Type 2 Diabetes

https://dlcs.io/pdf/wellcome/pdf-item/b2106331x/0

https://www.longdom.org/open-access/court-of-last-appeal--the-early-history-of-the-highfat-diet-for-diabetes-2155-6156-1000696.pdf

In Two Cases of the Diabetes Mellitus, Rollo and Cruickshank described the treatment of two patients suوٴering from glycosuria, polyuria and polydipsia with a combination of organic and inorganic salts and a diet restricted in vegetable food, and made largely of meat and fat [1]. Нis was based on the observation that, while both animal foods and vegetable foods are nutritious and will support life, glucose, found in the urine of patients with diabetes and therefore obviously connected to the disease, can be found in large quantities in vegetable foods but only in trace amounts in meat and fat. Нe diet was eوٴective for one of Rollo’s patients, but not the other. Redfearn subsequently published a report of the successful application of Rollo’s method in his own patient [2] and Rollo’s supporter John Latham published many case studies of the diet in his 1811 book Facts and Opinions Concerning Diabetes [3]. Rollo’s method seems to have become widely disseminated; circa 1830 the American adventurer Josiah Harlan, who had taught himself medicine from a popular encyclopaedia, prescribed an animal matter diet to a client in the Punjab, with what results we do not know, according to Ben MacIntyre’s life of Harlan, Нe Man Who Would be King [4]. Нe inconsistent response to the diet seen in Rollo’s first two cases, and in the cases of Latham, can be explained by its high protein content. In the later researches of Woodyatt and others, protein has a glucose value of 58%, due to a high proportion of gluconeogenic amino acids. Hadden gives an analysis of Rollo’s diet for patient 1, Captain Meredith, as supplying 160 g carbohydrate, 136 g protein and 135 g fat [1]. Нus only 50% of the energy from this diet is in the form of the nutrient, fat, which has the lowest requirement for insulin; nor is the diet as low in carbohydrate (from bread and milk, and later, when Captain Meredith returned to Ireland, potatoes) or as permissive with regard to non-starchy vegetables as modern thought would recommend. Captain Meredith lived another 15 years aіer adopting Rollo’s diet, dying in Newfoundland at the age of 49 - according to Hadden, death was probably due to macrovascular complications

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"I have now brought the history of Diabetes down to that period when Dr. Rollo first published his celebrated Treatise, a work which ought to be in the hands of every practictioner who is anxious for the fullest information upon the subject.: a work which, like the discovery of sugar in Diabetic Urine, equally marks an important area in this disease: a work which teaches us to cure what Willis taught us only to know, and which will convey his name, with that of his learned predecessor, down with honor to the latest posterity. And let not any thing which may occur in the following pages be construed to detract from that honorable distinction to which he is so justifly entitled; for his observations on the absolute necessity of a pure animal diet will stand the test of experience, when speculations, with respect to medicine in this disease, by every physician who has hitherto existed, (and even those by Dr. Rollo himself) may probably be altogether neglected and forgotten: I must refer the reader to the work itself, which in its more enlarged form is, if possible, rendered much more important by the many communications therein made from a great number of very ingenious correspondents."

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"so that not only may it exist where little of vegetable nutriment has been taken, and consequently where but little sugar can be produced, but where animal matter has alone been eaten:"

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Though Bouchardat (1806-1886) read his first memoir to the Academy of Sciences in 1838, and the final edition of his book appeared in 1875, he came into prominence through important contributions in the decade 1840 to 1850. Like Rollo and all other founders of the dietetic treatment, he considered diabetes a disease of digestion. According to his theory, normal gastric juice has no action upon starch, which is digested in the intestine; but in diabetes, an abnormal ferment digests starch in the stomach, and glycosuria, polyuria, and other symptoms result. He claimed to demonstrate the presence of diastase in the vomitus of diabetics and its absence in that of normal persons. Hypertrophy of the stomach and atrophy of the pancreas in diabetic necropsies were also held to support his theory; and he was thus the first to suggest an influence of the pancreas in the causation of diabetes, and the originator of the attempt to produce it by pancreatectomy in dogs. For sugar determination in urine, he used fermentation, the polariscope, and the Frommherz copper reagent. By the fermentation method he showed the presence of sugar in diabetic blood, but found none in normal blood. At how low an ebb was the Rollo treatment at this time is shown by the pleading and arguments of Bouchardat. He begs all friends of truth to hear him; whatever be the original cause of glycosuria, diabetics, who otherwise all die, are actually saved when his dietetic treatment is used. 

