Epoché (XIII), 28. 1. 2021
A synopsis of our reading of The Normal and the Pathological by Georges Canguilhem
Part I/Ch. 2 “Auguste Comte and the “Broussais’s Principle”” (pp. 47-64)
Part I/Ch. 3 “Claude Bernard and Experimental Pathology” (pp. 65-89)
Abridgment by: Sebastjan Vörös
[his outline and commentary of the whole book can be found here]
Chapter II: Auguste Comte and “Broussais’s Principle”
Comte took over the quantitative conception from François Broussais’s De l’irritation et de la folie:
“Comte credits Broussais, rather than Bichat, and before him, Pinel, with having declared that all diseases acknowledged as such are only symptoms and that disturbances of vital functions could not take place without lesions in organs, or rather, tissues. But above all, adds Comte, ‘never before had anyone conceived the fundamental relation between pathology and physiology in so direct and satisfying a manner.’ Broussais described all diseases as consisting essentially ‘in the excess or lack of excitation in the various tissues above or below the degree established as the norm.’ Thus, diseases are merely the effects of simple changes in intensity in the action of the stimulants which are indispensable for maintaining health.” (47)
Comte then raised “Broussais’s nosological conception to the level of a general axiom”, and seemingly accorded it the same dogmatic value as Newton’s law or d’Alembert’s principle. Actually, little by little, he practically claimed the intellectual paternity of this principle for himself, by virtue of applying it systematically (48). The following passage is particularly telling:
“Until Broussais, the pathological state obeyed laws completely different from those governing the normal state, so that the exploration of one could have no effect on the other. Broussais established that the phenomena of disease coincided essentially with those of health from which they differed only in terms of intensity. This brilliant principle has become the basis of pathology, thus subordinated to the whole of biology […] Those engaged in the encyclopedic task of compiling and classifying knowledge will extend Broussais’s principle primarily to moral and intellectual activities where it has not yet received a worthy application, hence their diseases surprise or move us without instructing us. […] In the general system of positive education, besides its direct usefulness for biological problems, this principle will be an appropriate logical preparation for analogous procedures in any science. […] I do not hesitate to state that Broussais’s principle must be extended to this point and I have often applied it to confirm or perfect sociological laws.” (49-50)
Comte believes that, given the fact that in experimentation one introduces various changes into the conditions so that one may observe (measure) their effects and finally deduce specific laws which govern their modifying influences (50), one may conceive of diseases as spontaneous experiments which allow a useful comparison between an organism’s abnormal states and its normal state (51). In this regard, and again following Broussais, he maintains that “the pathological state is not at all radically different from the physiological state, with regard to which […] it can only constitute a simple extension going more or less beyond the higher or lower limits of variation proper to each phenomenon of the normal organism” (51).
The implications of this are significant:
“Consequently, every conception of pathology must be based on prior knowledge of the corresponding normal state, but conversely, the scientific study of pathological cases becomes an indispensable phase in the overall search for the laws of the normal state. The observation of pathological cases offers numerous, genuine advantages for actual experimental investigation. The transition from the normal to the abnormal is slower and more natural in the case of illness, and the return to normal, when it takes place, spontaneously furnishes a verifying counterproof. In addition, as far as man is concerned, pathological investigation is more fruitful than the necessarily limited experimental exploration. The scientific study of morbid states is essentially valid for all organisms, even plant life, and is particularly suited to the most complex and, therefore, the most delicate and fragile phenomena which direct experimentation, being too brusque a disturbance, would tend to distort. […] Finally, the study of anomalies and monstrosities conceived as both older and less curable illnesses than the functional disturbances of various plant or neuromotor apparatuses completes the study of diseases: the ‘teratological approach’ [study of monsters] is added to the ‘pathological approach’ in biological investigation.” (51-2)
C. points out two things:
(1) With regards to Comte’s basic proposition that a pathological phenomenon always has its analogue in a physiological phenomenon, he mentions “the particularly abstract quality of this thesis” and the absence of any precise medical example to illustrate it: [example] “How is a sclerotic artery analogous to a normal one, or a systolic heart identical to that of an athlete at the height of his powers?” C. provides another counterexample from Siderits: “During digestion the number of white blood cells increases. The same is true at the onset of infection. Consequently this phenomenon is sometimes physiological, sometimes pathological, depending on what causes it.” (52).
