A Prehistory of the Diathesis-Stress Model: Predisposing and Exciting Causes of Insanity in the 19th Century

On October 18, 1866, a 31-year-old Henry Maudsley (1835–1918), a dominant figure in late 19th-century British psychiatry (1, chapter 8), began his address to the Harveian Society of London, “On Some of the Causes of Insanity” (2), as follows:

The diathesis-stress model, an influential conceptualization of psychiatric illness over recent generations (3–5), postulates that etiologic factors underlying psychiatric illness can be divided into those that are present from an early age and are temporally stable in their effect (diathesis) and those that are temporally discrete, occurring close in time to disorder onset (stress).

Reviews of this model trace its origins to Paul Meehl, Manfred Bleuler, and David Rosenthal in the 1960s (6–8), although earlier conceptual antecedents are sometimes noted (4, 5). I could find no review of the prehistory of this theory, to which Maudsley’s lecture is our entry point, articulating as it does what I call the “predisposition-excitation framework” (PEF) for the etiology of insanity. In the 19th century, the theory that disease could be understood as arising from predisposing and exciting causes was widespread and was applied, for example, to hereditary disorders (9), public health (10), infectious diseases (11), cancer (12), gout (13), and epilepsy (14).

I reviewed 25 representative psychiatric textbooks and one dictionary, all published in or translated into English between 1800 and 1910 (Table 1). Of those, seven (27%) had no section that systematically reviewed the causes of insanity. Of the remaining 19, 17 (89%) described the PEF. I review 10 of them here in an effort to illustrate the range of views on the PEF. Additional quotations from these authors are provided in Table 2. Among the 10 reviewed texts, seven provided lists of predisposing and exciting causes, and these are summarized in Table 3. Below, before the main history covering the 10 reviewed texts is presented, a prequel includes two earlier texts that anticipate the PEF. The remaining seven texts that address the PEF are summarized through quotations in Table 4.

Prequel

Burton (1621)

In the first edition of The Anatomy of Melancholy, Oxford don Robert Burton (1577–1640), in his section “Melancholy in Disposition,” discusses how individuals react to “melancholy provocations”:

In the 1620s, Burton, a depression sufferer, captured key features of the diathesis-stress model. Stressors reflected “melancholy provocations,” and the diathesis was captured by a range of terms: humor, temperature, rational soul, and carriage.

Louis (1749)

Among the precursors to the PEF were attempts to understand human heredity in the 18th century, illustrated by a 1749 essay by Antoine Louis (1723–1792) (17, 18). Louis was critical of the deterministic hereditary theories then popular (see quotation in Table 2), noting both the great variation in “the temperament of children born from the same father and from the same mother” (17, p. 308) and that parents commonly can receive a disease “from their ancestors and transmit it to their posterity without having themselves ever been attacked by the disease” (17, p. 315). As summarized by López-Beltrán, Louis concluded that it is not “the disease itself which is transmitted to children but rather a disposition to the disease … [which] will only take effect with the concurrence of external causes” (17, p. 315). While aware of the tendency for children to inherit the traits and diseases of their parents, before the 18th century, physicians noted several irregularities in this process, including differences between siblings and disorders skipping generations. They concluded that diseases were not themselves hereditary, but rather their predisposition, which fully emerged only in the setting of “exciting” causes.

Main History

Prichard (1837)

In the first of two texts, published a year apart in England and France, James Cowles Prichard (1786–1848) began his section “Of the Causes of Insanity” as follows:

He describes six “predisposing causes of insanity” and then the “moral” (or psychological) and physical “productive” (i.e., exciting) causes of insanity.

Prichard’s predisposing causes include stable traits (constitutional predisposition, temperament), demographic characteristics (age, sex), prior disorders, and education (Table 3). His moral productive causes are largely emotional in nature (care, anxiety, apprehensions), and the physical productive causes include substances of abuse, head injury, sexual excesses, and biomedical problems.

Prichard describes how predisposing and exciting causes interrelate:

He illustrates this process in the reaction of different individuals to excess alcohol consumption (quotation in Table 2).

Esquirol (1838/1845)

In his section “Causes of Insanity,” Jean-Étienne Esquirol (1772–1840), a dominant figure in early 19th-century French psychiatry (20), writes: “The causes of mental alienation are as numerous, as its forms are varied.” He lists several possible typologies, including “physical or moral” and “predisposing or exciting” (21, p. 30). He then enumerates a range of causes that are predisposing, including sex, temperament, and character, but then adds that insanity is “also produced by causes, whose influence is more immediate, and easily appreciated,” that is, exciting causes (21, p. 30).

