Depression is widely known as the common cold of the mental illnesses. It is also the most common reason for psychiatric assistance and hospitalization. Nevertheless, there is a great deal of heterogeneity within the disease. Indeed, one may speak of numerous “depressions” rather than a homogeneous disease. Theodore Millon, quoting Coyne, says:
“Increasingly, theoretical statements about the nature of depression start with an acknowledgment of its heterogeneity and the complexity and interdependence of it. Yet beyond that, authors tend to lapse into a singular frame of reference that is predictable from their discipline and their indoctrination. The study of depression is thoroughly fragmented and efforts at integration have been few and generally feeble and unsatisfactory. Investigators in genetics, biochemistry, experimental psychopathology, and epidemiology generally do not stay abreast of developments in other fields that have direct bearing on their work.”
There are numerous hypotheses concerning the origins of depression. First, there is the characterological predisposition approach, which is the most popular approach. According to this position, characterological disorders are primary, and depression is a secondary feature of these diseases. Individuals may be predisposed to depression because of self-defeating behaviors, alienation from others and poor coping patterns.
Next, there is the complication hypothesis. This position explains that depression influences personality rather than the other way around. Personality may be altered depending upon the duration of the depression. Sufficiently long-term depression may alter the individual’s personality. Then there is the attenuation hypothesis. From this perspective, personality disorders result from alternative or attenuated expressions of disease processes which constitute the underlying pathways of depression. Thus, for example, cyclothymia might be regarded as an attenuated form of full-blown bipolar disorder. These traits, according to this hypothesis, arise from constitutional factors.
Next, there is the coeffect hypothesis. From this perspective, depression and personality occur alongside each other as a result of a third variable, although each possesses a distinct psychobiological origin. Thus, the two are equi-primordial and neither causes the other. For the modification hypothesis, also known as the pathoplasty approach, it may merely be personality features which influence both how responsive depression is to treatment, as well as how it manifests itself. Depressive symptoms may serve a great deal of important psychological gains, such as obtaining nurturance from others, rationalizing subpar performance, safely expressing anger towards others, and avoiding undesirable responsibilities .
According to the orthogonal hypothesis, personality disorders are totally distinct and separate from personality disorders. The one exhibits a high degree of comorbidity with the other, however, because both result from similar conditions. According to the overlapping symptomatology hypothesis, comorbidity of depression and personality disorders results from the overlapping of criteria used to measure each disorder. Thus, affective abnormalities are seen as resulting from personality disorders, rather than there being a distinct mood disorder occurring alongside a personality disorder. This is particularly true, it is argued, of cluster B personality disorders.
According to the heterogeneity hypothesis, numerous distinct sources contribute to the genesis of both personality disorders and depression. Thus, Theodore Millon states “Various configurations of genetic/constitutional factors in conjunction with environmental variables may combine to produce differing vulnerabilities to expressions o depression or personality pathology. A heterogeneous population arises from these various combinations including a subset of individuals who evidence both symptoms of personality disorder and depression. The heterogeneity hypothesis is most consistent with Millon’s biopsychosocial conceptualization of personality and psychopathology.” So intimately linked is depression with the personality disorders, that a personality-counterpart to the mood disorder was discussed a great deal among the DSM-IV Personality Work Group. Older DSM models spoke of a dysthymic disorder, which was later acknowledged to encompass a great variety of subtypes. Indeed, depressive disorders tended to be seen as affective rather than distinctly social or cognitive in nature. It would fall to Theodore Millon to articulate a variant of depressive disorders that would represent a pervasive, underlying personality pathology.
According to Kahlbaum (1882), and anticipating the modern diagnostic category of bipolar disorder, depression and mania were both two copmonents of one disease. Kraepelin (1896) borrowed from Kahlbaum and distinguished between personality and temperamental variants of cyclothymia. Thus, even very early on in the history of psychiatry, the distinction between a depressive personality vs. a distinctly depressive mood disorder, made itself known. Kraepelin, like his predecessor, believed that “maniacal-depressive insanity” included both periodic and circular abnormal mood states, and considered them to be distinct components of a single disorder. He was convinced that these mood abnormalities occurred independently of environment, and were based overwhelmingly upon the individual’s constitution. Kraepelin began to articulate what would come to be seen as a distinctly depressive personality in the 8th edition of his “Psychiatrie” (1909-1915):
“There are certain temperaments which may be regarded as rudiments of manic-depressive insanity. They may throughout the whole o life exist as peculiar forms of psychic personality, without further development; but they may also become the point of departure for a morbid process which develops under peculiar conditions and runs its course in isolated attacks. Not at all infrequently, moreover, the permanent divergencies are already in themselves so considerable that they also extend into the domain of morbid without the appearance of more severe, delimited attacks.”