(2) With regards to Comte’s view of the reciprocal nature of the clarification between the normal and the pathological, he points out that Comte still insists that the normal and its true limits must be determined first: “Strictly speaking, knowledge of normal phenomena, based solely on observation, is both possible and necessary without knowledge of disease […]”. However, there is a serious gap here, because Comte provides us with no criterion of what constitutes a normal phenomenon; in fact, when he does talk about “the normal” he talks about a “harmony of distinct influences, those exterior as well as interior”, which is “a qualitative and polyvalent concept, still more aesthetic and moral than scientific” (53).
In general, Comte’s identity theory amounts to denying the qualitative difference between disease and health (admitted by the vitalists) and asserting a homogeneity expressible in quantitative terms (53). However, as C. points out, the terms used in doing so (cf. above: “simple extension going more or less beyond…”) have a peculiarly qualitative ring to them. Since this vocabulary was taken over from Broussaird, C. provides a short account of the latter’s theory as exposed in De l’irritation et de la folie (53-4).
For Broussais, the “vital primordial fact” was “excitation”: “Man exists only through the excitation exercised on his organs by the environment in which he is compelled to live.” Basically, the surfaces of contact are exposed to two kinds of excitation: external (foreign bodies), which gets transmitted to the central nervous system, and internal (influences of the brain), which consists of backward excitations transmitted to the tissues by the central nervous system. Life is sustained by the continual application of these multiple sources of excitation (54).
What does it mean if we apply this physiological doctrine to pathology? It would mean figuring out how “this excitation can deviate from the normal state and constitute an abnormal or diseased state” (54). There are two possible deviations – (i) one brought by deficiency, (ii) the other by excess. For Broussais, in pathology, (ii) outweighs (i). In general, Broussaird equates the terms “abnormal”, “pathological” and “morbid” (they are used synonymously): the distinction between the “normal or physiological” and the “abnormal or pathological“ is, in his eyes, a simple quantitative one defined in terms of deficiency and excess. C. concludes his presentation with the following words: “This then, in summary, is the thesis whose fortune certainly owes more to the personality of the author than to the coherence of his text.” (55)
What follows is C’s critique:
Obviously, Broussais confuses cause and effect: “A cause can vary quantitatively so that it nevertheless both continues and provokes qualitatively different effects.” Example: a quantitatively increased excitation can first produce pleasure, then pain. However, there is a larger issue at stake here:
“In such a theory two points of view are being constantly mixed together, that of [a] the sick man who is experiencing his illness and who is tested by it, and that of [b] the scientistwho finds nothing in disease that cannot be explained by physiology. But the states of an organism are like those found in music: the laws of acoustics are not broken in cacophony – this does not mean that all combinations of sounds are agreeable.” [!!!]
Broussais’s position can be developed into two slightly different directions, depending on whether one stresses homogeneity or continuity.
(i) Bégin, for instance, opts for continuity (cf. example on p. 56); however, as C. makes it clear, continuity can be compatible with heterogeneity: the continuity of the middle stages does not rule out the diversity of the extremes [!] (56).
(ii) Both Broussais and Comte strive towards homogeneity, but their vocabulary betrays difficulties in sustaining such a view consistently: “excess” or “deficiency” exist in relation to a norm (= scale deemed valid and suitable); however, when talking of a “normal (physiological) state”, we are no longer talking simply of a “disposition which can be revealed and explained as a fact, but a manifestation of an attachment to some value”; in general, an “ideal of perfection” can be found generally soaring over attempts at a positive definition of a “normal state” (56-7).