Bucknill and Tuke (1858)

The 1858 textbook of John Charles Bucknill (1817–1897) and Daniel Hack Tuke (1827–1895) (1, chapter 7) was among the most influential in mid-19th-century Britain. Their section “Of the Causes of Insanity” begins: “The Causes of Insanity may be either predisposing or exciting” (22, p. 240). They then list specific predisposing causes and both moral and physical exciting causes (Table 3):

Addressing a question of interest to modern diathesis-stress researchers, they were aware of how these causes might interact:

Griesinger (1861/1867)

Wilhelm Griesinger (1817–1868) was the most influential psychiatrist in mid-19th-century Germany, holding the first university chair and aggressively arguing that psychiatric illness should be considered a brain disease (23). In the second edition of his textbook (24, 25), he writes in his chapter “The Causes of Insanity”:

He outlines how these two kinds of causes interact developmentally (Table 2, quotation 1) and provides a “worked example” of the multiple kinds of causes in alcoholism (Table 2, quotation 2). He illustrates the role of predisposing and exciting causes:Given his biological orientation, he sees predisposing causes as having a dominant role:But, as evidence of his pluralistic outlook, he gives psychological factors their due:

His list of predisposing and exciting causes (Table 3) resembles that of other authors, with an expanded set of physical exciting causes.

Hammond (1883)

William A. Hammond (1828–1900) was a colorful late 19th-century American alienist who was the Surgeon General of the United States Army during the Civil War and later developed a largely outpatient neuropsychiatric practice in New York City (26). In his Treatise on Insanity in Its Medical Relations (27), his overview chapter “Causes of Insanity,” opens:

His specific list of predisposing causes (Table 3) resembles those of earlier writers. He then describes “exciting causes,” writing that they “are those which stand to the disease as its immediate producers. They are very numerous.…” (27, p. 654). His list of physical exciting causes is even longer than that of Griesinger, adding drug exposures and environmental toxins (Table 3).

Tuke (1892)

In the Dictionary of Psychological Medicine (28), the editor, Daniel Hack Tuke, wrote the article “Statistics of Insanity,” a section of which was entitled “Causation.” He notes that the U.K. “Lunacy Commissioners” adopted an official classification of the causes of insanity and collected data on these causes in 136,478 admissions from a wide range of asylums between 1878 and 1887. The proposed typology divided the causes into moral and psychological types (with six specific moral and 22 physical causes listed), with each listed as predisposing or exciting. So, for a decade in the late 19th century in the United Kingdom, the PEF became official. Here are Tuke’s comments, which indicate a considerable sensitivity to the problem of distinguishing between types of causes:

Kellogg (1897)

Theodore H. Kellogg (1841–1931), superintendent of Willard State Hospital, wrote a section on “The etiology of insanity” in his Textbook on Mental Diseases (29) which began:

Kellogg’s definition of predisposing causes was straightforward: “those conditions, internal or external, which favor, without actually causing, the development of Insanity” (29, p. 69). He defined exciting causes as “those which form not the favoring tendency, but the immediate occasion of the attack” (29, p. 92). Sometimes, he comments, the same factor can be both predisposing and exciting causes: “[I]ntemperance may cause general ill health or special disease of nervous centers and strongly predispose to Insanity, or it may excite an outbreak of alcoholic mania” (29, p. 92).

His descriptions of specific psychical causes are detailed. He gives this specific example of “the cumulative action of psychical causes”:

And this of “constant daily repetition of lesser moral shocks”:Otherwise, his list of predisposing and exciting causes resembles those of other authors (Table 3).

