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2. A Discourse-Analysis of the Scientific Progress Regarding Beriberi
2.1 From Positive to Negative Causation
2.2 Visualisation of the Revolutionary Phase
3. Scientific Progress and the Transition of Paradigm.
3.1 Modes of Scientific Progression
3.2 Validating the Iterative Schema Using Historical Material
By turn of the 20th century, medical researchers and practitioners were confronted with a disease ravaging largely the tropical zones. Called beriberi its main pathological symptoms comprised decreased muscle function, degeneration of peripheral nerves, and paraplegia. People suffering from this disease constantly grew weaker, eventually losing their ability to walk. In the end, heart dilatation often lead to a sudden death. Despite beriberi’s pathological appearance and its symptomatology, the disease’s etiological cause, however, seemed mysterious and obscure. As medical dictionaries around the turn-of-the-century reveal, beriberi was attributed to myriad reasons. From infection1 to food deficiency to the influence of atmospheric conditions, or due to previous diseases such as malaria.2 By 1920, however, these numerous explanatory attempts were discarded and reduced to a single cause: a vitamin deficiency.3 And still today this is considered to be beriberi’s true etiological factor. How this change of knowledge came into being and which philosophical inferences can be drawn from it shall be the guiding principle of this thesis.
The theoretical fundament for this inquiry adheres to a concept elaborated by Thomas S. Kuhn in his seminal work The Structure of Scientific Revolutions (1962). There, Kuhn claims any mature science to depend both on paradigms and revolutions. A paradigm is to be understood as an unquestioned framework for scientists—comprising theories, instruments, metaphysical assumptions, etc.—which both directs the scientists’ perception to specific problems and provides the pathway to their solution. A paradigm thus guides thoughts and imposes methodologies. Although this seems to yield the problem of a one-way road, causing scientists to recognise only what is predicted by a paradigm, Kuhn considers this a necessary structure of any science and terms this normal science. Otherwise, scientists would not see things at all—the perceived stream of data would be meaningless without a specific guideline for how to interpret phenomena.4 This ‘paradigm-stabilisation’, however, entails the built-in moment of paradigm shift caused by the recognition of anomaly. That is, with a paradigm come certain expectations, and these expectation, in turn, enable scientists to recognise contradictions to the paradigm’s predictions. Occasionally, when anomalies build up to such an extent that the prevailing paradigm fails to sufficiently solve the contradictions, the paradigm must be superseded. This phase is what Kuhn refers to as extraordinary science: When science enters a state of crisis and generates new theories in order to overcome anomaly. At the end of such a crisis, a new paradigm will be born. Kuhn calls the structure of this transitional period a scientific revolution.
As will become apparent in the light of this historical study, the scientific progress concerning the etiology of beriberi entered such a crisis, bringing about a paradigm shift away from the earlier medical paradigm of disease-causation. Whereas at the beginning of the 20th century, diseases were thought to be mainly caused by external factors,5 the discovery of vitamins—which was a direct result of the research into beriberi’s etiology—shifted this paradigm into a new theory of vitamin-deficiency, revealing that diseases which appeared no different from those caused by external factors could also originate from a deprivation of internal factors. It is, thus, my endeavour to scrutinise this transitional period.
To this end, I shall undertake two related analyses. First, I will trace the scientific progress in respect to the research into the disease’s etiology by means of a discourse-analysis of the period 1900 to 1920. I show this period to be marked by five methodological changes—which I will refer to as ‘observational shifts’—that fostered the scientific investigations and altered the perception of the disease, ultimately revealing it to be a vitamin deficiency. For the sake of brevity I have confined this linguistic analysis mainly to an intra-scientific discourse studying only articles from the medical journal The Lancet. Following this discourse-analysis I shall, in the second part of this thesis, attempt to reach further into the structure of this transitional period. I will present a model aiming to describe the inherent development of the gradual shifting of paradigm. Thereby, I identify the underlying structure of this shift as an iterative paralleling of cumulative and discontinuous processes. However, this approach does not seek to give a general theory of paradigm change. Rather, it tries to reconstruct this historical period in order to give a detailed description of a scientific progress that stands out as a scientific revolution.
