Depression and mood disorders


 Depression raises many questions. Why, for example, is it cyclical? It is well known that this psychopathology tends to resolve itself on its own and reoccur after a period of full or partial remission, when it becomes chronic. Drugs, at best, accelerate a remission that occurs in the natural course of the illness. If we exclude dysthymia, the other forms are characterized of severe depression are characterized by an on-off pattern. Depression is either there or it is not. Patients often describe entering or emerging from the “illness” as sudden, sometimes unexpected events. This is a peculiarity of severe depression”.(Ugazio, 2013, p.223).

When other psychopathologies become chronic, they tend to remain over time: the severity of the symptoms fluctuates but the disorder remains.This is not the case with depression. Why?

The enigmatic connection between depression and art raises another question. How come people with a triple negative vision -of themselves, of the world and of the future (according to Beck’s famous definition) – are they able to create important works and among them some of the greatest artistic masterpieces? Why do they often make notable works, not only in the field of art, but also in the economic, professional and business worlds? And why do people with depressive organizations contribute to creating, as now many studies have shown, the negative events that tend to hit them more frequently than in other organizations? Finally, how come people with a great ability to sever ties and with such a keen sense of loneliness as the chronically depressed, break up the couple relationship with so much difficulty? Linares and Campo (2000) stress, and rightly so, that severe depressed patients, as well as bipolar patients, are among the few psychiatric patients to establish a stable and meaningful couple relationship.

Valeria Ugazio answers many of these questions and others in:

Ugazio, V. (2010). L’appartenenza negata[The denied belonging]

Terapia Familiare94, 41-59


Permitted and Forbidden Stories

by Valeria Ugazio

6th chapter (223-260)

New York: Routledge, 2013


One of the thesis put forwards in this book by Ugazio is that the semantic of belonging dominates the conversation in families where severe unipolar and bipolar depressions develop.

“The most important thing for members of these families is to be included as part of the family, as well as being part of the wider community. The reason is that within the same family group there are also those who are excluded, marginalized or rejected. Expulsion from the group, or not belonging to a family, is seen by such people as an irreparable disgrace, whereas the greatest good is to be well-established and respected within the groups to which they belong, including family and community”. (Ugazio,2013 p.228 )

When the semantics of belonging has a long history in a family, extending back over several generations, those who are black sheep, or have been disowned, defrauded or forgotten co-position themselves with individuals who are respected, or worthy of being remembered for their actions, or have simply been included by divine grace among the elect. Illegitimate births, desertions, abandonments are matched with fortunate events such as inheritances, fairytale weddings, professional honors, dazzling careers. Life for some seems to have been harsh, while for others it has been particularly kind. Some members of the family are adored and admired while others are ignored or become the object of aggression and violence.(Ugazio, 2013,p.) As far as we know, this is what happened in Virginia Woolf’s family.

Even if serotonin deficiency were really the cause of the depression, as has been heralded for years by biological psychiatry and by the pharmaceutical industry, the questions to which Ugazio answers, like others that depression raises, would receive no response.


It appears that this is not the case. The available studies do not show that serotonin deficiency has a causal effect on depression

Starting from 2000, the thesis that depression is a brain disease, similar to asthma or diabetes, its alleged staggering growth in the West and the efficacy of serotoninergic drugs have been severely challenged, especially in the United States. The debate developed about depression and the SSRIs has undermined the credibility of psychiatry itself, hypothesizing deep  collusion between psychiatry and Big Pharma. The reasons are not lacking. Our data show that around 25 percent of depressed patients have low levels of serotonin or norepinephrine (Valenstein, 1998; Horwitz and Wakefield, 2007). If the hypothesis of serotonin deficiency were etiopathologically correct, then it would explain only a limited part of cases. But it is not correct, at least etiopathologically. The low levels of serotonin found in these patients may indeed be the consequence rather than the cause of depression. No empirical evidence has shown that chemical imbalance is the cause of depression. Indeed, we know that exactly the opposite happens in apes.

To know more: A.V.Horwitz and J.C. Wakefield (2007) The loss of sadness.  New York: Oxford University Press

The results that had the greatest resonance concern the efficacy of Prozac and other SSRIs and their secondary effects as they emerged from double-blind clinical trials. These are staggering results. Presented as miraculous, these drugs have identical or slightly superior effects to placebo. This data is dubbed the “dirty little secret” because the big Pharma knew it very well.


It seems so, and this is the most worrying fact. The Federal Drug Administration knew this and was silent.

The increase in suicidal behaviour has been shown for children, adolescents and young adults so much so that the Federal Drug Administration recently concluded that: “SSRIs duplicate the risk of suicidal thoughts and behaviors in depressed subjects up to the age of 24 “(Kirsch, 2010, p. 151).


Certainly not as much as it would seem; the alarming data, released in the last twenty years, are generally inflated. The diagnoses and the pharmacological treatments for this disease have increased because the diagnostic criteria have changed. 

The DSM, starting from its third edition in 1980,  introduced criteria so little discriminating and decontextualized for the diagnosis of “major depression” that come together inside this diagnostic category both normally sad people due to negative events, as well as patients suffering from clinical depression. Two and a-half-thousand  years of Western clinical tradition has  been swept away by the last three editions of the DSM. Even the traditional psychiatric distinction between “endogenous” depressions – caused by internal processes, in the absence of negative external events – and “reactive” depressions – triggered by losses and other negative social events – is ignored.

West is not facing an implosion into depression. Serious forms of unipolar and bipolar depression remain infrequent. It is the criteria for diagnosis that have changed: sadness has been transformed into a mental disorder and clinical depression has  equated with the manic-depressive psychosis, now dubbed bipolar disorder.

To know more:

  • Greenberg G. (2010). Manufacturing Depression. The Secret History of a Modern Disease. New York: Simon & Schuster.
  • Healy, D. (2004). Let Them Eat Prozac. New York: New York University Press
  • Horwitz, A.V. e Wakefield J. C. (2007), The Loss of Sadness. How Psychiatry Transformed Normal Sorrow into Depressive Disorder, Oxford University Press, New York.
  • Kirsch I. (2010), Antidepressants: The Emperor’s New Drugs?, Basic Books, New York.
  • Joiner T. E. e Coyne J. C. (a cura di) (1999), The Interactional Nature of Depression, Ame­rican Psychological Association, Washington DC.
  • Linares J. L. (2010), Depressione e distimia: basi relazionali e guide per l’intervento. [Depression and distimia]. Terapia Familiare., vol. 94, 79-94.

  • Loriedo C. e Jedlowski M. (2010), Aspettative totalizzanti e relazioni familiari nella depres­sione [, Ter. Fam., vol. 94, 60-78.
  • Pettit J. W. e Joiner T. E. (2006), Chronic Depression. Interpersonal Sources, Therapeutic Solutions, American Psychological Association, Washington DC.
  • Prince J. e Gardner R. (1999), Sociophysiology of Depression, in Joiner e Coyne (1999).
  • Ugazio, V. (2010). Quello che la serotonina non spiega.[What setotonin does not explain].Terapia Familiare94, 7-20