Krafft-Ebing (1903/1904)

Richard von Krafft-Ebing (1840–1902), from Vienna, authored the most widely read psychiatric textbook in the German-speaking world in the 1870s and 1880s (30, 31). In his last edition, translated into English in 1904, he wrote in “Causes of Insanity”:

Krafft-Ebing suggests that predisposing causes can lead to exciting causes, which can precipitate illness. Being of an organic bent, Krafft-Ebing viewed predisposing causes as most important: “In general, experience teaches that predisposing influences are of much greater importance than accidental causes, and are of themselves sufficient to induce insanity” (31, p. 138). In particular, he emphasized heredity as the most important predisposing cause: “By far the most important cause of insanity is transmissibility of psychopathic dispositions or cerebral infirmities by way of heredity” (31, p. 157). However, he also suggested that in the setting of strong emotions, particularly if chronic, as in “household trouble,”

His specific list of predisposing and accessory/exciting causes is typical, with an extensive set of physical exciting causes. In discussing the psychic causes, he gives emphasis to depressive emotions and comments on the sex differences in the exciting emotional causes of insanity (Table 2).

De Fursac (1903/1905)

In his Manual of Psychiatry (32, 33), after introducing the complexity of the causal pathway to insanity, the French psychiatrist Joseph Rogues De Fursac (1872–1942) began his section “Etiology” with predisposing causes:

He divides predisposing causes into those that are “exerted upon communities and not individuals” and those that affect individuals directly. He emphasizes, as a key individual predisposition to insanity degeneration, a popular concept in late 19th-century France (34, 35). He introduces exciting causes:De Fursac then notes that, unlike predisposing causes, exciting causes may be preventable:He then provides a theoretical example of such effects (Table 2). Aside from his reference to degeneration, his list of predisposing and exciting causes is typical.

Maudsley (1895)

I now return to the writings of Maudsley, later in his life when he had become a committed materialist preferring physiological to psychological explanations (1, p. 235). Nonetheless, he explored implications of the question posed by Burton more than two centuries earlier:

He points out the specificity between each individual’s psychological constitution and their susceptibility to particular exciting causes:

He then notes how much predisposition can be affected by rearing and education:

Other Texts Adopting the PEF

Readers interested in further descriptions of the PEF, including comments from Benjamin Rush, may wish to review selected quotations from each of the seven unreviewed textbooks in Table 4.

Discussion

From this rich selection of texts, 13 conclusions are noteworthy. First, over a long stretch of psychiatric history, which contained disagreements about psychiatric nosology, the appropriate role of physical restraints, purging and bleeding, and the best form of asylum care, a surprising degree of consensus was seen on the value of the PEF.

Second, for modern theorists, diatheses are, by definition, “internal” to the organism and stressors “external” (5). That viewpoint was not adopted by most PEF advocates. Exciting causes were often somatic diseases, or physiological states like pregnancy or substance abuse, making this category broader than the stressful life events emphasized in most recent diathesis-stress models (4). Furthermore, predisposing causes extended beyond classical “internal” factors such as genes or temperament. Climate, education, occupation, and marital status were often listed as important predispositions to insanity.

Third, exciting causes in the PEF often include “symptoms” such as anxiety, which may conflate the causes of “insanity” with its prodromal symptoms. This has been an important methodological issue in modern stress research (37, 38).

Fourth, a conceptual debate in contemporary diathesis-stress models is whether the two causes need to be independent (4). Krafft-Ebing addresses this for the PEF, noting that predispositions can lead to “affects, passions, and perverse manner of life,” which can constitute exciting causes, a process termed “stress generation” in the modern literature (39).

Fifth, the time scale of stressors is debated in diathesis-stress models (4). While most authors assume acute effects, Kellogg (29) notes longer time intervals where “constant daily repetition of lesser moral shocks” can precipitate insanity. This perspective parallels modern researchers moving beyond acute events to include chronic stressors (38) and “daily hassles” (40).

Sixth, Maudsley anticipates modern diathesis-stress models that emphasize onsets arising from a diathesis-stressor match (5) when he notes “special susceptibilities where a moral cause will strike it with most effect.” His observations address another concern in modern theories, namely, whether predisposing and exciting causes add or interact in their risk impact (4).

Seventh, De Fursac noted a practical consequence of the PEF: exciting causes are easier to prevent than predispositions. Maudsley’s thought experiment of the individual “transplanted early into new and different social conditions” anticipates ideas of primary prevention.

Eighth, a threshold effect for stressors, postulated in some diathesis-stress models, is invoked by Kellogg. In “the cumulative action of psychical causes,” he reports that some individuals can endure substantial “loss of fortune” but with repeated adversities, their threshold is reached and insanity occurs.

Ninth, while differentiating predisposing and exciting causes is sometimes easily done (i.e., Tuke), the distinction in certain cases can be quite difficult (i.e., Kellogg). Several authors agree with De Fursac in suggesting the utility of the PEF from a “didactic standpoint.”

Tenth, in the United Kingdom, PEF achieved “official status” with the Commissioners of Insanity requiring its coding on cases admitted to asylums under their jurisdiction, as did California State Hospitals and St. Elizabeths Hospital. Table 5 provides predisposing and exciting causes of insanity from commitment forms for 15 patients admitted to Mendocino State Hospital in California between March 14 and April 29, 1909.

Eleventh, did the PEF evolve over the 19th century in response to the dramatic advances in medical knowledge, such as the microbial revolution (41)? Surprisingly, the texts suggested no major changes, although increasing conceptual sophistication was seen, for example, in Kellogg and the later writings of Maudsley.

Twelfth, what explains the PEF’s popularity over place and time? Answers to this question can enlighten us about the course of our own more recent history. The PEF is multicausal, developmental, and pluralistic, with intuitive, commonsense appeal. This contrasts with the two leading monocausal theories of 20th-century American psychiatry: psychoanalysis and biological psychiatry. In the place of the ideological struggle characterizing American psychiatry then, pitting social, psychological, and biological explanations against each other, each suggesting that they had the only “real” explanation for psychiatric illness, the PEF accepted the complementarity of these diverse perspectives.

Finally, while the PEF was popular during the 19th century, it was not the only etiologic framework available. Esquirol mentioned dividing the causes of insanity into those that are “physical” and “moral” (42, p. 30). Emil Kraepelin, in his section “The Causes of Insanity,” noted that it was “necessary to distinguish between the two great groups of causes, i.e., external and internal ones” (43, p. 9). However, in my review of these texts, the PEF was the most frequently mentioned etiologic framework.

The PEF was a precursor not only to the diathesis-stress model but also to the biopsychosocial model of George Engel proposed in the 1970s (44), as well as the multiperspectival view of psychiatry developed by Paul McHugh in the 1980s (45). While the PEF was not discussed in philosophical terms in the texts reviewed, its perspective aligned with the integrative pluralism of Sandra D. Mitchell (46, 47) and other philosophers of science and psychiatry in recent decades (48–51). Furthermore, the PEF was nondoctrinaire in nature, appealing to psychiatrists of varying theoretical perspectives. In particular, it was advocated for by Griesinger, who, with his strong support for a neuropathological focus for psychiatric research, set the research agenda for academic psychiatry in the German-speaking world for much of the rest of the 19th century (52), and by Krafft-Ebing, well known for his emphasis on the organically oriented degeneration theory (53). Finally, the PEF was not so bland as to be devoid of interesting predictions, and it provided support for both advocates of hereditary-constitutional and environmental etiologic approaches to insanity. An attraction of the PEF noted by many authors is its ability to explain why various individuals exposed to the same objective stressor react in strikingly different ways.

The spirit of the PEF is well reflected in these modest words about the etiology of schizophrenia from Manfred Bleuler, one of the founders of the modern diathesis-stress model (4):

Conclusions

The modern diathesis-stress model of psychiatric illness has a long, rich prehistory. A majority of psychiatric textbooks from 1800 to 1910 in Western Europe and North America propounded versions of the PEF, which bears substantial resemblance to the diathesis-stress theories of today as well as other pluralist etiologic models of psychiatric illness. Indeed, the consistency of the PEF over place and time was remarkable. No psychiatric diagnosis, not even mania or melancholia, was as stable over this period (54–56).

Many of the conceptual issues in recent debates on the diathesis-stress theory were anticipated by these earlier writings, including the appropriate time scale for exciting stressors, the independence of stress and diathesis, the additive or interactive nature of their relationship, and the importance of “matching” predispositions and stressors.

While its widespread use and durability could result from many factors, including its popularity in general medicine, its content also likely played a role. The PEF proposed a nuanced, developmental, and pluralistic view of the etiologic pathways to psychiatric illness antithetical to the monocausal schools of psychoanalysis and biological psychiatry that dominated U.S. psychiatry for much of the 20th century. While not rigorous by current research standards, the PEF was commonsensical rather than ideological. It presented an intuitively reasonable and clinically validated model that, while sometimes difficult to apply to any specific patient, provided a constructive framework for generations of our predecessors. The PEF helped them conceptualize the various pathways to illness in the diversity of the patients for whom they were trying to care.