This discourse-analysis aims to trace a paradigm shift that constitutes a transition from a positive to a negative disease conception. ‘Positive’ refers here to the notion that mainly external factors were held responsible for disease causation. These factors were either assumed to be of pathogenic origin or poisons that would lead to the formation of beriberi. The change into a ‘negative’ conception, on the other hand, refers to the recognition of the absence of substances necessary for health. By around 1912 these substances were gradually known as vitamines [ sic ].6
Within this revolutionary period, I have identified five smaller periods that are associated with methodological changes structuring the investigations into beriberi’s etiology. As stated above I will refer to these as ‘observational shifts’, for each of these periods facilitated a change of investigation strategy that altered both perception and theoretical approaches for researchers and practitioners. Accordingly, these observational shifts play a major role in the transition from one paradigm into another.
Moreover, this discourse-analysis is limited to a period from 1900 to 1920. The reason for selecting this interval is not, however, arbitrary. Although beriberi had been known for a long time to occur mostly in the world’s tropical zones—thereby causing severe economic and political problems for the colonised areas of Great Britain or the Netherlands—by the turn of the 20th century the disease appeared ever more frequently on European terrain. Especially in Britain, where beriberi occurred prevalently on the ports because sailors were often affected by the disease, the newfound proximity provoked a much stronger attention to scientific investigations. It is in virtue of these circumstances that I restricted the scope of this thesis’ analysis to scientific articles from the English medical journal The Lancet from 1900 onwards.
Around 1900, medical researchers and practitioners were committed to a paradigm that predicted external factors for disease causation. Concerning beriberi this paradigm provided two major theories—the germ-theory and the intoxication-theory—which were thought suitable to solve the puzzle of the disease’s etiology. In addition to these theories, the scientific discourse also named dietary and hygienic conditions as plausible factors for beriberi’s origination. Each of these approaches provided plausible arguments that could—at least to some extent—explain the formation of beriberi. This circumstance, however, inhibited a concentration on one single line of investigation and instead produced a myriad of vague explanations.
An article from April 14th 1900, for instance, reveals the role that was given to hygienic factors. It reports an outbreak of beriberi among a crew on a fishing vessel. The crew is said to have lived in “overcrowded” and “ill-ventilated” cabins.7 Moreover, it is noted that the crew should have noticed “a most nauseous smell”8 emanating from the debris the ship carried. On the other hand, a different article proposes the theory of germs. There, the author utters the wish for a bacteriological investigation, for it is “the only scientific guide for action.”9 Or Bullmore, a surgeon to the Falmouth hospital, who, on the contrary, adheres to the intoxication-theory, who proposes the factor of alkaloidal poisoning due to disarranged gastric secretion and suggests an“auto-infection”.10 His article even reflects on further ideas proposed by researchers. For instance, the suggestion for factors such as a “rice insect”11 or the possibility of a microorganism.12 And with the ending of the year, Ronald Ross proposes the possibility (insisting this not to be a theory) of arsenic poisoning due to “tinned and bottled fruits“13 and therefore also assumes beriberi to be a kind of intoxication caused by canned food.
Nearly a year passes until, in October 1901, The Lancet eventually publishes a paper commenting on Ross’ suggestion of arsenic poisoning. There, the author14 supports Ross’ hypothesis by stressing a most probable connection between beriberi and foodstuff. I argue that the grounds for the author’s reason why “the illness is to be connected in some ways or other with diet rather than with an infective process”15 has its roots in the medical history of the disease. I shall not give an overall account here, for many others have sufficiently elaborated on this topic,16 but it seems necessary to mention that both Takaki and Eijkman already reliably showed at the end of the 19th century that there is an intimate connection between a diet solely consisting of milled white rice and the outbreak of beriberi. By administering non-milled rice or even eradicating all rice from the diet, Takaki and Eijkman made evident that the consumption of white rice is linked to the disease.17 Around 1900 this rice-theory, however, was mainly dismissed, for it was only seen as a practical experience unable to prove the theory.18
With this brief historical background let us return to the article from October 19th. Although the author stresses a dietary explanation for the causation of beriberi, rice is rejected to be the cause: “It is noteworthy that in these cases of beriberi outbreaks on British ports, rice, which has been suspected for good reasons to be associated with the disease in the East, has formed no part of the sufferers.”19 According to the author, the sailors’ diet did not consist of rice. This statement yields the historical circumstance that the disease, at that time, had not yet been considered a consistent, singular entity. Beriberi in “the East” seems to differ from European beriberi on British territory because “it is, of course, possible that the peripheral neuritis which is the chief characteristic of the malady of the European sailors may not be due to the same cause as tropical-beriberi.”20 However, I shall not focus on this distinction in this thesis. Instead, I wish to illustrate that rice, as a causal factor, had at