Downloaded from 158 &dquo;dysrhythmia&dquo; is the consequence of the disruption of external routines, particularly the social routines that would act as zeitgebers for behavioral and mental rhythms, and the sleep-wake cycle; disordered biological rhythms are in this view the result of abnormal masking influences on what are essentially normally regulated endogenous rhythms. The disorder would be comparable with dysregulations underlying shift-work disturbances. The debate represents one variant of the classical debate in psychiatry between those who emphasize endogenous and exogenous causation. The primary source of the illness is either located internally, that is, in &dquo;the clock,&dquo; or in the environment, that is, in &dquo;the social zeitgebers.&dquo; Both concepts can be reconciled. In the first place, disrupted social routines resulting, for example, in changes in sleep timing might entail changes in light exposure, which then in turn would affect the central pacemaker. In such cases the latter would produce a truly abnormal output. Furthermore, pacemakers may have interand intrapersonal variability in the susceptibility to light and alterations of light schedules.Whatever the cause of the &dquo;dysrhythmia&dquo; (i.e., a primary or a secondary abnormality in the circadian regulation), the existence of it is generally accepted, provided that dysrhythmia is taken as a descriptive term covering a broad variety of abnormalities in form, amplitude, and phase positions of all possible kinds of rhythms. In view of the clinical phenomena, such as diurnal variation of mood and early morning awakening, it is understandable that much attention has been paid to the regulation of the sleep-wake cycle. The attention has grown in light of findings that manipulations of this cycle and exposure to bright light induce considerable changes in disturbed mood. These observations constitute the core arguments underlying chronobiological theories of affective disorders. However, the argumentation is precarious. A number of questionable assumptions are tacitly implied. The first is that the various &dquo;dysrhythmias,&dquo; particularly those concerning the sleep-wake cycle, can be interpreted as products of specifiable anomalies in the regulation of this cycle. The second questionable assumption is that if this were true the clinical effects of the manipulation of sleep-wake cycles or exposure to light are the results of their impact on these regulatory anomalies. The third assumption is that , if the former assumption might be valid, this would prove that the affective disorders are caused by these anomalies. Despite its attractiveness, this reasoning is weak. Even if coherent links between some dysregulation and clinical response to manipulations of sleep-wake cycles or exposure to light would be demonstrated, this would not necessarily imply that this link is causal, nor would it show that affective disorders result from this dysregulation. The latter may still be an epiphenomenon.Nevertheless, in view of the wide dispe...