Bouchardat in the clinical field ranks with Claude Bernard in the experimental field. He is easily the most brilliant clinician in the history of diabetes. He resurrected and transformed the Rollo treatment, and almost all the modern details in diabetic therapy date back to Bouchardat. He was first to insist on the need of individualizing the treatment for each patient. He disapproved the rancid character of the fats in the Rollo diet, but followed an intelligent principle of substituting fat and alcohol for carbohydrate in the diet. He forbade milk because of its carbohydrate content. He urged that patients eat as little as possible, and masticate carefully; also (1841) he inaugurated the use of occasional fast-days to control glycosuria. Subsequently he noted the disappearance of glycosuria in some of his patients during the privations of the siege of Paris. 

Though the introduction of green vegetables is credited by Prout to Dr. B. H. Babington, the honor of thus successfully breaking the monotony of the Rollo diet, properly belongs to Bouchardat. He recommended them as furnishing little sugar, a little protein and fat, but especially potassium, organic acids, and various salts. He also devised the practice of boiling vegetables and throwing away the water, to reduce the quantity of starch when necessary. As a similar trick he "torrefied" (i.e., charred and caramelized) bread to improve its assimilation; possibly this is the origin of the widespread medical superstition that diabetics may have toast when other bread must be forbidden. He invented gluten bread; this started the idea of bread substitutes, from which sprang the bran bread of Prout and Camplin, Pavy's almond bread, Seegen's aleuronat bread, and the numerous later products. 

Bouchardat also first introduced the intelligent use of exercise in the treatment of diabetes, and reported the first clinical experiments proving its value. He showed that carbohydrate tolerance is raised by outdoor exercise; and to a patient requesting bread, he replied: "You shall earn your bread by the sweat of your brow." 

There is a modern sound to his complaints of the difficulties of having treatment efficiently carried out in hospitals, of the lack of adequate variety of suitable foods, of deception by patients, and of how, even when improved in hospital, they break diet and relapse after returning home. He advocated daily testing of the urine, to keep track of the tolerance and to guard against a return of sugar without the patient's knowledge. 

He followed Mialhe in giving alkalies, viz. sodium bicarbonate up to 12 to IS gm. per day, also chalk, magnesia, citrates, tartrates, soaps, etc., also ammonium and potassium salts; he found them often beneficial to the patients but not curative of the glycosuria. He told a patient: "You have no organic disease; there is merely a functional weakness of certain parts of your apparatus of nutrition. Restore physiological harmony and you will attain perfect health." 

He used glycerol for sweetening purposes, and introduced both levulose and inulin as forms of carbohydrate assimilable by diabetics, for reasons which well illustrate his intellectual keenness. On giving cane sugar to diabetics, he had found only glucose excreted. Was the levulose utilized or changed into glucose? Levulose proved under certain conditions to be more easily destroyed in vitro than glucose. Accordingly he gave levulose and inulin to diabetics, and found no sugar in the urine. Therefore he recommended levulose for sweetening purposes, and inulin-rich vegetables for the diabetic diet.

Main Works:

• Manuel de matière médicale de thérapeutique et de pharmacie, (1838, fifth edition 1873) – Materia medica manual of therapeutics and pharmacy.

• Eléments de matière médicale et de pharmacie (Paris 1839) – Elements of materia medica and pharmacy.

• Nouveau formulaire magistral, etc. (1840, 19th edition 1874).

