Depression is sometimes referred to as the common cold of psy-chopathology. Consistent with this aphorism, epidemiological studies demonstrate that depressive disorders are indeed rather common across the life span. Given the importance of the social relationships and context to understanding depression, it seems likely that culturally informed and diverse research will yield important findings about those critical components of human cognition, emotion, and social relationships that underlie risk for depression, as well as those that serve to aid in recovery from these disorders. Most researchers believe it is unlikely there is a direct effect of hormones on depression, but rather that they indirectly increase risk via any one of several mechanisms, including: the effects of hormones on brain development, the development of secondary gender characteristics that are generated by these hormones, or the hormonal changes that occur during the pubertal transition may interact with life events and the social context.

Depressive disorders are characterized by etiological heterogeneity, which means that many diverse causal factors or causal pathways can lead to the same clinical outcomes. Women are at higher risk for depressive episodes beginning at early adolescence and then throughout the life span. Unipolar depressive disorders can onset at any point in the life span, but are most prevalent in late adolescence through early to mid-adulthood. Bipolar disorder (BD)s generally onset before mid-adulthood; new cases are rare thereafter. More severe cases of unipolar and bipolar disorders are characterized by a chronic/recurrent course. Both unipolar and bipolar disorders are commonly comorbid with other forms of psychopathology; overall severity and poorer outcome over time is associated with comorbidity. If gender differences are of interest, the effects of potential etiological factors are measured in persons of both genders and their associations with depressive disorders are statistically compared across genders.

This chapter provides some questions and answers so that people can see for themselves. Most theories of love predict that, as time goes on, the passion in a relationship will begin to falter. According to the triangular theory of love, passion is the quickest component of a relationship to develop but also the quickest to die down. If they always need the thrill of the early days of a relationship, they may find themselves flitting from one relationship to the next without ever experiencing any deeper satisfaction. A mismatch of stories is not as obvious as disagreement over political beliefs, the desire to have children, or religious affiliation, but it can be just as challenging to a relationship. When people end serious relationships, they often go through a period in which they are just not ready to enter a new relationship.

Modern personality science has made considerable advances in terms of understanding the nature and distribution of core individual differences across people that offer a more nuanced understanding of personality than prescientific models such as the humoral theory. Nonetheless, current models of personality risk for depression share much in common with these ancient notions, including the proposition that personality and temperamental dispositions toward depressive disorders emerge from biological systems, the properties of which can vary across people, creating differences in their basic reactivity to important classes of stimuli. Depressive episodes are not characterized by disinhibition, but other elements of low constraint may be an outcome of depressive behaviors. Personality traits are important correlates of depressive disorders, and a rich tradition and large empirical literature indicate that traits relevant to basic emotional processes may predict risk for these conditions.

The aim of applied research on depressive disorders is to stimulate the development of treatments for these conditions and to evaluate their efficacy. The role of mental health care systems is to facilitate access to these treatments including interventions focused on ameliorating symptoms and preventive approaches intended to forestall their development. Intervention research focuses on testing which interventions are successful at treating various clinical problems in the population. For conditions such as depressive disorders, they are evaluated by the magnitude of change in symptoms and functioning measures among patients who receive the intervention, compared to patients who are exposed to some condition. Treatments for unipolar and bipolar depressive disorders take many forms including psychotherapies and biological interventions such as medicines and electroconvulsive therapy. Among the most studied and best validated psychotherapies for depressive disorders are those that use behavioral and cognitive techniques to target symptoms and maintaining factors in the depressive disorders.

This chapter aims to highlight and clarify the particular ways in which scientific disciplines have approached understanding the variety of experiences people call depression, and to demonstrate how the knowledge generated by science has shed light on their human understanding of depression and resulted in improved identification and treatment of these conditions. Diagnoses of depressive disorders differ from colloquial meanings of the term depression often used to refer to more temporary reactions to those more troubling manifestations of the concept that are the province of psychopathological research. One important difference is that diagnoses fit the concept of a syndrome. A syndrome is a set of signs and symptoms that appear together in time in a coherent pattern. In the case of psychiatric disorders such as depression, symptoms are those problems that can be described by someone experiencing them but that are not readily observable by others, such as thoughts of hopelessness.

The aim of genetic research on depressive disorders is to clarify the distal causal mechanisms that lead to individual differences in risk for developing these conditions. Genetic influences on unipolar depression overlap considerably with those for Generalized Anxiety Disorder (GAD), as well as those for NE. This suggests that genetic influences may drive comorbidity across anxiety and depressive disorders. Bipolar disorder (BD) and schizophrenia have shared genetic influences, as do bipolar and unipolar depressive disorders. The classic animal model of depression derived from studies of dogs exposed to repeated, uncontrollable, inescapable shocks. Animal models hold promise for helping to potentially identify endophenotypes of depression that could be useful targets for neuroscience or genetic approaches in humans. All the major theoretical models of the etiology of depressive disorders invoke mechanisms that are instantiated in biological processes including reactivity to emotionally salient stimuli and stress reactivity.

Stress is a central component of many lay conceptions of the causes of depression. The concept of stress, so ubiquitous and easily understood when used in common language to describe psychological distress and challenge, is actually a rather complex construct to measure and model for scientific study. There are a limited number of research designs that are actually adequate for exploring the role of stress in depressive disorders. A few studies have found that positive events may be related to recovery from depression, specifically positive events that represent an end to chronic stress or ongoing deprivation. Stress generation describes the ways in which individual differences in personality and behavior are intimately tied to the creation of stressful circumstances. Patients who are exposed to an environment characterized by high levels of “expressed emotion” by close others fare the worst over time.

Any theoretical model of depressive disorders must be consistent with people’s broader understanding of human psychology, including the origins and functions of their psychological processes. A number of theorists have offered models of depressive disorders that emphasize the possible adaptive significance to their species of these conditions and related emotions. The purpose of such models is twofold: to provide a conceptualization of depression that is consistent with evolutionary theory, and to describe how the etiology of depression may be understood as involving normal processes of adaptation. If depressive disorders and normal experiences of grief, sadness, and guilt emerge from shared mechanisms, then perhaps depression shares with these normal experiences their adaptive functions as well. Many of the evolutionarily based models generated to explain the existence of depression focus on the interpersonal and social contexts of depression.