length been considered but was pushed aside by the prevailing paradigm predicting external agents to be the only causal factor. Consequently, poisons or germs seemed the most likely culprits, for they ‘invade’ the human body. Rice, on the other hand, is said to rarely form a sailor’s diet, and even if, as Bullmore states, “on examination I have always found it excellent on ships where beri-beri has broken out.”21 Additional evidence for this type of reasoning can be drawn from the inaugural address from Patrick Manson delivered before the Epidemiological Society of London in November 15th in 1901. There, he claims that the germ-theory of beriberi is “much more plausible than the foregoing” [rice-theory] and thus considers beriberi to be a “germ disease”.22 But Manson not only believes germs to be the sole factor but also claims that “[t]he fundamental nerve lesions […] resemble those produced by several well-known organic poisons, and are probably the results of the direct action of some such poison.”23 According to Manson, this theory has many advocates. However, this inaugural address is not only important for the fact that a certain paradigm was responsible for the rejection of the rice-theory, but—to a greater degree—this address uncovers a synthesis of the former rather disconnected theories into new interrelating structures. To explain this I shall again cite Manson in his own words:
To my mind, the theory which confirms best to all the known facts in respect to the etiology and pathology of beri-beri is to the effect that this disease is purely an intoxication produced by a toxine elaborated by a germ whose nidus is located outside the human body. […] Granted that a place or ship can become infected, we have still to find the particular medium in which the germ operates, and the particular portal through which its toxine enters the human body. (Manson 1902, p. 12, My italics.)
As a matter of fact, Manson not only believes in a single but in a cluster of factors. Poisoning, overcrowding, intoxication, and even to some extent the factor of rice find, at the end of 1901, a synthesis in Patrick Manson’s disease explanation. This new structure ultimately renders his perception on beriberi as a place disease.
There is a marked tendency among the students of this subject to regard, not without reason, rice as the nidus of the germ; but, if rice be the medium, how is it that the disease sometimes occurs in individuals who have not consumed this cereal? […] The answer to this may be, that the germ clings to the walls, the wood, the utensils of the place; and that when cereals are brought in this germ drops into them and infects them. Thus infected, when consumed, wether on the premises or exported elsewhere, they may cause the disease. […] This is speculation, but I think we have distinct evidence to show that beri-beri is, in a sense, a place disease. (Manson 1902, p. 16, My italics.)
Finally, with this interrelation, Manson can put forward a coherent theory that fits the phenomenon. It is, however, necessary to mention that Manson does not entirely discard the rice-theory or any other dietary explanations, for he acknowledges the practical experiences made by Eijkman and Takaki.24 Yet, from his address one can clearly see his conviction of rice, if any, to be merely a passive factor in the causation. In general, the scientific commu-nity lacks unanimity about beriberi’s distinct cause. Articles from 1902 reveal this discordance. For instance, in a report from the Norwegian Scientific and Literary Society it is said that “[n]one of these theories [infectious disease due to microbes, insufficient food, rice- or fish-intoxication, auto-intoxication, etc.] explained in a satisfactory way the appearance of late years of the disease in Europe and especially on European sailing ships.“25 For that reason Vilhelm Uchermann, a Norwegian physician who is quoted by the same article, urges for a more general theory of intoxication “by tainted vegetable or animal food.”26
However, apart from Uchermann’s general theory of intoxication, the medical sciences seem to focus more specifically on the “intimate connection between a certain disease in rice and beriberi in man“.27 This theory of a “certain disease in rice” still goes hand in hand with a medical paradigm predicting external agents for disease causation. That is, the majority of physicians, pathologists, or practitioners who theorise rice as the main factor in the for-mation of beriberi, conjecture that “rice may become a vehicle of the beriberi infection.“28
In the following years, this theory appears to gain traction. The medical perception now, indeed, recognises rice and other foodstuff as a “vehicle” for the onset of beriberi. Two articles from 1904—one from February 20th, the second dating from November 26th—take this view. The former is a report about Patrick Manson’s assessment of the potential curative effect of water-cress on beriberi. It is stated that Manson, besides discarding water-cress’ curative effect, proposes a general hypothesis of malnutrition; maintaining that a deficiency of any foodstuff would render a body susceptible to diseases such as beriberi.29 This very idea of susceptibility is also presented in the latter article from November 26th. There, it is said that an exclusive rice diet could predispose the human body to illness.30
No further articles on beriberi appear in the next three following years. It is therefore plausible to assume that during this time, research focused on the theory of susceptibility, i.e. whether the consumption of food triggers beriberi. But historical data suggests that, instead of pursuing Manson's wider theory of general malnutrition in order to explain the susceptibility’s cause, scientists focused solely on rice as the main factor. Still, guided by their medical paradigm they only perceived external factors to be the susceptibility’s cause. Meaning, that with the consumption of rice a poisonous agent must be ingested.