From this, C. develops a major objection to Broussais’s thesis:
“The ambition to make pathology, and consequently therapeutics, completely scientific by simply making them derive from a previously established physiology would make sense only if, first, the normal could be defined in a purely objective way as a fact and, second, all the differences between the normal state and the pathological state could be expressed in quantitative terms, for only quantity can take into account both homogeneity and variation. […I]t must be evident that neither Broussais nor Comte fulfilled the two requirements which seem inseparable from the attempt with which their names are associated.” (57)
C. then goes on to provide a more in-depth explanation as to why this is the case for the two authors (cf. Broussais, 57-63; Comte, 63-4). In doing so, he turns back to the people who had influenced the two said authors, particularly John Brown, Samuel Lynch, and Xaivier Bichat. With what purpose does he undertake such ideational archeology?
“It must be said that this disinterment of an obsolete nosology was not intended to amuse or to satisfy the vain curiosity of a scholar. In a unique way it approaches a precise statement of the profound sense of the thesis now before us.” (61)
More specifically, he shows how in these authors the ideal of quantitative analysis was ripening (often to absurd proportions); and how the terminological confusion (especially through the appropriation of Bichat’s works) slipped into the thesis under investigation.
Chapter III: Claude Bernard and Experimental Pathology
Claude Bernard never referred to Comte when dealing with the topic in question; but, adds C., he could not ignore Comte’s opinions, as it is well known that he read Comte closely and “with his pen in hand” (65). In general, however, it is “a very difficult and delicate task” to delineate Bernard’s precise views on the “nature and meaning of pathological phenomenon”, since there is no complete critical edition of his works and secondary literature is strongly divided on most, if not all, issues (66).
C. starts with a general observation:
“In Bernard’s work, the real identity -should one say in mechanisms or symptoms or both? – and continuity of pathological phenomena and the corresponding physiological phenomena are more a monotonous repetition than a theme.” (67)
“Bernard considered medicine as the science of diseases, physiology as the science of life. In the sciences it is theory which illuminates and dominates practice. Rational therapeutics can be sustained only by a scientific pathology, and a scientific pathology must be based on physiological science.” (67)
So, we have the following sequence (in order of importance and influence): physiology [theory] → pathology → therapeutics [practice]. In Bernard’s own words:
“Common sense shows that if we are thoroughly acquainted with a physiological phenomenon, we should be in a position to account for all the disturbances to which it is susceptible in the pathological state: Physiology and pathology are intermingled and are essentially one and the same thing.”
Bernard uses the example of “diabetes” to substantiate his view, for it is a disease which, according to him, consists solely in the disorder of a normal function: “Every disease has a corresponding normal function of which it is only the disturbed, exaggerated, diminished or obliterated expression.” (68)
In this regard, Bernard was actually at odds with many physiologists of his day, who believed that disease was an extra-physiological entity that was superimposed on the organism. According to Bernard, the study of diabetes no longer allows for such an opinion. All the symptoms of diabetes – polyuria, polydipsia, polyphagia, autophagia and glycosuria – are not new phenomena, but merely more intensified (“excess”) forms of normal processes (68).