• De la glycosurie ou Diabète sucré son traitement hygiénique, Paris, (1875, second edition 1883) – On glycosuria or diabetes mellitus and its hygienic treatment.

• Traité d'hygiène publique et privée basée sur l'etiology, 1881 – Treatise on public and private hygiene, based on etiology.[2]

The First Case of Diabetic Retinopathy 

(Eduard von Jaeger, Vienna 1853) by FRANZ FISCHER 

We have before us the plates and documentation of a case of retinitis (retinopathy) in diabetes mellitus, the first of its kind. It derives from the Beitrage zur Pathologie des Auges by Eduard von Jaeger for the year 1855. That it was the first such case we have the best guarantor, Theodor Leber. In 1875, he collected the cases from the literature - there were 19 in all, of which Jaeger's case was the first - and coined the term retinitis diabetica. So characterized, Jaeger's case wanders through the literature. After Leber he found no-one more appreciative. We thought it stimulating as well as conducive to the continuity of research to exhibit this case. 

It is no accident that the observation was made in Vienna, and made by Eduard von Jaeger. In the second half of the 18th century and subsequently, Vienna was very fruitful medical soil, a place where the new seed of ophthalmology could flourish. We see Joseph Barth, the gifted individualist, Georg Joseph Beer (first professor, 1818), the first teacher and founder of scientific ophthalmology, Friedrich Jaeger, Ritter von Jaxtthal (Eduard's father), Professor at the military medical Joseph's Academy (Josephinum), the most sought-out eye-surgeon in Europe. In the so-called II Vienna Medical School, Eduard von Jaeger with Ferdinand von Arlt and K. Stellwag von Carion was an outstanding champion of the specialty. As the son of Friedrich von Jaeger and grandson of the great Joseph Beer, Eduard von Jaeger had glittering prospects. 

Nevertheless, and with all his personal accomplishment, he was denied what he felt to be his heart's desire: only at the age of 65 did he become Professor at the II Ophthalmic Clinic, Vienna, not long before his death (5 July, 1884). His main creative work lay in ophthalmoscopy. The best witnesses on his account are two competent ophthalmologists: Ludwig Mauthner (in the obituary): "Eduard von Jaeger's career is inextricably bound up with the history of the ophthalmoscope. He was one of the first who turned Helmholtz's discovery to practical use. He also produced an improved form of Helmholtz's instrument very soon for everyday practice. Eduard von Jaeger was the greatest ophthalmologist the world had yet seen." Then Maximilian Salzmann (in the preface to the reworked Atlas of 1890): "The time has its expectations, which Eduard von Jaeger, linked with the appearance of his Atlas has satisfied in full measure. His work is recognized as the most important in the field of ophthalmoscopy and has become a foundation on the basis of which numerous young doctors have been introduced into this important oculists' discipline." So much for the environment and personality of our author. 

And now for the case. The description begins as follows: "The gardener Wilhelm W., then 22 years old, of slender physique and medium height, had always been healthy and strong in childhood and adolescence. However, 4 years previously, through catching cold, he developed a disorder which repeatedly kept him in bed with slight fever and swelling of the right foot, loss of strength and appearance. As this continued, the phenomenon of a diabetes emerged, coupled with marked anorexia, dry throat, frequent vomiting after eating and feelings of great decline and weakness. For a short time the patient had also complained of frequent cough with much sputum and feelings of oppression and pressure in the chest. " 

We now shorten this account. 5 weeks before he had experienced a disturbance of vision: transient seeing of flashes and "slight clouding of the outer half of the visual field in the left eye". The clouding had spread to the other eye and was increasing. The sight in the left eye had temporarily improved. The disorder had steadily increased. It is stated: "The patient presently appears very ill and low, is thin and has a sallow complexion." Then a "disturbance of the visual field in the middle" with reduction of visual acuity is described. Passing to the ophthalmoscopic findings: The media had appeared quite transparent and normal. The peripheral parts of the fundus were free from lesions. 