However, pushed forward by this paradigm, research entered—to use Kuhn’s terminology—a phase of crisis when around 1907 science had to face the anomaly that not every consumption of rice per se renders a person ill. Ultimately, this anomaly laid the focus solely on a specific type of rice and thereby had a lasting effect on the scientific methodology.
In his article from June 1907, William Fletcher, a British surgeon working in Malaysia, gives an account of an experiment which he conducted between December 1905 and December 1906 in a lunatic asylum in Kuala Lumpur. Due to an outbreak of beriberi inside one of the asylums, where 94 out of 219 inmates were affected by the disease, and of whom 27 died, Fletcher saw this as an opportunity for commencing an experiment in order to falsify the rice-theory.31 He put two groups each on a different kind of rice with the expected outcome that both sorts would produce beriberi:
It was fully expected that the patients on Bengal rice would suffer from beri-beri to the same extent as those who remained on the Siamese variety and that the result of the experiment would be a refutation of the rice theory. (Fletcher 1907, p. 1778.)
Fletcher questions the rice-theory as it was formerly contended by Braddon, i.e. the difference between Siamese rice—what Braddon called “uncured” (milled white rice)—and Bengal rice—called “cured” (non-milled rice). Fletcher was, like many other medical researchers and practitioners at that time, convinced that rice per se develops a beriberi-producing poison. In order to disprove the theory that only uncured rice causes beriberi, Fletcher formed two groups from which one was placed on cured while the other was administered uncured rice. Each group was situated in different wards of the asylum. This arrangement gave Fletcher the additional opportunity to verify Manson’s theory of place-disease. The results obtained by the experiment, however, proved all expectations wrong. The group on uncured rice suffered from beriberi, whereas the party on cured did not. And even when the groups swapped places, yet continued with the same diet, no change occurred. Consequently, Fletcher’s experiment involuntarily disproved Manson’s place-disease theory and proved Braddon’s rice-theory to be correct:
Contrary to expectation, the result of the experiment, so far as it goes, is to prove the truth of Dr. Braddon’s contention that uncured rice is the cause of beri-beri. It remains to be proved whether the cause of the disease amongst the eaters of the uncured rice is a poison contained in the rice or whether there is something essential to the human economy which is supplied by the cured rice whilst it is absent in the uncured. […] If this be the case the deficiency of proteid [ sic ] matter in the diet may be the actual cause of the disease, or, what is more likely, the lack of nutriti vematter [ sic ] in the rice may induce a condition in the patient which renders him an easy prey to some external agency—bacterial or protozoal—which is the actual cause of beri-beri. (Fletcher 1907, p. 1778. My italics.)
Fletcher concludes from this experiment three possible kinds of explanation which reconciled the observations best: (i) a poison contained in the rice; (ii) a deficiency disease due to nitrogen starvation; and (iii) uncured rice renders the human body susceptible to an invasion by a specific agent.32
In the end, this experiment initiated an observational shift leading research to only focus on a specific kind of rice and its assumed pathogenic action. During the years 1907 and 1908, Fraser and Stanton—arguably the most prominent figures in the experimentational proof of the rice-theory—conducted a similar trial to that of Fletcher33 with similar findings. In an article released in 1909 they present their findings, claiming that their experiment suggests, yet does not prove, that “place per se or considered as a nidus of infection has no influence upon the development of beriberi.”34 Their experiment was designed as follows:
For the purpose of the inquiry it was necessary to observe two parties of men under similar conditions as to environment, &c., and whose food-supply was definitely known. In view of the suggestion made by numerous observers that the disease may be bacterial or protozoal in origin, it was desirable that the places chosen should have been hitherto uninhabited or that no case of beri-beri should have occurred there for some time previously; further, the places should be in an isolated district sufficiently remote from towns or villages to exclude as far as possible the entrance of a supposed infection. Such a situation would also have the advantage, on account of the absence of shops, that the men under observation could not readily obtain food other than that supplied to them. It is obvious that the conditions required for such an investigation could not be secured in a public institution, as in all such in these States beri-beri is known to be endemic. Various places were visited with a view to securing satisfactory conditions, and it was finally decided to carry on observations with regard to some 300 Javanese indentured labourers employed in the work of road construction in a remote part of the Jelebu district in the State of Negri Sembilan. (Fraser; Stanton 1909, p. 451.)