C. points out that, while this claim can be demonstrated for polyuria, polydipsia, polyphagia and autophagia, it is not so easily demonstrated with regards to glycosuria (= the excretion of glucose into the urine.). Bernard seems to be aware of this and contends that glycosuria is a “masked and unnoticed” phenomenon in the normal state, which becomes noticeable only in its exaggerated forms. However, he never actually proves what he is propounding (68):
“It is striking to document here that, in trying to furnish a particularly convincing fact favoring his interpretation in a case where he felt especially challenged, Bernard found himself forced to admit this same fact without experimental proof – by reason of the theory – by supposing that its reality was situated beyond the limits of sensibility of all the methods used at that time for its detection.” (69)
In fact, more recent research has shown that there is “no normal glycosuria”. However, if this is the case, then “what physiological phenomenon does diabetic glycosuria exaggerate quantitatively?” (69)
C. indicates that Bernard is most well known for his finding that sugar found in the animal organism is produced by this same organism and is not just something introduced through feeding (= glycemia = the presence, or the level, of glucose in one’s blood). Further, he showed that blood normally contains sugar and that urinary sugar is a product usually eliminated by the kidneys when the rate of glycemia exceeds a certain threshold (69-79):
“In other words, glycemia is a constant phenomenon independent of food intake to such an extent that it is the absence of blood sugar that is abnormal, and glycosuria is the consequence of glycemia which has risen above a certain quantity, serving as a threshold. In a diabetic, glycemia is not in itself a pathological phenomenon – it is so only in terms of its quantity; in itself, glycemia is a ‘normal and constant phenomenon in a healthy organism’.” (70)
The reason why Bernard was so vehement in expounding his thesis was because of the contrarian voices in academia. For instance, Jaccoud (professor at the Faculty of Medicine in Paris) claimed that glycemia is an inconstant, pathological phenomenon and that the production of sugar in the liver is a pathological condition (70). Diabetes, in his view, is not an exaggeration of a normal physiological operation, but rather “the expression of an operation completely foreign to life”. In short, it is “the essence of the disease” (70-1).
“If we really want to understand the meaning and significance of the assertion of continuity between normal and pathological phenomena, we must bear in mind that the thesis toward which Bernard’s critical demonstrations are directed is one which admits a qualitative difference between the mechanisms and products of the vital functions of the normal state and those of the pathological state.” (71)
This contradiction between his thesis and that of his opponents is particularly strongly underlined in Bernard’s following statement:
“Health and disease are not [1 – discontinuous view] two essentially different modes as the ancient physicians believed and some practitioners still believe. They should not be made into distinct principles, entities which fight over the living organism and make it the theater of their contest. These are obsolete medical ideas. [2 – continuous view] In reality, between these two modes of being, there are only differences of degree: exaggeration, disproportion, discordance of normal phenomena constitute the diseased state. There is no case where disease would have produced new conditions, a complete change of scene, some new and special products.” (71)
In light of this, Bernard draws the following general conclusion:
“These ideas of a struggle between two opposing agents, of antagonism
between life and death, between health and sickness, inanimate and living nature have had their day. The continuity of phenomena, their imperceptible gradation and harmony must be recognized everywhere.” (72)
The merit of Bernard is definitely in having denied the antithesis accepted until then between the mineral and the organic, plant and animal, and of having affirmed the material identity of all physicochemical phenomena regardless of their setting and appearance. He was not the first to assert the identity of the products of the laboratory and those of ‘living’ chemistry (that idea was conceived by Wöhler in 1828), but he was the first to assert the physiological identity of plant functions and corresponding animal functions. In short:
“Bernard denied all of these antitheses, and the discovery of the glycogenic function of the liver is one of the most beautiful results of the desire to ‘recognize everywhere the continuity of phenomena.’” (73)
Now, there is an ongoing debate as to whether Bernard was a materialist or vitalist (73). C. maintains that this is a very nuanced question. On the one hand, and from the physicochemical point of view, Bernard does not accept the distinction between the organic and the mineral realm, i.e., he asserts the homogeneity of matter within and outside the living form. On the other hand, Bernard argued for the originality of the living form and its functional activities:
“Along with Lavoisier I believe that living things are tributaries of the general laws of nature and that their manifestations are physical and chemical expressions. Unlike physicists and chemists I am far from seeing vital actions in the phenomena of the inanimate world – on the contrary I believe that the expression is particular, the mechanism special, the agent specific although the result is the same. No chemical phenomenon exists inside the body as it does outside of it.” (74)
In sum, then: “it seems clear that for Bernard, recognizing the continuity of phenomena does not mean ignoring their originality”. But couldn’t we then say the same with regards to the relation between phenomena existing in the diseased organism and phenomena existing in the healthy one? (75)
According to C., Bernard supported his general principle of pathology with verifiable arguments, experimental protocols, and methods for quantifying physiological concepts. However, in spite of his undeniable progress in logical precision, his thought is still not free of ambiguity (75).
