Alcohol: A Dangerous and Unnecessary Medicine, How and Why by Martha Meir Allen (warren buffett book recommendations txt) π
"It sloweth age, it strengtheneth youth, it helpeth digestion, it cutteth phlegme, it cureth the hydropsia, it healeth the strangurie, it pounces the stone, it expelleth gravel, it keepeth the head from whirling, the teeth from chattering, and the throat from rattling; it keepeth the weasen from stiffling, the stomach from wambling, and the heart from swelling; it keepeth the hands from shivering, the sinews from shrinking, the veins from crumbling, the bones from aching, and the marrow
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The economic loss to a people from beer and wine drinking is worthy of serious consideration since a bottle of wine or its equivalent in beer could diminish by ten to fifteen per cent. the amount of work done by these type-setters experimented upon by Professor Aschaffenberg.
Professor Kraepelin says:β
βI must admit that my experiments, extending over more than ten years, have made me an opponent of alcohol.β
He says again:β
βThe laborer who wins his livelihood by the working power of his arm strikes at the very foundation of his power by the use of alcohol.β
Professor Aschaffenberg says of moderate doses:β
βAny quantity of alcohol must be regarded as considerable which causes a disturbance, even if only transitory, of bodily and mental efficiency.β
Dr. Reid Hunt, chief of the Division of Pharmacology, Hygienic Laboratory, United States Public Health and Marine Hospital Service, made some very interesting experiments to determine the physiological changes upon animals which would result from the strictly moderate use of alcohol. These are described in Bulletin No. 33 of the Hygienic Laboratory, published in 1907. Mice and guinea-pigs were used. The food, usually oats, was soaked in diluted alcohol, at first of five per cent. strength, then gradually increased to forty or fifty per cent. By carefully observing the weight of the mice, and not increasing the strength of the alcohol too rapidly, it was possible to keep the animals for months on this diet without any material loss of weight. After the lapse of weeks, in some cases, and months in other cases, these alcohol fed animals were given small doses of a poison known as acetonitrile. Other mice to whom no alcohol was fed were given similar doses of this poison. In the first series the mice which had received alcohol died from about one-half the quantity of acetonitrile required to kill those which had not received alcohol. In the second series with a somewhat stronger dilution the alcohol mice succumbed to one-half to one-third the dose necessary to kill the non-alcoholized animals. In no case was enough alcohol given for any symptoms of intoxication to appear, nor was there any outward indication of any injury being done by the alcohol. In another experiment a mouse was kept for four months on a diet of oats soaked in water, then 0.5 milligram of acetonitrile per gram body weight was injected. The mouse recovered. It was then fed on oats soaked in an alcoholic solution which was gradually increased to 45 per cent. After a little more than a month of this diet 0.2 milligram acetonitrile per gram body weight proved fatal. The weight of the mouse had remained about the same throughout.
Alcohol increased the susceptibility of the guinea pigs also.
Dr. Hunt says on page 33 of the bulletin:β
βThese experiments with alcohol and acetonitrile are of interest in another connection. The greatest advance in recent years in our knowledge of the physiological action of alcohol has been the clear demonstration that alcohol is oxidized in the body, and may replace fats and carbohydrates and to a certain extent, the proteids of an ordinary diet. So clear has been this demonstration that the view that alcohol, in moderate amounts, should be regarded as a food is almost universally accepted by physiologists, and the drift of opinion is certainly toward the view that it is in all respects strictly analogous to sugar and fats, provided always that the amount used does not exceed that easily oxidized by the body. Under these premises it would be expected that alcohol in a diet would have the same effect upon an animalβs susceptibility to acetonitrile as has dextrose, for example. This is by no means the case, however; on the contrary, the action of these substances in this regard is entirely different. Mice fed upon oats soaked in a solution of dextrose or upon cakes containing considerable dextrose, or upon rice, show a very distinct increase in their resistance to acetonitrile; such mice may recover from two or three times the dose fatal to controls. (Controls are the animals fed in the ordinary way without alcohol or in this case dextrose.βEd.) While these facts are not sufficient to justify the conclusion that in many cases alcohol has not a true food value, yet they are sufficient to indicate caution in applying, without further consideration, the brilliant and very exact results on the proteid sparing power of alcohol to practical dietaries.β
Various other experiments were made, but there is not room here for a record of them.