I shall recapitulate the experiment's structure here: As can be drawn from Figure 2, Fraser and Stanton formed different groups (parties), each of them administered with two sorts of rice. On May 12th 1907, party one (No. I) was given “uncured” white rice (characterised by a “W”), whereas at around the same time, though different location, party two (No. II) was supplied with “cured” parboiled rice (characterised by a “P”). On July 1st No. I was, then, split into two groups: No. IA and No. IB. Hitherto, no beriberi occurred in No. I. Between August and September, however, both No. IA as well as No. IB developed cases of beriberi. Until that time No. II remained healthy. This changed, though, when Fraser and Stanton swapped the diet between the two parties on October 19th. On April 9th 1908, No. II—having been fed only on white rice for a period of seven months—eventually developed several cases of beriberi. Whereas No. IA/B, since the change of diet, did not develop any symptoms whatsoever. For the sake of accuracy, a third party (No. III) was employed. Administered solely parboiled rice during the entire time from August 19th 1907 to June 1st 1908, none of the workers from No. III developed any beriberi symptoms. Lastly, Fraser and Stanton maintain that “[i]n three instances in which definite outbreaks of beri-beri occurred among parties on white rice, substitution of parboiled rice was followed by a cessation of the outbreaks.”35
Although different in their initial goals36, I argue that the results acquired by Fletcher, Fraser, and Stanton had a lasting influence on the prevailing paradigm. They did so by initiating a shift between 1907 and 1909 away from the theory of place-disease, and away from rice per se as the medium, towards a new observational structure that now focused on a specific distinction: cured versus uncured rice. Yet, besides this new focus that gradually perceived some sort of deficiency, researchers and practitioners nevertheless continued to adhere to the theory of intoxication.
Evidence for this observational shift can further be drawn from an article published on May 8th 1909. There, Fraser and Stanton’s observations are regarded to “largely dispose of the theory of infection either of person or place.”37 Moreover, it is stated that “there […] be no question as to the incrimination of uncured rice. The point now remaining to be demonstrated is whether the symptoms of the disease are the result of a nitrogen starvation or are due to a toxin produced in the rice by some organism.”38
Ultimately, 1907 saw a development in the scientific consensus towards an ever-sharper medical perception, gradually changing the prevailing paradigm. Around that time, however, it seems that this rice-theory was not yet altogether acknowledged. For medical researchers and practitioners still favoured rather diverse explanations. In a meeting of the Society of Tropical Medicine and Hygiene on beriberi, a compilation of hypotheses of beriberi’s etiology is proposed. These include infection, food-intoxication, sanitary conditions, storage time, or overcrowding.39 Ultimately, Patrick Manson (president of the society at that time) urges that “[u]ntil the germ or the toxin of beri-beri was discovered, and until direct experiments could be carried out and the results watched, it would not be possible to decide the question.”40 Neither of these theories, however, triumphed.
In 1910 The Lancet published two papers on beriberi, both pertaining to the attempt to discover the deficiency-causing agent which had been hypothesized by a minority of scientists to be the factor of the milled (cured) rice; opposed to a germ or a toxin, how it was urged by Manson. One of the articles, dating from December 17th and titled The Etiology of Beri-Beri41 , was written by Fraser and Stanton, who describe another experiment conducted with cured and uncured rice. I argue that with this experiment, they established the third observational shift in respect to the scientific progress of beriberi’s etiology.
With the appearance of their article, new terms emerge in the scientific discourse that identify new factors—such as substance, the pericarp, and rice-polishings 42 —that are thought to play major parts in the origination of beriberi. The analysis reveals that these terms, which found their way into the scientific language and related to the onset of beriberi, seem to have replaced the foregoing terms of “poison”, “intoxication”, “germs”, or alike. If anything, these latter terms merely show up in the scientific discourse mainly to be disproven.43 I argue that this transition is—in accordance with Fleck—to be explained by the concept that (i) new theories are commonly accompanied by the application of a new language; and (ii) this new language reshapes the conception of the research object:
At any rate, once a statement is published it constitutes part of the social forces which form concepts and create habits of thought. Together with all other statements it determines “what cannot be thought in any other way.” (Fleck 1979, p. 37.)