The crucial issue is – as it was with Bichat, Broussais and Comte – “a deceptive mingling of quantitative and qualitative concepts in the given definition of pathological phenomena”. This ambiguity, says C., is very instructive as it reveals the problem that lies at the heart of the identity thesis:
“Is the concept of disease a concept of an objective reality accessible to quantitative scientific knowledge? Is the difference in value, which the living being establishes between his normal life and his pathological life, an illusory appearance which the scientist has the legitimate obligation to deny?” (76).
Bernard uses two expressions interchangeably, namely:
(1) “quantitative variations”, which refers to homogeneity; and
(2) “differences of degree”, which refers to continuity.
However, these two concepts do not imply the same logical requirements:
(@1) Asserting the homogeneity of two objects, I must define the nature common to both.
(@2) Asserting the continuity, I can only interpolate between the two extremes all the intermediaries, without reducing one to the other, by divisions of progressively smaller intervals (76). For this reason, some authors (defenders of “facile relativism”, cf. below) refused to define either of the two extremes, claiming that there is “no perfect health”, i.e., “no completely normal state”, which is to say that there exist only sick men. However, as C. points out, this could just as easily mean that there are no sick men, i.e., that there are only healthy men, which is absurd. The reason for this move seems to be that physicians are aware it entails a revival of the problem of the existence of the perfect and the ontological argument (77).
The background issue here is of a philosophical nature. Namely, (perfect) health does not exist (in the strict sense), because it is a norm:
“Strictly speaking a norm does not exist, it plays its role which is to devalue existence by allowing its correction. To say that perfect health does not exist is simply saying that the concept of health is not one of an existence, but of a norm whose function and value is to be brought into contact with existence in order to stimulate modification. This does not mean that health is an empty concept.” (77) [!!!]
Now, Bernard does not buy into the “facile relativism” argued for by those who deny that there is such a thing as perfect health, etc.; the reason for this is twofold: (i) in his thought, the assertion of continuity implies that of homogeneity; and (ii) in his view, it is always possible to give the concept of the normal an experimental content (77).
C. tries to shed light on the issue with the following two examples:
(i) if the renal mechanism is considered in terms of its results(presence of sugar in diabetic urine) disease is the appearance of a new quality (i.e., diabetic urine is qualitatively different form normal urine);
(ii) if the renal mechanism is considered in itself (relation between the renal filter and the composition of blood) disease is only a quantitative variation (i.e., glycosuria is the glucose overflowing a given threshold) (78).
(b) alkaptonuria (rare inherited genetic disorder in which the body cannot process the amino acids phenylalanine and tyrosine):
(i) in light of the end result, alkaptonuriac urine has a new quality (black colouring);
(ii) in light of the overall process, alkaptonuria can be brought about by a massive absorption of tyrosine (78-9).
“Thus, we have a pathological phenomenon which can be defined in terms of quality or quantity depending on one’s point of view, depending on whether the vital phenomenon is considered in terms of its expression or its mechanism.” (79)
Put differently: a given pathological phenomenon X =
(a) defined in terms of quality iff considered in terms of its expression
(b) defined in terms of quantity iff considered in terms of its mechanism. (!)
However, can we really choose one’s point of view? Shouldn’t scientific pathology, if it is to be scientific, consider real causes and not apparent effects, functional mechanisms and not their symptomatic expressions [= i.e., shouldn’t it prefer (b) over (a)]?
“All of this would be indisputable if physiological functions could
be considered as mechanisms, thresholds as barriers, regulations as
safety valves, servo-brakes or thermostats.” (79)
But is this feasible?