In the summary Dr. Hunt says:β
βIt is believed that these experiments afford clear experimental evidence for the view that extremely moderate amounts of alcohol may cause distinct changes in certain physiological functions, and that these changes may, under certain circumstances, be injurious to the body. The results also afford further evidence that in some respects the action of alcohol as a food is different from that of carbohydrates, and finally that in all probability certain physiological processes in βmoderate drinkersβ are distinctly different from those in abstainers.β
Professor Chittenden, of Yale University, has made extensive researches upon alcohol and digestion. A full report of these may be found in the βPhysiological Aspects of the Liquor Problem.β In the Medical News, vol. 86, page 721, Professor Chittenden says of the theory that alcohol is a food similar to sugar and fats:β
βIt is, I think, quite plain that while alcohol in moderate amounts can be burned in the body, thus serving as food in the sense that it may be a source of energy, it is quite misleading to attempt a classification or even comparison of alcohol with carbohydrates and fats, since, unlike the latter, alcohol has a most disturbing effect upon the metabolism or oxidation of the purin compounds of our daily food. Alcohol, therefore, presents a dangerous side wholly wanting in carbohydrates and fats. The latter are simply burned up to carbonic acid and water, or are transformed into glycogen and fat, but alcohol, though more easily oxidizable, is at all times liable to obstruct, in some measure at least, the oxidative processes of the liver, and probably of other tissues also, thereby throwing into the circulation bodies such as uric acid, which are inimical to health; a fact which at once tends to draw a distinct line of demarcation between alcohol and the two non-nitrogeneous foodsβfat and carbohydrate.β
Dr. S. P. Beebe, now of the Cornell Medical College Laboratory, New York City, has made some very valuable experiments with alcohol. It is well known that impairment of the functions of certain organs results in the appearance in the urine of nitrogeneous compounds which do not normally occur there. In certain diseases of the liver the same quantity of nitrogen may be excreted as in health, but a portion of it is in the form of acids never found in the urine during health. Dr. Beebe, with this knowledge in mind, sought to discover the effects of alcohol upon the excretion of uric acid in man. Most of the experiments were made on the same person, a young man in good health, of regular habits, unaccustomed to the use of alcohol in any form. Absolute alcohol, diluted with water, whisky, ale, and port wine were used at different times. Dr. Beebe reported his experiments in the American Journal of Physiology, vol. 12, No. 1. His conclusions are given as follows:β
βAfter a consideration of these experiments, it hardly seems possible to doubt that alcohol, even in what is considered by the most conservative as a moderate amount, causes an increase in the excretion of uric acid, and this effect is seen almost immediately after taking the alcohol. The following points indicate that the effect is due to a toxic effect on the liver, thereby interfering with the oxidation of the uric acid derived from its precursors in the food: Alcohol taken without food causes no increase. The maximum increase occurs at the same time after a meal as it does when purin food but no alcohol is taken. Alcohol is rapidly absorbed and passes at once to the liver, the organ which has most to do with the metabolism of proteid cleavage products.
βThere is no evidence that the alcohol has merely hastened the excretion of urates normally present in the blood; the increased excretion means that a larger quantity has been in circulation, and although it is classed by Van Noorden among the substances easily excreted, still most physiologists would consider the presence in the blood of this larger quantity as undesirable. Certainly in pathological conditions it might be harmful.
βIf we accept the origin of the increased quantity of uric acid to be in the impaired oxidative powers of the liver, the results of these experiments will have greater significance than can be attributed to uric acid alone. For the impaired function would affect other processes which are normally accomplished by that organ, and the possibilities for entrance into the general circulation of toxic substances, of intestinal putrefaction, for instance, would be increased. The liver performs a large number of oxidations and syntheses designed to keep toxic substances from reaching the body tissues, and if alcohol, in the moderate quantity which caused the increase in uric acid excretion, impairs its power in this respect, the prevalent ideas regarding the harmlessness of moderate drinking need revision.β
Dr. Winfield S. Hall, professor of physiology at the Northwestern University Medical School, Chicago, has interpreted these researches of Beebe and Hunt in a very striking way. He says that they prove that the oxidation of alcohol in the body is a protective oxidation, the same as the oxidation of any other poisonous substance by the liver. His views have such an important bearing upon the commonly accepted theory that alcohol is in some sense a food that they are given here, somewhat abbreviated, as a fitting finish to this chapter. Dr. Hall says:β
βThe fact that alcohol is oxidized in the body has been generally misunderstood. The first impression naturally was: βFoods are Oxidized; Alcohol is Oxidized; therefore alcohol is a food.β But many difficulties appeared. A real food promotes muscular, glandular and nerve activity, and its oxidation maintains body temperature. But alcohol disturbs muscular, glandular, and nervous activity, and its oxidation does not maintain body temperature. When one eats a real food it is assimilated largely by muscle tissue and is oxidized for the purpose of liberating the life energy. When one ingests alcohol it is carried by the blood to the tissues, mostly to the liver, where it is oxidized, as any toxine would be, for the purpose of making it harmless. Its oxidation liberates heat energy but this energy cannot be utilized by the body even for the maintenance of body temperature. If a food is defined as a substance which, taken into the body, is assimilated and used either to build or repair body structure, or to be oxidized in the tissues to liberate the energy used by the tissue in its normal activity, then alcohol is not a real food.
βBut, if alcohol is not a real food, what is the significance of its oxidation? It has been long known that the liver produces oxidases and that it is the site of active oxidation of mid-products
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