For a better understanding of the scientific progress it is now necessary to briefly explain Fraser and Stanton’s second experiment:
1 American Pocket Dictionary (1898), p. 68.
2 A Dictionary of Medicine (1890), p. 104.
3 Stedman’s Dictionary (1920), p. 121.
4 Kuhn, therefore, implicitly draws an important distinction between observation and mere sense perception, for the former already entails the guideline and framework of how to cope with data, whereas the latter lacks this kind of directed noticing.
5 This paradigm of disease-causation by external factors is supported by the fact that by the first quarter of the 19th century the germ-theory found growing consensus and finally established with the findings of Pasteur and Koch at the end of the century. But also the intoxication-theory explained diseases having the pathological appearance of degenerated tissue by the infiltration of poisons.
6 The initial spelling had an additional ‘e’ since Casimir Funk, the chemist who coined this term, supposed these substances to be compounds of amines crucial for life (vita). On the basis of that supposition, he merged these two words: vita-amine. He was, at the time he discovered their chemical properties, however, not aware of the numerosity of substances that we nowadays call vitamins. Only after he proposed this term did other analyses show that not all ‘vitamines’are amines. But as it was already entrenched as a technical term, the word was simply truncated by removing the ‘e’so that the emphasis on amines was diminished.
7 Cruchet (1900), p. 1082.
9 Ensor, (1900), p. 1041.
10 Bullmore (1900).
11 Ibid., p. 873.
13 Ross (1900), p. 1677.
14 The article does not provide the author’s name.
15 “Beri-Beri and arsenical poisoning” (1901), p. 1059.
16 Arnold (2010); Carpenter (2000); Lonsdale, Marrs (2017).
17 Eijkman (1897); Takaki (1906).
18 Manson (1902).
19 “Beri-Beri and arsenical poisoning” (1901), p. 1059.
21 Bullmore (1900), p. 873.
22 Manson (1902), pp. 11, 12, 13. Manson’s opinion surely stems from the germ-theoretical doctrine that circulated around this period. Lauren N. Ross’ paper The doctrine of specific etiology (2018) draws special attention towards this paradigmatic supposition of pathogenic agents that came with Koch and Pasteur at the last quarter go the 19th century.
23 Manson (1902), p. 11.
24 Manson (1902), p. 8–11.
25 “Beri-Beri“ (1902), p. 225.
27 Ibid., p. 448.
28 Ibid., My italics.
29 “Water-Cress as a Specific for Beri-Beri” (1904), p. 521.
30 “The Food of the Japanese Soldier in Connexion with Beri-Beri” (1904), p.1512.
31 It must be said that already at the turn of the 20th century “rice-theory” referred to the idea that only a specific kind of rice was be responsible for the onset of beriberi. As mentioned above Eijkman and Takaki both sufficiently proved evidence in favour of this theory. However, Fletcher refers to William Braddon who, around 1900, recognised that Chinese immigrants in Malaya who consumed milled and polished rice had a higher chance of catching beriberi than the Tamils who ate non-milled rice. See: Bruyn, George W.; Poser, Charles M. (2003), p. 12.
32 Fletcher (1907), p. 1778.
33 The difference is that Fraser and Stanton, unlike Fletcher, sought proof in favour of the rice-theory and, thus, conducted experiments built to eliminate the theories of infection, intoxication, or place disease in the first place.
34 Fraser; Stanton, (1909), p. 452.
35 Fraser; Stanton (1909), p. 455.
36 Fletcher, on the one side, whose experiment was designed in the first place to disprove Braddon’s theory of the formation of beriberi due a specific type of rice, and Fraser and Stanton, on the other, who conducted their trial in favour of Braddon’s theory.
37 “Is Beri-Beri Caused by Rice?” (1909), p. 1334. At this point it seems necessary to note that a“theory of infection” goes hand in hand with the theory of germs, for these enter the human body causing infective processes.
39 “Beri-Beri” (1909), p. 1181.
41 Fraser; Stanton (1910).
42 I must, however, admit that “pericarp” and “rice-polishings” are not at all ‘new’ terms. As far as I am concerned, Christiaan Eijkman was the first who explicitly pointed to the fact that rice-polishings, i.e., the layer of rice rubbed off by milling (pericarp), causes beriberi.
43 Following this discourse-analysis I shall visualise this gradual transformation of terms in paragraph 1.2.1. However, I recommend the reader turning to this visualisation whenever she or he feels to align this historical outline with visual illustration.
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