Atwater and Benedict,[28] and Beebe[29] and Mendel,[30] have shown that alcohol is a “protein sparer,” and can, to some extent, take the place of fats and carbohydrates. This is what is meant by calling alcohol a “food.” Always, however, it fails to pass some test by which true foods are measured. Apart from its effect on the nervous system, among which must be figured its action on the blood vessels which causes a loss of body heat, Mendel has shown that in moderate doses (96 cc. daily) it increases the output of uric acid and allied (purin) bodies derived from the tissues, a fact which distinguishes it from all other foods. These poisonous or drug effects must always be considered, together with any alleged nourishing effects. Alcohol is still used by some as a rapidly available fuel-food in fevers, and when ordinary foods cannot be readily digested and made available. But this is done to a much less degree than formerly, now that its narcotic and poisonous effects are more fully understood. Sugar and water often serve quite as useful a purpose.
It seems reasonable, on the evidence herein presented, to class alcohol among the narcotic or “deadening” drugs, such as ether or chloroform. Indeed, Aschaffenburg[31] has recently called attention to the growth of the ether habit in eastern Germany, where this drug is used as a so-called stimulant, while in reality the effects are well known to be narcotic, or deadening.
The laboratory and the life insurance records simply give exact expression to what has long been a matter of common knowledge to the employer of labor and to leaders and commanders of men; to wit, that the influence of alcohol on any large group of men, whether they be artisans or soldiers, is harmful and lowers the efficiency of the group. Individual susceptibility varies, but the man who thinks he is an exception and can indulge with safety may find that he is mistaken only after serious damage to the body has been done and perhaps a definite loss sustained in happiness and achievement.
Stockard,[32] in his experiments on animals, has demonstrated conclusively that the germ cells of males can be so injured by allowing the subjects to inhale the fumes of alcohol that they give rise to defective offspring, although mated with vigorous untreated females. The offspring of those so treated when reaching maturity are usually nervous and slightly undersize. These effects are apparently conveyed through the descendants for at least three generations. Such evidence establishes at least the probability of the transmission of serious ill effects to human offspring through alcoholic indulgence of the male parent.
Much of the statistical evidence that has been produced on both sides of this question of the transmissibility of the effect of alcohol is misleading unless very critically analyzed, but the results of exact laboratory experiments can hardly be gainsaid.
Those who trifle with alcohol should at least take the precaution to be periodically examined in order to detect the earliest signs of ill-effect. One’s own feelings are not safe guides, and may fail to warn of danger until serious damage has been done.
In 1914, at the annual meeting of the National Council of Safety, at which there were present representatives from several hundred large industries, the members unanimously voted to abolish liquor from their plants. It has been well stated by Quensel[33] that “work and alcohol do not belong together, especially when the work demands wideawakeness, attention, exactness and endurance.”
The restrictive and prohibitive measures of the French and Russian governments, the well known opposition of the Kaiser to alcohol and the warnings uttered by Lord Kitchener and leading British statesmen, are sufficient evidence that the condemnation of alcohol represents the deliberate judgment of the world’s strong men.
[1] United Kingdom Temperance and General Provident Institution of London, Annual Report, 1910.
[2] Sceptre Life Association, Annual Report, 1912.
[3] Scottish Temperance Life Assurance Company, Annual Report, 1912.
[4] The Abstainers and General Insurance Company, Ltd., Annual Report, 1912.
[5] McMahon, T. F.: The Use of Alcohol and the Life Insurance Risk. Proceedings of the Association of the Life Insurance Medical Directors of America, 1911, Twenty-second Annual Meeting, p. 473; Medical Record, LXXX, p. 1121.
[6] Lounsberry, R. L.: Proceedings of the Life Assurance Medical Directors. October, 1913.
[7] