The Aetiological Turn (The Nineteenth Century)

Abstract

Beginning in the 1830s, medical investigators began to think of organic disorders as having single causes that were both universal and necessary. For this to be possible required a radical shift in the way doctors defined diseases: from symptoms to causes. The so-called aetiological approach to disease meant that every case of the disease had the same cause. This, in turn, meant that any prophylactic or therapeutic measures directed at that cause, which were effective in one case, would be effective in every case. The crux of the matter now shifted to identifying a disease’s causation, beyond dispute. And when it came to pellagra, this was precisely the problem. By the middle of the nineteenth century, all the medical actors involved agreed on the close link between pellagra and maize consumption. What they disagreed on was the exact causal nature of that link, propounding two divergent, indeed mutually exclusive, explanatory models. How the cultural dominance of one explanatory model, at the expense of another, came about; what it tells us about the nature of Italian medical science in the second half of the nineteenth century; and what its dominance meant for sufferers, is the subject of this chapter.

The Aetiological Turn and the Pellagra Epidemic

By the middle of the nineteenth century, all the medical actors involved agreed on the close link between maize and pellagra. What they disagreed on was the exact causal nature of that link, propounding two divergent, indeed mutually exclusive, explanatory models. The fact that one of these, more culturally influential, turned out to be the ‘wrong’ one, and the other, less culturally successful, turned out to be the ‘right’ one, allows us to study a history of ‘stasis, of delay, of digression’, to quote David Wootton, when ‘bad ideas … triumph over good’. Did this result in what Wootton has called ‘bad medicine’: medicine that did far more harm than good? (Wooton 2007, pp. 14, 26). How the cultural dominance of one explanatory model, at the expense of another, came about; what it tells us about the nature of Italian medical science in the last few decades of the nineteenth century; and what its dominance meant for sufferers, is the subject of this chapter.

Italian medical investigators had been debating the nature, causes and treatment of pellagra, which they recognised as a new disease, since the 1760s—as we saw in the previous chapter. At the turn of the century, two of them, Francesco Fanzago and Giambattista Marzari, had become embroiled in a priority dispute over the idea that the disease was at least in part a result of increasing maize consumption by the poor peasants of northern Italy. They were certainly on to something; but this was not their main concern. What they wanted to understand was what sort of illness pellagra was—its nature—and how it could be classified. And understanding its nosology could only be achieved by determining its most prominent signs and symptoms.

In general terms, during the late eighteenth and early nineteenth centuries, understanding disease causation took a secondary place to understanding the nature of a disease. For the medicine of the time, every disease had a lengthy list of causes associated with it. And pellagra was no exception: climate (the burning sun), hard labour, dire poverty, habit (alcholism), heredity and—with Fanzago and Marzari—diet. To impose a sense of order on the existence of multiple causes for every disease, doctors broke them down into different sorts, such as ‘proximate’ and ‘remote’. The latter, in turn, were distinguished into ‘predisposing’ and ‘occasioning’. Doctors would bring to bear this variety of possible causes—combined with a patient’s temperament, sex and age—as variables in understanding, and so treating, individual cases. In the particular case of pellagra, this variety of causes also explained to contemporaries how its effects could vary so widely from patient to patient.

However, beginning in the 1830s, a few European researchers began to think of several different organic disorders as having single causes that were both universal and necessary. For this to be possible required a radical shift in the way doctors defined diseases: from symptoms to causes. The so-called aetiological approach to disease, championed by Ignaz Semmelweis in his explorations of puerperal fever, meant that every case of the disease had the same cause (Codell Carter 1985, pp. 44–60). This, in turn, meant that any prophylactic or therapeutic measures directed at that cause, which were effective in one case, would be effective in every case. The aetiological approach offered a coherent means of explaining a bewildering range of facts and observations about a disease, whilst making the search for prevention and cure more focused. The crux of the matter now shifted to identifying a disease’s causation, beyond dispute. And this was precisely the problem.

Aetiological Arguments

When it came to the study of pellagra, the first to shift the focus to aetiology was the community physician, hospital director and later university lecturer, Filippo Lussana (1820–97). In 1856, Lussana developed his ideas into a book-length study, co-authored with the pathologist Carlo Frua. It begins with a chapter on the aetiology of pellagra, which occupies a full third of the book (Lussana and Frua 1856). If the content here is partly traditional, surveying each of the by-now standard range of causes in turn, it offers a radical departure by singling out a cause which Lussana considered ‘essential’. That is: ‘a dietary regime of insufficient plastic nutritive regeneration’ (Lussana and Frua 1856, p. 124). For Lussana, the deficiency of a maize-based diet was thus the primary cause of pellagra, with all other factors being secondary. It was the key to understanding the disease’s pathogenesis and possible therapeutics, which is discussed in the rest of the book. We thus have a necessary cause, if not yet a single one.

The dispute did not begin until thirteen years later, with the work of Cesare Lombroso—the originator of what I referred to above as the ‘wrong’ theory. If the Veronese doctor Lombroso (1835–1909) is best known today as the originator of criminal anthropology, which brought him international fame—the infamy came later—some of his first published works were on pellagra and he would continue to investigate and write on the subject for the rest of his life—amounting to some 200 publications in all (Baima Bollone 1992; Frigessi 2003). Lombroso first noted a link between the consumption of maize and the spread of pellagra in the Italian region of Lombardy in 1863, whilst he was a lecturer in mental illness at Pavia University and director of the insane ward at the city’s hospital. This first period of research culminated six years later in Lombroso’s monograph on the ‘clinical and experimental study of the nature, cause and therapy of pellagra’ (Lombroso 1869).

Here, Lombroso explicitly espoused the aetiological agenda, in a book intended to identify the factor which, as he puts it, ‘is the exclusive cause of pellagra’. And he found it in ‘spoilt maize covered with penicillium glaucum’. This idea, which is the focus of the book, is not presented as hypothesis but as fact; there is no room for doubt. ‘And so is destroyed, a priori, that doctrine which had pellagra deriving from an insufficient plastic diet’—clearly referring to Lussana’s work (Lombroso 1869, p. 349). Lombroso spent most of the following decades fleshing out what became known as the toxicozeist (or spoilt maize) theory of pellagra causation, with laboratory investigations, to counter Lussana’s use of chemical studies in support of what would later become known as the deficiency theory.

With toxicozeism, Lombroso turned a factor or principle discussed by Lussana as a possible, secondary cause of pellagra—spoilt maize—into the necessary, single cause of the disease. Moreover, it was one for which he (Lombroso) now, triumphantly, took sole credit. If Lombroso tended to see pellagra-like effects of spoilt maize everywhere, and if his experiments with potential toxins worked better in the lab than in real life, this did not stop him from being surprised and dismayed when people did not replicate his findings and agree with his conclusions. This was at a time time when open and direct confrontation was an accepted part of scientific dispute (de Bont 2013). Views had to be defended and opponents swiftly and decisively dealth with.

Opposition to Lombroso came in part from Lussana, who in 1872 responded with another study of pellagra. That Lussana too had embraced the issue of causation was evident from the book’s title, ‘On the causes of pellagra’; but Lussana could not share Lombroso’s conviction that the ‘common mold’ penicillium glaucum underwent a harmful toxic alteration in contact with maize (Lussana 1872). Lussana used this second book to refine his ideas, stressing that maize was not a cereal-based disease, along the lines of ergotism, but the result of a diet deficient in ‘azotates’ (as an idea, a precursor to proteins). He did offer a compromise with Lombroso, in singling out ‘poor quality and spoilt maize’ as particularly low in azotates. But in essence, Lussana’s work was a refutation of Lombroso’s.

In response, Lombroso quickly dashed off a thirty-page ‘polemical letter’ to Lussana (Lombroso 1872). Lombroso argued that the toxin was most harmful when ingested over protracted periods, as Lussana should have known. Not only was Lussana wrong about pellagra’s aetiology; Lombroso more or less claimed the study of its aetiology for himself, since only he had the right idea and the right methodology. Lombroso apologises for his argumentative tone, but there was too much at stake, when on his doctrine ‘depends the wellbeing of thousands of people’. Indeed, as this debate over causation raged throughout the 1870s, reported pellagra cases in Italy climbed to 100,000 cases (MAIC 1879, pp. 324–325).

Lombroso and Lussana differed over the key question of whether maize was a sufficiently nutritional food when consumed by hard-labouring peasants as a staple. In 1878 the director of the insane asylum in Ferrara, Clodomiro Bonfigli (1838–1919), drew on Lussana’s theory and his own experience to argue for the ‘dietary insufficiency’ of maize (Bonfigli 1878). When Bonfigli’s article was republised in La Rivista, Lombroso immediately answered back in the same periodical, which he amplified into book form two years later (Lombroso 1880). Bonfigli replied in turn with a lengthy article in Il Raccoglitore Medico, an important medical periodical which often hosted controversies of this kind. Bonfigli substantiated his findings and directed his fire at Lombroso (Bonfigli 1879).

In particular, Bonfigli was critical of the strichnoid toxin which Lombroso claimed to have isolated two years earlier and promptly baptised ‘pellagrozeine’. Bonfigli accused Lombroso of wanting to establish pellagrozeine as the single cause of pellagra at all costs, even though, as Bonfigli affirmed, peasants refused to eat moldy maize (Bonfigli 1879). The gap between the socially orientated Bonfigli and the laboratory-focused Lombroso could not have been wider. Bonfigli and Lombroso locked horns over everything from the quantities of maize eaten by field hands and the digestibility of maize and its relationship to malnutrition, to the existence of cases of pellagra without maize. As a result, they also differed on preventive and therapeutic measures. For Bonfigli, these came down to resolving ‘the most serious and urgent social question of the pauperism of the rural classes’. Lombroso countered that this would mean ‘a social revolution’; the money Bonfigli proposed spending to improve the diet of the rural poor would be better spent on providing maize-drying ovens so people would not have to eat spoilt maize.

Lussana did not let that get away and returned to the fray with a short article entitled ‘Professor Lombroso’s hallucination’, which cites a range of studies against Lombroso’s toxicozeist theory (Lussana 1883). Lussana refers to Lombroso’s virulent comments against both him and Bonfigli as evidence of Lombroso’s unbalanced mental state, diagnosing him—only partially tongue-in-cheek—as a mattoide. The irony is that mattoide was a term Lombroso himself had coined to label the mad genius: that is, mad on the surface but normal underneath, and so distinguished from what Lombroso labelled the criminally insane. Lussana refers to Lombroso as a ‘poor delusional’ who in his ‘frenzied delirium’ sees the spoilt maize toxin everywhere.

The Nature of Scientific Controversy and Cesare Lombroso’s Success

With the benefit of hindsight, it is all too tempting to side with Lussana and Bonfigli in the debate: not only because their deficiency theory would eventually prove to the ‘right’ one, but because Lombroso appears as the bully of the piece. However, on closer reading of the treatises, articles and short notices, it is not immediately apparent why one theory—Lombroso’s toxicozeist hypothesis—would become the influential one, affecting government policy, whilst the other—the dietary insufficiency hypothesis—was marginalised.

The participants disputed both facts and the interpretation of those facts, according to their differing theoretical positions. A history of science approach can help us here, encouraging us to understand the past on its own terms, by reconstructing the ‘reasonableness’ of the arguments, whilst also allowing us to appreciate the range of factors involved, such as social interests and political struggles (Daston 2009). Even in the most internalist of scientific controversies, broader ‘social’ aspects come to the fore, including issues like academic status and power relations (Brante and Elzinga 1990). In the case of Lombroso and pellagra, we might reduce these aspects to three: media fame, scientific fashion and politico-economic expediency.

Let us begin with fame. By the 1880s, at an international level, Lombroso was Italy’s most read author, hailed as the founder of a new science: criminal anthropology. Lombroso’s was an increasingly loud and powerful voice. He was becoming a very public figure: at once doctor, philosopher, anthropologist, sociologist and political commentator (Forno 2010). (The role of the doctor as public intellectual and media star has resurfaced during the COVID-19 pandemic, in Italy as elsewhere.) Lombroso worked tirelessly to shape public opinion, mobilise intellectuals and organise a ‘school’ of followers able to penetrate the apparatus of the State. As a positivist scientist, he saw himself as the bearer of a mission to educate, inform and influence, especially in the field of public health. And when it came to pellagra’s aetiology, Lombroso unceasingly and bullishly drove his message home, publishing a seemingly endless flow of long and short articles in both scholarly journals and the popular press, book and article reviews, and book prefaces. He combined a populist approach, (over-)simplifying complex scientific ideas, with a narrative and provocative writing style.

In developing his toxicozeist theory of transmission, Lombroso rode the scientific fashion for bacteriology, the success of which was allowing medicine as a profession to regain the prestige it had lost earlier in the century. The bacterial hypothesis forcefully suggested that each disease was caused by a bacterium; determining causation was thus reduced to a matter of identifying the single bacterium concerned. In the five years between 1879 and 1884, the causative organisms for leprosy, typhoid, malaria, diptheria, cholera and tetanus were identified (Shortt 1983). There may have been many germ theories of disease—focusing, variously, on chemical poisons, ferments, degraded cells, fungi, bacteria or parasites—but proponents tended to subsume these into a single theory in order to strengthen their position (Warboys 2000).

