How to Live - Eugene Lyman Fisk (top 100 novels of all time .txt) 📗
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Horsley, Sir Victor: Discussion on Alcohol in Therapeutics, Med. Rec., 1912, LXXI, p. 951. Read before the Hunterian Society.
Hunter, Arthur: Can Insurance Experience be Applied to Lengthen Life? Proceedings of the Association of Life Insurance Presidents, Eighth Annual Meeting, 1914, pp. 27–37.
Kelynak, T. M.: The Drink Problem, London, Methuen & Company, 1907.
Landau, Anastazy: Beitrage zur hehre vom Purinstoffwechsel und zur Frage über den Alkoholeinfluss auf die Harnsaureausscheidung, Deutsch. Arch. f. klin. Med., XCV, 1908–9, pp. 280–328.
Miller, Joseph L.: The Physiologic Action, Uses and Abuses of Alcohol in the Circulatory Disturbance of the Acute Infection, Jour. A. M. A., 1910, LV, pp. 2034–2037. Read in the joint session of the Sections of Practice of Medicine and Pharmacology and Therapeutics of the A. M. A., Sixty-first Annual Session, held at St. Louis, June, 1910.
Neff, Irwin H.: The Problem of Drunkenness, Proceedings of the Fifteenth International Congress on Hygiene and Demography, Washington, 1912, IV, p. 510.
Phelps, Edward Bunnell: The Mortality from Alcohol in the United States, Proceedings of the Fifteenth International Congress on Hygiene and Demography, Washington, 1912, Vol. I, p. 813.
Proceedings: Association of Life Insurance Medical Directors, October, 1911.
Report of the Committee of Fifty on: Physiological Aspects of the Liquor Problem, Houghton, Mifflin & Company, two volumes, 1903.
Togel, O., Brezina, E., and Durig, A.: Ueber die kohlenhydratsparende Wirkung des Alkohols, Biochem. Ztschr., 1913, I, 296; Editorial, Jour. A. M. A., 1913, LXI, p. 967.
Williams, Henry Smith: Alcohol, How it Affects the Individual, the Community and the Race, The Century Company, New York, 1909.
Woods, Robert A.: The Prevention of Inebriety: Community Action, Proceedings of the Fifteenth International Congress on Hygiene and Demography, Washington, 1912, IV, p. 517.
Additional Notes on AlcoholThere has lately been undertaken at the Nutrition Laboratory of the Carnegie Institution at Washington a very broad and comprehensive study of the effect of moderate doses of alcohol on the healthy and normal human body. The immense scope of the investigation planned may be judged by the fact that under the physiological division of the research, as laid out by Professors Raymond Dodge and E. C. Benedict, there are seven main sections and one hundred and sixty subdivisions. The program has been arranged after conferences, either in person or by letter, with the leading physiologists of the world, and may take ten years to complete.
The psychological program, carried out with the co-operation of Dr. F. Lyman Wells, has already been completed and the results recently published.[34] These results must be accepted as the testimony of pure science, free from all bias or even remote suggestion of propaganda. They were based upon experiments with moderate doses of alcohol (30 cubic centimeters, or about 8 teaspoonfuls, and 45 cubic centimeters) upon ten normal subjects, very moderate users of alcohol, and may be summarized as follows:
A very simple reflex act, the “knee-jerk,” a nervous mechanism controlled by a center at the lower level of the spinal cord, was markedly depressed, the time of response being increased 10 per cent. and the thickening of the muscles concerned in the act decreased 45 per cent. In some subjects the larger dose, 45 cubic centimeters, practically abolished the knee-jerk.
The eye-lid reflex, elicited by a sudden noise, showed the next largest effect, the time of response being increased 7 per cent. and the degree of movement decreased 19 per cent.
Other nervous mechanisms, or reflex arcs, at the higher levels of the cord, were next investigated: (1) eye-reaction to suddenly appearing stimulus, and (2) speech reaction to visual word stimuli. Dose A (30 cubic centimeters), accelerated the eye-reaction, while dose B (45 cubic centimeters) positively depressed it, agreeing with the simple reaction experiments of Kraepelin. This was the only instance of acceleration of movement of the voluntary muscles through alcohol, all the other tests showing it to be a consistent depressant. The speech reaction showed a positive depressant effect of 3 per cent.
Free association of ideas and memory tests were also made, and showed practically no effect from alcohol, but, unfortunately, the smaller dose only was used in these tests.
The sensitiveness to electrical stimulation was decreased 14 per cent.
Motor co-ordination, as evidenced by eye-movements in fixating seen objects, was next investigated. The velocity of these movements was decreased 11 per cent. Finger-movements, measured in an exceedingly delicate way, were reduced in speed 9 per cent.
The effect on the pulse while these tests were made was observed, and electrocardiograms taken. The pulse was found to be accelerated, but not increased in force, that is, the “brake” was taken off the heart, but no driving force supplied by alcohol. The condition of the circulation was impaired by the narcotic effect of alcohol on the cardio-inhibitory center which holds the heart action in check.
According to the investigators, the effect is to “decrease organic efficiency.” This should shut off such little debate as still persists with respect to alcohol having any value as a heart stimulant.
While these investigations only confirm in part the contention of the Kraepelin school that alcohol first acts by depressing the higher centers, and tend to show that its first and most profound effect is on the lower levels of the spinal cord and the simpler nervous mechanisms, it confirms the view of these and other investigators, that the total effect of alcohol is that of a narcotic, depressing drug, even in the smallest doses usually taken as a beverage.
