From The Aesthestics of Disengagement: Cotemparary Art and Depression Christine Ross


In the last three decades or so, pyschopharmacology has made hypothetical suggestions as to what might be the underlying biological cause of depression (for example, serotonin imbalance) following the presumption that a disease is modeled on the medication that treats it. Hence, for instance, when a medication is said to elevate serration (a mono-amine neurotransmitter present in the mammalian brain), it is presumed that patients helped by that medication must have seratonion defiency. Tricylic antidepressents such as iipramines, for example, were found to block the synaptic reuptake of monoamines into the presynaptic neurons. Based on this drug effect, Joseph J Schidkraut postualted in 1965 that depression resulted from insuffifencies of the monoamine neuro-transmitters (espeically norepinephrine and serotonion.) Tricylic antidepresseants were made more widely availble as a result. But research in this area is far from conclusive. According to Brian Leonard and David Healey's study on the differential effects of anti-depressents, although it has been accepted for more than thirty years, "that a reative deifict in noadreliane, seratonion and possible dopamine in the limbic (emotional) regions of the brain is primarily responsible for the symptoms of depression, direct evidence "for a primary deficit in such neurotransmitters in depression is limited" (190)

In contrast to the previous belief (in the 1960s and 1970s) that depression was either reactive--triggered by stressful life events and best handled by pyschotherapy--or more rarely endogenous--biological in origin (the result of a spontaenous neurological imbalance or a  genetic predisposition and best treated with pharmacatherapy--the consens today is that this descriptivei dichtomy is not meaningful and that depression should be seen to be both reactive and endogentous. This means that, although one type of depression has biological features, these features are likely to have been triggered by life events and that although another type of depression, ius crealy related to pyschsocial difficulturies, it will often respond to pharmacotherapy. It is clear, however, that depression is a mental illness with corporeal ramifactions. Many symptoms of depression, such as sleep disturbance, weight loss or gain, faituge, lack of energy, and pyschomotor retardation or agitaiton are phyiscal... (184)

The instution of slow time is both endemic and crucial to depressed subjectivity. As Ehrenberg convincingly argues, depression is a "pathology of time (the depressed is without a future) and a pathalogy of motivation (the depressed is without energy, his movement is slowed down, his parole is slow) (150)

In all these (social, interpersonal and sociological) perspectives, disconnection is a state that amplifies or predisposes a personto depression in one way or another. Yet connection does not, by itself protect one from depression and might, in certain circumstances, provoke it. This is one of the main paradoxies of depressive disorders... (127)

James Coyne:
Defentional problems continue to plague the study of depression, and they are not going to be readily resolved. There remains considerable disagreement as to what extent and for what purpose a depressed mood in realtively normal persons can be seen as one end of a continum with the mood disturbance seen in hospitalised pyschatric patients and to what extent the clinical phenomena are distinct and discontinuas with normal sadness and unhappiness. Should we limit the term depression to those people who are most distressed and seeking treatment. And what do we make of the "merely miserable" that we have defined out of the depressed category? If we agree to make a sharp distinction, where is that to be drawn? What of the differences among the depressed persons? The positions on these questions that one t akes have major implicaitons for who one studies and who one treats and how, what data are going to be considered realvent, and how one organizes data...We cannot pretend to resolve those controversies, b ut we can at least identify them. They are striking differences among depressed persons that invite some form of subtyping...However, efforts to derive such subtypes are generally controversial, and any scheme is likely to be more satiscatory for some purposes then others. Confronted with all of this ambiguity and confusion, one must be cautios and not seek more precision than the phenonomena of depression can afford... (67)

Benjamin Leftist Meloncholia.