We shall explore the link between bacteriology and pellagrology further in the following chapter. Meanwhile, Lombroso was able to document how the consumption of poorly dried and stored maize—itself a widespread reality at the time—was linked to the development of a pellagra-causing toxin. From Lombroso’s new base at the University of Turin (from 1878), he was able to develop a well articulated scientific research programme based on laboratory analysis, the results of which his followers elsewhere in Italy endeavoured to duplicate and build upon. And the science was important, for it allowed Lombroso to be more ‘convincing’ than either Lussana or Bonfigli.

Knowledge of metabolism and foods did not allow the latter two doctors to articulate clearly the precise relationship between maize subsistence and pellagra. Their use of generic expressions like the ‘meagre nutritive physiological value’ of maize did not quite cut it when compared to Lombroso’s well articulated—if ultimately flawed—laboratory methodology (Vanni and Missiroli 1987). At a time when chemical methods and experimental physiology dominated medical research, influenced by figures like (first) Justis von Liebig and (later) Robert Koch, setting up a laboratory for his clinic became a point of honour to the clinician (Büttner 1992). This is evident in Lombroso’s magnum opus on the clinical and pathological science of pellagra, published in 1892. Its 400 pages detail the numerous experiments on live animals, drug trials on living humans and autopsies on dead ones—113 in total—all made possible by the extensive resources Lombroso had at his disposal, in terms of personnel and funding (Lombroso 1892). Lombroso bombarded his readers with detailed tables and illustrations of all sorts, the latter alone covering a range of topics, from the micro-organisms of spoilt maize to the gaits of pellagra victims (Fig. 3.1).

Fig. 3.1

The micro-organisms of spoilt maize. From: Cesare Lombroso, Trattato profilattico e clinico della pellagra, 1892

Expediency also had a part to play in the success of Lombroso’s aetiological model. It suited government, which sought a clearly identifiable enemy and practicable solutions; and it suited the ruling bourgeois and agrarian classes, in identifying pellagra’s origins as ‘hygienic’ (public health) rather than the ordering of society (peasant poverty). From the 1880s, a series of proposed laws fighting pellagra had failed to receive parliamentary assent, because they interfered with the maize-related interests of landowners, millers and traders (De Bernardi 1984, pp. 690–692). Watering down the legislation, combined with a new liberal-left government in office, more receptive to social issues, finally allowed legislation to pass. Lombroso’s proposed measures brought no social disruption and the cost to the public purse was minimal.

Finally, on 21 July 1902, the Italian parliament passed the country’s first law dedicated to countering the harmful effects of pellagra (Perisutti 1902). It prohibited the sale of unripened or spoilt maize, whether in the form of grain or flour, and trade in all products made from unripened or spoilt maize. Following Lombroso’s suggestions, the law mandated the installation of public maize-drying ovens in affected areas, authorised the free distribution of salt to pellagrins and obliged municipalities to report new cases of pellagra in a timely fashion and keep up-to-date statistics. A fund of 100,000 lire a year was to be set up to allow local authorities to implement these measures.

Paradoxically, and rather perversely, the anti-pellagra law was not only long overdue, combatting a disease that had ravaged maize-growing areas of the country since the middle of the eighteenth century; it also came too late. By 1902, pellagra rates had been declining for a decade, as diets had slowly improved, partly due to emigrants’ remittances, as we shall see in chapter four. Moreover, the law put the weight of the Italian state to only one of the theories accounting for pellagra’s aetiology: which turned out to be the ‘wrong’ one.

The Dispute’s Impact on Pellagra and Pellagrology

Lombroso complained that ongoing opposition to his aetiological ideas had harmed his career and reputation, whilst also causing ‘large sums of money’ to be wasted on ‘false causes’ (Lombroso 1892, pp. vii, viii, xviii). Yet it was Lombroso’s own theory which can be accused of having had the more deleterious effects—certainly on the lives of pellagra sufferers, if not necessarily on medical investigation into the nature of the disease.

Take the following exchange. In 1883 Lombroso contacted the founder of the town of Mogliano Veneto’s Hospice for Pellagrins, Costante Gris, to propose a trial. Gris was to treat forty pellagra sufferers with drugs alone, without modifying their diet, following Lombroso’s instructions. However, after five months, with the patients as ill as ever, Gris decided on his own initiative to reverse the experiment. ‘By means of the restorative diet alone’, Gris later informed Lombroso, ‘and without the use of the aforementioned medicines, I obtained much better results than with the first method’ (Vanzetto 1992, pp. 122–127, 136). Their collaboration and their correspondence ceased after that.

This was ‘bad medicine’ indeed. By dismissing the idea that a change of diet could cure pellagra, and by relying on chemical substances like lead acetate and arsenious acid instead, Lombroso was treating pellagrins with what amounted to dangerous poisons. Moreover, in eschewing a diet-based treatment, he effectively eliminated the one effective remedy available—and which was perceived as such at the time, at least by some. Lombroso stubbornly continued in this conviction until his death in 1909.

What impact did the dispute have on Italian medical practitioners more broadly? If Lombroso was able to dominate the pellagra debates at the higher echelons of medical science and government, the situation down on the ground played out quite differently. A look at the aetiological models adopted by asylum and town doctors, who treated pellagrins on a day-to-day basis, suggests that practitioner responses were not clear-cut. If we have polarised the pellagra dispute hitherto, construing it as a two-sided debate, much as Lombroso himself saw it, in fact it was multi-sided, almost fluid—as are indeed most controversies in science (Engelhardt and Caplan 1987).

For the Venetian asylum director Cesare Vigna (1819–92), the aetiology of pellagra saw medical investigators divided into, not two, but four camps: ‘unicists’, who favoured either one of the two dominant explantory models based around maize; ‘dualists’, who opted for a mixture of the two main theories; and ‘pluralists’, who continued to acknowledge a wide range of causal factors in the generation of pellagra (Vigna 1879, p. 448). These divisions are borne out by work that we have carried out on the thousands of diagnoses of the pellagrous insane referred to the Venetian asylums of San Clemente (for women) and San Servolo (for men). Throughout the latter two decades of the nineteenth century, the patient records continue to refer to multiple causal factors: heredity, sunstroke, poverty and hard labour being the key ones. This may be a throwback to the pre-aetiological age; but it may just as likely refer to the difficulties faced by nascent clinical psychology in coming to grips with causation in a disease like pellagra that mixed physical and mental aspects, a topic we shall return to in Part II.

Gauging the opinions of community-funded town or district doctors (medici condotti) is more difficult. The case notes they submitted to the two Venetian insane asylums when referring a patient for admission are inconclusive. More helpful is a 1912 survey of 242 condotti with experience treating pellagrins (Camurri 1912). The survey found that they were divided, much like asylum doctors: 87 town doctors (or 35%) were found to favour dietary insufficiency, 79 (32%) opted for spoilt maize intoxication, 66 (27%) preferred a mixture of both of these theories, and the remaining 15 (6%) favoured a range of other causes, including alcoholism and infection.

There is no evidence that Lombroso’s predominance here harmed the careers of either Lussana or Bonfigli. Lussana continued his research in the neurophysiology of the brain and was professor of physiology, first at Parma (1860–67) and then at Padua (1867–89), the years of his long-running dispute with Lombroso. Bonfigli likewise continued to publish widely and translated several works of German psychiatry. After a successful tenure at the Ferrarese insane asylum (Beltrami and Guerra 2015), in 1893 he took up directorship of the Santa Maria della Pietà asylum in Rome and the chair of psychiatry at Rome’s ‘La Sapienza’ University. He was elected to the 20th legislature of the Italian Parliament, 1897–1900, where he spoke on issues regarding public health and asylum legislation.

Finally, the effect of this predominance on the broader research agenda were less that might be expected. If the 1902 pellagra law suggests some kind of ‘closure’—a defining element of scientific controversies—in fact the Italian dispute over pellagra’s aetiology remained open and unresolved, even whilst the disease continued to decline in Italy. Lombroso’s may have been an intimidating presence in the field of pellagrology throughout the last three decades of the nineteenth century and into the twentieth, but this did not actually stifle investigation and debate. The field’s main journal, the Rivista pellagrologica italiana, may have been a Lombrosian stronghold, founded (in 1900) and directed by one of his former pupils, Giuseppe Antonini; but its pages provide ample evidence of the continuing vivacity, urgency and variety of the investigations into the disease. Indeed, as we shall see in the next chapter, the first decade of the twentieth century saw more Italian publications on pellagra than any other. And with them came a final brilliant, internationally divisive, but short-lived idea.