The possible reactions are more complex than those supposed by Kraepelin, and there is evident in the higher centers (the effect on highest brain functions, were not measured by Dodge and Benedict) a power of “autogenic reinforcement,” which is well exemplified by the ability of a half-intoxicated person to sober up under some shock or strong incentive. When social conditions do not stimulate this reinforcement, but, on the contrary, dull and retard it, as in convivial company, there is reinforcement of the lower, more animal mechanisms of the nervous system, and we have exhibited revolting and foolish reactions to alcohol, which are consistent with these findings.
The slight effect on memory and free association is explained partly by the methods used in the laboratory (difference in time of recognizing words suddenly exposed a second time), which are more in the nature of “short cuts” and perhaps not so accurate a reproduction of normal memorizing as those employed by Kraepelin and Vogt (memorizing numbers and verse), and partly by the power of “autogenic reinforcement,” which it is difficult to eliminate in a laboratory test.
This, the latest contribution of science to the study of alcohol, gives added proof that the higher mortality among so-called moderate users of alcohol is largely due to the unfavorable effect on the protective mechanism of the body.
This has been further emphasized by the studies of Reich[35] at the University of Munich, who found that the resistance of blood cells to salt solution and to typhoid bacilli was less among alcohol users than among total abstainers.
Konrádi[36] has found that comparatively few antibodies against cholera germs develop in persons who consume alcohol daily in fairly large quantities and who had been inoculated against cholera. Pampoukis[37] has observed that alcoholics are not favorable subjects for inoculation against rabies. The Pasteur Institute in Budapest has made similar observations, based on twenty-five years’ experience.
Additional References[34] Benedict, E. C.: The Psychological Effects of Alcohol, The Carnegie Institution, Washington, D. C., 1916.
Benedict, E. C.: The Psychologic Effect of Alcohol on Man, The Journal A. M. A., 1916, lxvi, p. 1424.
[35] Reich, H. W.: Ueber den Einfluss des Alkoholgenusses auf Bakterizidie, Phagozytose und Resistenz der Erythrocyten, beim Menschen, Arch. f. Hyg., 1916, lxxxiv, 337.
[36] Konradi: Ueber den Wert der Choleraschutzimpfungen, Centralbl. f. Bakteriol., I. O., 1916, lxxvii, 339.
[37] Alcohol and Immunity, Jour. A. M. A., 1916, lxvi, p. 962, p. 1122.
SECTION VNOTES ON TOBACCO
It is the purpose of this section to present as fairly as possible the evidence relating to the effects of tobacco on the human body, so that those who smoke may correctly measure the probable physical cost of the indulgence. The extremes of opinion on this subject are well expressed in the following verses:
“Hail! Social Pipe—Thou foe to care,
Companion of my elbow chair;
As forth thy curling fumes arise,
They seem an evening sacrifice—
An offering to my Maker’s praise
For all His benefits and grace.”
Dr. Garth.
“A custom loathsome to the eye, hateful to the nose, harmful to the brain, dangerous to the lungs, and the black stinking fume thereof nearest resembling the horrible Stygian smoke of the pit that is bottomless.”
James I.
Tobacco is a plant, Nicotiana Tabacum of the order Solanaceæ, which includes Atropa Belladonna, or “Deadly Nightshade,” Hyoscyamus, or “Henbane,” Solanum Dulcamara, or “Bitter Sweet,” all powerful poisons, and likewise the common potato and tomato, which are wholesome foods. The cured leaves are used for smoking and chewing, or when powdered, as snuff.
Prior to the middle of the 16th Century, the use of tobacco was confined to the American Indians. In 1560 the Spaniards began to cultivate tobacco as an ornamental plant, and Jean Nicot, the French Ambassador at Lisbon, introduced it at the court of Catherine de Medici in the form of snuff. Smoking subsequently became a custom which spread rapidly throughout the world, although often vigorously opposed by Governments. In the 17th Century, smoker’s noses were cut off in Russia.
Tobacco contains a powerful narcotic poison, nicotin, which resembles prussic acid in the rapidity of its action, when a fatal dose is taken.
The percentage of nicotin present varies according to the brand and the conditions under which it is cultured.
The following figures have been given by the various authorities.
London Lancet[38] .64 to 5.3 per cent. French Dept. of Agriculture[39] .22 to 10.5 " " Connecticut Agricultural Experiment Station[40] 2.89 " " (Home grown—after fermentation.) U. S. Dept. of Agriculture[40] .94 to 5. " " (Domestic.)Aside from nicotin it also contains small quantities of related substances—nicotellin, nicotein, a camphoraceous substance termed nicotianin, said to give tobacco its characteristic flavor, and likewise a volatile oil developed during the process preparation. On heating, pyridin (a substance often used to denature alcohol), picolin, collidin, and other bases are formed, as well as carbolic acid, ammonia, marsh gas, cyanogen and hydrocyanic acid, carbon monoxide (coal gas) and furfural. Furfural is a constituent of fusel oil, which is so much dreaded in poor whisky. The smoke of a single cigaret may contain as much furfural as two ounces of whisky.
The complex constitution of tobacco and the smoke from its combustion has caused much debate as to the substances that are responsible for its charm and its ill effects, which are to be described. No one can doubt the serious injurious effects from such a powerful poison as nicotin if taken in any but the most minute quantities (one to three milligrams have produced profound poisoning in man).
It has been maintained by some that nicotin is practically destroyed in the process of smoking, and that the effects of tobacco are limited to the decomposition products resulting from the burning tobacco, especially pyridin. But pyridin is also formed in the burning of cabbage leaves, and cabbage leaves do not possess any attractions for smokers, neither do they produce the well-known effects that smoking and chewing tobacco produce. No doubt pyridin and furfural are factors in the drug effects of tobacco, but recent painstaking experiments by
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