1998) e
Weissman MM, Onset of psychopathology in
offspring by development phase and parental depression, Journal of the
American Academy of Child and Adolescent Psychiatry, 1998, 37: 933-942.
[3] Rice F (2002), Harold G e
Thapar A, The genetic aetiology of
childhood depression, Journal of Child Psychology and Psychiatry, Jan 2002,
43: 65-79.
[4] Bear MF (2002),
Connors BW e Paradiso MA, Neuoroscienze
esplorando il cervello, Masson, 2002.
[5] Guidetti V (2005), Fondamenti di neuropsichiatrica dell’infanzia
e dell’adolescenza, Il Mulino, 2005.