On the other hand, the site and vicinity of the transverse section of the optic nerve (in the extent of the extravasate illustrated in the picture) is dull in color, less translucent, more blood-red, and the optic nerve cross-section is so completely covered by the aforesaid color change as to be no longer perceived and can only be recognized by the union of the retinal vessels. 

"Anomalous redness of the optic fundus" and "radiate spreading of the optic fibers in the vicinity of the optic nerve" were reported. Then it states: "In the region of this anomalous coloring of the optic fundus there are to be perceived a considerable number of apparently uniformly distributed blood-red flecks, some punctate, some striate or otherwise shaped, of the most various size, which seem to lie in the plane of the retinal vessels, i.e., deep to the retina, are predominantly elongated, and whose arrangement and orientation correspond partly to the optic expansion and partly to the paths of the retinal vessels, particularly the veins. Between the flecks, at some distance from the optic disc, there also appear numerous irregular, rounded, light-yellow spots whose brightness makes them very obvious." 

It then states that the retinal vessels in the region of the optic disc were hazy. The arteries showed an especially brilliant media. The diameters of the arteries and veins were significantly increased above normal. The description ends as follows: "The left eye exhibits objectively and subjectively exactly the same appearances, though to a lesser degree and the patient is still capable with its aid of getting about in the street and even doing some work as a gardener." 

We note that plate and text are quite consistent. The text, based on the author's principle, is descriptive, not explanatory. The illustration is quite true to life and free from any exaggeration. The lithography and color printing, carried out by the Imperial and Royal Court and State Press in Vienna is an amazing technical achievement for a hundred years ago. 

What was Eduard von Jaeger describing? At the fundus: an edema of the optic disc and adjacent retina, streaked and radially arranged hemorrhages at some distance from the disc, light-yellow spots, to be explained later, as essential features. The question whether this complied with the concept of diabetic retinitis (retinopathy), then and now, may be answered as follows. Th. Leber (1875) remarked of Jaeger's case that it resembled the retinitis occurring in albuminuria. Later, the edema (with the star figure in the macula) were counted as characteristics of albuminuric (nephritic, angiospastic) retinitis as against diabetic retinitis. What can we say today? Diabetic retinopathy embraces a whole range of retinal lesions: "blood-spots (anatomically: capillary aneurysms) at the outset, hemorrhages and white degenerative foci subsequently, and finally vascular and connective tissue proliferation, vitreous hemorrhage, retinal shrinkage, etc. (retinitis proliferans), though these stages are not always observed. As always with retinopathy, the edema is not part of the fundus picture. It is the view of not a few workers today that, when an edema appears, the case is one of nephritic and not diabetic retinopathy. We believe, however, that diabetic retinopathy can, exceptionally, imitate nephritic retinopathy. Edema formation is shown especially by young diabetics, as confirmed by R. Thiels and our own observations. Frankly, we cannot share Thiels' view (1956) that this depends on the special nephropathic forms of diabetes, the KimmelstielWilson glomeruloscleroses. The fact that most Kimmelstiel-Wilson cases are heralded by retinopathy without edema formation is an argument against. Therefore nothing prevents us from acknowledging Jaeger's case as one of true diabetic retinopathy, despite any similarity with albuminuric retinitis. Jaeger's case admits of another interpretation. The indistinct disc, the numerous radially arranged hemorrhages, the markedly reduced visual acuity - all are very suggestive of a thrombosis of the central vein of the retina. This is not at all an uncommon event in older diabetics (with advanced arteriosclerosis), in any case commoner than in non-diabetics; in young diabetics it was unknown. Now, J. Dietzel and P. White have recently observed a central vein thrombosis in a young diabetic, followed by a retinitis proliferans in the other eye. This demonstrates that the angiopathy specific to diabetes (and not just the usual arteriosclerosis) is capable of producing such a picture. Jaeger's case in a 22-year-old diabetic could be interpreted in this sense; but, frankly, the fundus picture is not at all consistent and the appearance in both eyes arouses doubts. The possibility exists. Now for the "rounded light-yellow spots" in our fundus picture. That this referred to the usual retinal degenerative foci we believe can be dismissed without more ado. K. vom Hofe was the first (1938) to point out the frequency of such a finding in diabetic retinopathy, and we confirm this from our own experience. It only surprises us how little awareness of this there was until now. Vom Hofe interpreted the picture as lipid infiltration of the deep retinal layers or choroid and proved correct. For the picture certainly is not related to "choroiditis in diabetic retinopathy" as we have recently described it. How accurate, then, were Jaeger's observations!

 If we leave the fundus picture: the patient's age of 22 years leads to the following remarks. Until some 10 years ago, diabetic retinopathy below 40 years of age was an absolute rarity. Thus we find in a world-famous textbook of ophthalmology of 1935 that only a single case is quoted from the literature. A marked change has occurred here. The number of young diabetics is large and steadily increasing, due to insulin and other modern treatment. The young diabetic is becoming older and now experiences its vascular complications, notably nephropathy and retinopathYi at the age of 30 or 40, he is confronted with a gloomy fate. For us, this is the main problem of diabetes mellitus today. On the other hand, the practicality of oral treatment of diabetes is fading. 

And now back to Jaeger's case. At that time, and for one of his age, he was certainly a rarity. And it should be considered that in the pre-insulin era young diabetics died off very quickly without exception from comai young diabetics did not live to experience vascular complications. As for the duration of the diabetes - in our case barely longer than 5 years - the following may be noted. As far back as 1858, Albrecht von Graefe was struck by the fact that the ocular disorders in diabetes mellitus belonged to "an advanced stage of the general disease". It required intensive research up to our own time to reveal the role of the duration of the diabetes in the development of retinopathy. 

Today, many workers, notably Dolger (USA) adopt the standpoint that every diabetic will experience the "vascular complications" of nephropathy, retinopathy, etc., if he lives long enough, for 20 years or more. On the other hand, Joslin's school in the USA advances the view that the vascular complications can be prevented or at least postponed by precise management of the diabetes from the outset without interruption, with proper treatment and surveillance. The advocates of the "free diet" (which actually is not a free diet) for diabetic children and adolescents rather incline to Dolger's view. We ourselves acknowledged Joslin's requirements in various articles though, like other authors, we were well aware that in by no means a few cases, and despite the best monitoring of the diabetes, a retinopathy (and nephropathy) develops after quite a short duration of the diabetes, while others remain unaffected despite continuously poor monitoring and overlong duration of the disease (30 or more years). We sought to explain the "bad" cases by a special penetrating power of the diabetes on an unherited basis. 

We are further of the opinion that, not only the diabetes as such, but also the associated vascular constition are inherited, and in a decisive manner. On this, the findings have yet to be made known. Jaeger's case, with its relatively short duration of diabetes, therefore also falls outside the rule in this respect and requires a special explanation, as given above. What does the case tell us otherwise? We may pass over the classical diabetes symptoms. Nothing is said relating to albuminuria or nephritis. Th. Leber felt this as a defect in the completion of his task. Thanks to the exact illustration, we can say with fair certainty that a nephropathy did exist, indeed in the uremic end-stage. This is not surprising, since we know how much alike are diabetic retinopathy and nephropathy, both clinically and pathologically; and it is just in young diabetics that nephropathy, as Kimmelstiel-Wilson's glomerulosclerosis, runs a deleterious course. 

That the report contains nothing about the blood-pressure only evokes the late development of blood-pressure measurement. A hypertension would not be surprising; according to our findings, it is associated just like the nephropathy with the retinopathy of young diabetics. The disease was ushered in by an infection, as we know well today. We amplify: the course of the diabetes was also unfavorably influenced by infection. Unfortunately, the eradication of focal sepsis has been pushed into the background in modern diabetes treatment. The description even suggests pulmonary tuberculosis. Over and again, this disease plays a noteworthy yet too little noted role in juvenile diabetes, being the second cause of death after uremia. 