According to C., contemporary medicine [i] no longer thinks that glycosuria is only a function of glycemia, nor [ii] does it believe that the kidney simply prevents the filtration of glucose by means of a constant threshold: “The renal threshold is essentially mobile, and its behaviour, variable, depending on the patients.” (79)
(Counter)examples: (i) In subjects with severe hyperglycemia, glycosuria can be practically non-existent (so-called “pure hyperglycemia”). (ii) In subjects without hyperglycemia, glycosuria can sometimes be demonstrated (so-called “renal glycosuria”). (iii) Two diabetics under the same conditions and with the same glycemia in the morning and on an empty stomach can show variable glycosuria (79-80).
What conclusions can be drawn from this?
1. Conclusion I: introducing the qualitative notion of behaviour
“We are now led to modify the classic scheme, which linked glycosuria to basal disturbance by the sole intermediary of hyperglycemia, by introducing a new articulation between hyperglycemia and glycosuria: ‘renal behaviour’. By speaking of the mobility of the threshold, of renal behavior, a notion is introduced in the explanation of the mechanism of urinary secretion that cannot be entirely translated into analytical and quantitative terms. This amounts to saying that to become a diabetic is to change kidneys, a proposition which will seem absurd only to those who identify a function with its anatomical position. It seems permissible to conclude that by substituting mechanisms for symptoms in the comparison between the physiological and the pathological state, no difference in quality between the two states is eliminated at all.” [!!!]
2. Conclusion II: importance of the living organism taken as a whole
“This conclusion looms larger still when we stop dividing disease into a multiplicity of functional mechanisms gone wrong, and regard it as an event involving the living organism taken as a whole. This is very much the case of diabetes.” (80)[!!!]
Example: The idea that the fundamental disturbance in diabetes is hypoinsulinemia (diabetes mellitus) is the result of several findings: Von Mering and Minkowski’s discovery of experimental diabetes (1889), Laguesse’s discovery of the endocrine pancreas, Banting and Best’s isolation of the insulin (1920).
But – doesn’t this confirm that Bernard was right? No, it does not. Houssay and Biasotti, for instance, showed that the role of the pituitary and the pancreas were antagonistic in metabolism: if pancreas is removed from a healthy dog, he cannot survive for more than 4-5 weeks; however, if the removal of pancreas is combined with the removal of the pituitary, there is a considerable improvement in diabetes. Thus, it would seem that the action of insulin in the metabolism of glucides is not direct, since diabetes can be lessened without the administration of insulin (80-1).
“As far as internal secretions are concerned, as in the case of the nervous system, localizations are ‘privileged’ rather than absolute and what appears to be partial augmentation or diminution is in fact an alteration in the whole.” (81)
For instance (example), Rathery points out that metabolism of glucides depends on numerous factors: “(a) blood vascular glands; (b) the liver; (c) the nervous system; (d) vitamins; (e) mineral elements, etc.”, and that any of those factors can play a role in the development of diabetes (81-2).
C. points out that Bernard’s views are not so much wrong, as inadequate and incomplete (i.e., valid in only limited cases). Why so?
“They stem from the unwarranted extrapolation of a perhaps privileged case and, moreover, from a definition which is clumsy in terms of the point of view adopted. It is correct that certain symptoms are the quantitatively varied product of constant mechanisms of the physiological state.” (82)
Example: hyperchlorydia in the ulcerous stomach: in this case, says C., the mechanism in the state of health and those in the state of disease are the same; however, there’s a catch even here: for the essence of the disease lies not in hyperchlorydia, but rather in the fact that the stomach is digesting itself, which is a state very different from the normal state: “A function could be said to be normal as long as it is independent of the effect it produces. The stomach is normal as it digests without digesting itself. What is true of balance scales is also true of functions: fidelity first, then sensitivity.” (82-3)
Further, the reduction of all pathological cases to the explanatory scheme put forward by Bernard seems very remote.
