This chapter explores three ’classic’ studies of creativity and mental illness. The first is Jamison whose focus is on the connection between bipolar disorder and creativity. The second is Andreasen, who used structured interviews to analyze 30 creative writers, 30 matched controls, and first-degree relatives of each group. The writers had a higher rate of mental illness, with a particular tendency toward bipolar and other affective disorders. The third major work is Ludwig, who utilized the historiometric technique. All three studies have come under serious criticism. Many of the studies of Big-C creators are historiometric, akin to Ludwig’s work. Some such studies claim that eminent creators show higher rates of mental illness. A much more common approach is to look at everyday people and give them measures of creativity and mental health. Typically, researchers look at what are called subclinical disorders—in other words, they’re not clinically significant.

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.

The idea of the mad genius persisted all the way to modern times and was even promulgated in scientific circles. Not only was genius mad, but it was associated with criminality and genetic degeneration. The empirical research relevant to the mad-genius issue uses three major methods: the historiometric, the psychometric and the psychiatric. The historical record is replete with putative exemplars of mad genius. The mental illness adopts a more subtle but still pernicious guise-alcoholism. In fact, it sometimes appears that alcoholism is one of the necessities of literary genius. Psychopathology can be found in other forms of genius besides creative genius. Of the available pathologies, depression seems to be the most frequent, along with its correlates of suicide and alcoholism or drug abuse. Family lineages that have higher than average rates of psychopathology will also feature higher than average rates of genius.

Sadness and anxiety are normal human emotions and stress is a normal occurrence in our lives. When we’re feeling somewhat down, anxious or stressed, we can benefit from exercise, relaxation, recreation, eating nutritious foods, allowing time for sleep, and talking to a friend. Clinical depression and anxiety are very common conditions. This chapter looks at what they are, what happens to sleep, and what helps recovery of mood and sleep. It outlines what is known about treating insomnia in three forms of clinical depression: major depression, Seasonal Affective Disorder, and Bipolar Disorder. Research on how people respond to natural disasters has told us that within the first months of disaster, many people develop signs of anxiety, depression and posttraumatic stress. With respect to sleep, people with posttraumatic stress disorder tend to get somewhat less deep sleep, longer periods of being awake during the night, and an overall shorter sleep duration.

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.

This chapter focuses on identifying the primary features that appear to be common across all or several of diagnostic and statistical manual of mental disorders, as well as those that differentiate them from each another; and describing the continuum of severity that can exist within any one of these disorders. Understanding the full spectrum of presentation of depressive disorders is useful for identifying features that may explain variability in functioning and outcome over time across individuals with the same disorder. It may potentially point to targets for understanding the etiology of these conditions. One of the most important distinctions made in psychiatric classification systems and in the scientific literature on depressive disorders is between bipolar disorders (BDs) and the unipolar mood disorders. The idea that manic episodes reflect a unique etiological pathway and have different implications for functioning and outcome compared to unipolar depressive disorders has received considerable empirical support.

Depressive disorders are etiologically heterogeneous. Considerable progress has been made in describing depressive disorders across the life span their impact on behavior and functioning; their relationship to broader psychological systems; and identifying some of the processes within people and their environmental circumstances that may be involved in the etiologies of these disorders. The next decades of research on unipolar and bipolar mood disorders seem likely to focus much more explicitly on making connections across evidence derived from very different lines of research in order to provide more direct evidence for the mechanisms that underlie risk for and expression of depression and mania. Some areas of research on depression will necessarily become increasingly technological and specialized, areas like genomics. The challenge for psychopathologists will be to define the psychological and clinical constructs that are the most promising targets for exploration using these new technologies.