We may conclude: The case reported by Eduard von Jaeger in 1855 is unusual as regards age, duration of diabetes and fundus findings. It withstands any check by current standards. We are right to see in it the first observation of diabetic retinopathy. The strictly scientific approach of the author has saved the case from oblivion. Yet it is quite remarkable that our acquaintance with diabetic retinopathy should have begun in such an unusual way. And what is even stranger is that in Jaeger's case we encounter the problem case of diabetes mellitus today. Eduard von Jaeger published this case in his Beitriigen zur Pathologie des Auges (1855-1856). 

Just listen, in conclusion, to what our historian, J. Hirschberg, writes on this: "No sacrifice for science was too heavy for him. For his wonderful Contributions to the Pathology of the Eye he plunged into a debt of 20,000 gulden, which he gradually paid off from his earnings." Such was Eduard von Jaeger. May he be a model to all young ophthalmologists!

 Summary 

The priority of the case is certified by Th. Leber (1875). That the observation was made in Vienna and by Eduard von Jaeger (1855) is not a matter of chance. Though this case of diabetic retinopathy is unusual in many respects, the diagnosis is beyond doubt and satisfies any check. The author's comprehensive and very factual approach gives us cause, even today, for valuable inferences and reflections, and not only as regars the fundus appearances. The spirit of a true natural scientist reveals itself. 

References 

F. Fischer: Probleme der diabetischen Retinopathie. Klin. Mbl. f. Augenheilkunde 125 (1954): 666 - Einst und jetzt. Die historische Entwicklung der Retinopathia diabetica. Miinchner med. Wschr. 44 (1954)1287. - Die Retinopathie des jungen Diabetikers (unter 40 Jahren). Graefes Arch. 1957. - J. Hirschberg: Geschichte der Augenheilkunde. In Handbuch Graefe-Saemisch, Bd. XV, 1916. - Eduard von Jaeger: Beitrage zur Pathologie des Auges. 2. Lieferung, S. 33, Tafel XII. K. K. Hof- und Staatsdruckerei, Wien 1855. - Th. Leber: Uber die Erkrankungen des Auges bei Diabetes mellitus. Arch. f. Ophthalm. 21, 3 Abtlg. (1875): 206 - Die Krankheiten der Netzhaut. In Handbuch Graefe-Saemisch, Bd. VII12 (1914): 969. -1. Mauthner: Eduard von Jaeger. Wiener Med. Wschr. 28 (1884): 878 - Th. Puschmann: Die Medizin in Wien wahrend der letzten 100 Jahre. M. Pedes, 1884. - M. Salzmann: Ophthalmoskopischer Handatlas von Eduard von Jaeger, neubearbeitet und vergr6Bert. F. Deutike, Leipzig und Wien 1890. - L. Schonbauer: Das Medizinische Wien. Geschichte, Werden, Wiirdigung. Urban & Schwarzenberg Berlin und Wien 1944. in: Wiener Medizinische Wochenschrift 107 (1957) 969-972.

 “My patient, Mr. Banting having published for the benefit of his fellow sufferers, some account of the diet which I recommended him to adopt with a view to relieve himself of a distressing degree of hypertrophy of the adipose tissue. I have been frequently urged by him to explain the principles upon which I was enable to treat with success the inconvenient and in some instances distressing condition of the system. 

“The simple history of my finding occasion to investigate the subject is as follows: when in Paris in the year 1856, I took the opportunity of attending a discussion on the views of M. Bernard who was at that time propounding his now generally admitted theory of the liver functions. After he had discovered by chemical processes and physiological experiments, which it is unnecessary for me to recapitulate here, that the liver not only secreted bile, but also a peculiar amyloid or starch-like product which he called glucose, and which in its chemical and physical properties appeared to be nearly allied to saccharine matter, he further found that this glucose could be directly produced in the liver by the ingestion of sugar and its ally starch and that in diabetes it existed there in considerable excess. 

It had long been well known that a purely animal diet greatly assisted in checking die secretion of diabetic urine; and it seemed to follow, as a matter of course, that the total abstinence from saccharine and farinaceous matter must drain the liver of this excessive amount of glucose, aid thus arrest in a similar proportion the diabetic tendency. Reflecting on this chain of argument and knowing too that a saccharine and farinaceous diet is used to fatten certain animals and that in diabetes, the whole of the fat in the body rapidly disappears, it occurred to me that excessive obesity might be allied to diabetes as to its cause, although widely diverse in its development: and that if a purely animal diet was useful in the latter disease, a combination of animal food with such vegetable matter as contained neither sugar nor starch, might serve to arrest the undue formation of fat. 

I soon afterwards had an opportunity of testing this idea. A dispensary patient who consulted me for deafness, and who was enourmously corpulent, I found to have no distinguishable disease of the ear. I therefore suspected that his deafness arose from the great development of adipose matter in the throat, pressing upon and stopping up the eustachian tubes. I subjected him to a strict non-farinaceous and non-saccharine diet, and treated him with the volatile alkali alluded to in his Pamphlet, and occasional aperients and in about seven months he was reduced to almost normal proportions, his hearing restored and his general health immensely improved. The case seemed to give substance and reality to my conjectures, which further experience has confirmed. 

“When we consider that fat is what is termed hydrocarbon, and deposits itself so insidiously and yet so gradually amongst the tissues of the body it is at once manifest that we require such substances as contain a superfluity of oxygen and nitrogen to arrest its formation and to vitalize the system. That is the principle upon which the diet suggested in his pamphlet works, and explains on the one hand the necessity of abstaining from all vegetable roots which hold a large quantity of saccharine matter, and on the other beneficial effects derivable from those vegetables, the fruits of which are on the exterior of the earth, as they lose, probably by means of the sun’s action a large proportion of their sugar. 

“With regard to the tables of Dr. Hutchinson, referred to in his Pamphlet, it is no doubt difficult, as he says, to determine what is a man’s proper weight, which must be influenced by various cases. Those tables, however, were formed by him on the principle of considering the amount of air which the lungs in their healthy state can receive and apply to the oxidation of the blood. I gave them to Mr. Banting as an indication only of what the approximate weight of persons in proportion to their stature should be, and with the view of proving to them the importance of keeping down the tendency to grow fat; for, as that tendency increases, the capacity of the lungs, and consequently the vitality and power of the whole system must diminish. In conclusion, I would suggest the propriety of advising a dietary such as this in diseases that are in any way influenced by a disordered condition of the hepatic functions as they cannot fail to yield in some degree to this simple method of treatment if fairly and properly carried out; it remains for me to watch its progress in a more limited sphere. 

WILLIAM HARVEY, F.R.C.S. 

Surgeon to the Royal Dispensary for Diseases of the Ear 2, Soho Square 

April, 1864 

Griesinger in 1859 published an analysis of 225 cases of diabetes; and though only eight were his own and the others all from the litera ture, his contribution was valuable for clinical experiments and sound judgment. He compiled the first evidence indicating excess in sugars and starches as a cause of diabetes, but concluded that it could not be the most important cause, or many more persons and some entire races would have diabetes. He overthrew various current errors, but somehow convinced himself in painstaking experiments that diabetics may excrete large quantities of sugar in the sweat, as reported by several other authors. From the negative findings in necropsies, he regarded diabetes as generally a functional disorder. His most notable achievement was the demonstration, in three separate experiments on a single patient, of sugar excretion equalling exactly 60 percent of the protein of the diet.“ These facts, remaining constant under varied conditions, cannot be accidental; they seem much more to contain the law of the relation in which, in this individual on exclusive meat diet, the production and excretion of sugar stands to the quantities of ingested meat."