Example: when a woman suffering from Basedow’s [also: Graves’s] disease (= autoimmune disease that affects the thyroid) breathes into a closed space so that her oxygen consumption and correlatively basal metabolism could be measured, oxygen is always burned according to the chemical laws of oxidation, and it is precisely on this basis that one can calculate the variation in metabolism and term it abnormal:
“It is in this precise sense that there is an identity of the physiological and the pathological. But it could also be said that there is an identity of the chemical and the pathological. It will be agreed that this is one way to make the pathological disappear and not to clarify it. Isn’t this also true of the case where it is declared homogeneous with the physiological?” (83)
In sum, C. points out that Bernard’s theory is valid only in certain limited cases:
“1. as long as the pathological phenomenon is limited to some symptom, leaving aside its clinical context(hyperchlorhydria, hyperthermia or hypothermia; reflex hyperexcitability);
2. as long as symptomatic effects are traced back to partial functional mechanisms (glycosuria in terms of hyperglycemia; alkaptonuria in terms of the incomplete metabolism of tyrosine).” (84)
Yet even when narrowed down to these circumscribed cases, his theory runs into many difficulties. Examples:
(a) hypertension: hypertension is not merely an increase in the physiological arterial pressure, but also includes a profound alteration in the structure and function of the vital organs (heart, blood vessels, lungs, etc.), which constitutes a new way of life for the organism (= new behaviour!);
(b) hypersensitivity to a toxic substance: the latter is not merely a simple quantitative modification of a normal reactivity; first, one must inquire whether we’re not dealing merely with an appearance (of, say, the fact of poor renal elimination); second, one must distinguish between isotoxic tolerance (phenomena are changed only quantitatively) and heterotoxic tolerance (new symptoms emerge in relation to the changed cellular activity).
This can be generalized to all functions in the organism:
“The same is true of functional mechanisms, which can be easily experimented with separately. But in the living organism all functions are interdependent and their rhythms are coordinated: renal behavior can be only theoretically divorced from the behavior of the organism functioning as a whole.” (84)
Bernard focused on metabolic phenomena (diabetes) which were too unilateral to be generalized without some arbitrariness (84-5).
Example: Infectious disease: How could infectious diseases be explained in the framework of Bernard’s ideas? [i] The theory of inconspicuous infections [cf. also], promulgated by Charles Nicolle, or [ii] the terrain theory, advocated by Antoine Bechamp would allow the claim that infectious diseases have their roots in so-called normal state. But this widespread opinion is far from being unassailable:
[@ i] “It is not normal for a healthy subject to have diphtheria bacilli lodged
in his throat, in the same sense that it is normal for him to eliminate phosphates in his urine or contract his pupils when passing quickly from the dark into the light.” That is to say, a disease in a state of suspension or remission, is not a normal state.
[@ii] Even if it is a good idea to bear in mind the importance of the terrain(as Pasteur himself proposed) one should not too easily dismiss a microbe as an epiphenomenon: “It takes one last fragment of crystal to obtain the solidification of a supersaturated solution. Strictly speaking, it takes a microbe to make an infection.”
“It seems difficult to assert that the infectious state produces no real discontinuity in the history of the living being.” (85)
Example: Nervous disease: N. D. also doesn’t sit well with Bernard’s principles. For a long time, N. D.’s were described in terms of exaggeration and deficiency. This was also the tiđme when higher cognitive functions were considered as the sums of elementary reflexes and the brain centers as pigeon holes for images or impressions (85). In such a theoretical framework a quantitative interpretation of pathology seemed inevitable (85-6). However, the approaches of John Hughlings Jackson, Henry Head, Charles Scott Sherrington and, more recently, Kurt Goldstein altered the course of research and erected a framework in which facts took on a “synthetic qualitative value”. In this view, an act of a normal person must not be linked to an analogous act of a sick person without gaining insight into the sense and value of the pathological act for the possibilities of existence of the modified organism as a whole (86).
Conclusion: “In short, the continuity of the normal state and the pathological state does not seem real in the case of infectious diseases, no more than homogeneity in the case of nervous diseases.” (86)
Summary of Bernard’s contribution to the discussion of health-disease:
According to C., Bernard formulated the profound need of an era which believed in the omnipotence of a technology founded on science and which felt comfortable in life. Medicine as an art of living implied a science of life: efficient therapeutics assumes experimental pathology, which in turn cannot be divorced from physiology (86-7).
“But must it be deduced from this, with brutal simplicity, that life is the same in health and disease, that it learns nothing in disease and through it? The science of opposites is one, said Aristotle. Must it be concluded from this that opposites are not opposites?” (87)
Making this point succinctly:
“It is understood that medicine needs an objective pathology, but research which causes its object to vanish is not objective.” (87) [!]
“An organism’s behavior can be in continuity with previous behaviors and still be another behavior. The progressiveness of an advent does not exclude the originality of an event.” (87) [!]
On the distinctness of pathology/sickness:
“In the final analysis, would it not be appropriate to say that the pathological can be distinguished as such, that is, as an alteration of the normal state, only at the level of organic totality, and when it concerns man, at the level of conscious individual totality, where disease becomes a kind of evil? To be sick means that a man really lives another life, even in the biological sense of the word.” (87-8)
Example: diabetes (again): It is not a kidney disease (due to glycosuria) nor a pancreatic disease (due to hypoinsuinemia) nor a pituitary disease; instead,
“it is the disease of an organism all of whose functions are changed, which is threatened by tuberculosis, whose supperated infections are endless, whose limbs are rendered useless by arteritis and gangrene; moreover, it can strike man or woman, threaten them with coma, often hit them with impotence or sterility, for whom pregnancy, should it occur, is a catastrophe, whose tears – O, irony of secretions! – are sweet.” (88)
There is a certain artificiality in breaking a disease into symptoms, for what is a symptom without context or background? When an isolated symptom is termed pathological it is often forgotten that what makes it so is its inner relation to the totality of individual behaviour:
“Pathology, whether anatomical or physiological, analyzes in order to know more, but it can be known as pathology, that is, as the study of the mechanisms of disease, only insofar as it receives from clinical practice this notion of disease, whose origin must be sought in the experience men have in their relations with the whole of their environment.” (88)
But here, another issue crops up, namely the relationship between the physician and the patient. For, if our previous reflections were correct, how come the modern clinician more readily adopts the point of view of the physiologist than that of the sick person? C. maintains that this is so because of the fact that subjective morbid symptoms and objective symptoms rarely overlap (88-9):
“[Example:] It is simply capricious for a urologist to say that a man who complains of his kidneys is a man who has nothing wrong with his kidneys. For [i] the sick man the kidneys are a cutaneous-muscular territory in the lumbar region, while for [ii] the physicianthey are vital organs connected to others. The well-known fact about reported pains, whose multiple explanations have been very obscure up to now, prevents one from thinking that the pains experienced by the sick man as major subjective symptoms bear a constant relation to the underlying organs to which they seem to call attention. But most of all, the often prolonged latency of certain degeneracies, the inconspicuousness of certain infestations or infections lead the physician to regard the direct pathological experience of the patient as negligible, even to consider it as systematically falsifying the objective-pathological fact. Every physician knows, having learned it occasionally to his embarrassment, that the immediate sensible awareness of organic life in itself constitutes neither a science of the same organism nor infallible knowledge of the localization or date of the pathological lesions involving the human body.” (89)
This, says C., is perhaps why, until now, pathology has retained so little of that unique character which disease has for the sick man – of being truly another way of life. But note:
“Certainly pathology is correct in suspecting and rectifying the opinion of the sick man who, because he feels different, thinks he also knows in what and how he is different. It does not follow that because the sick man is clearly mistaken on this second point, he is also mistaken on the first. Perhaps his feeling is the foreshadowing of what contemporary pathology is just beginning to see, namely that the pathological state is not a simple, quantitatively varied extension of the physiological state, but something else entirely.” (89) [!]
Presenter: Barbara Borovšak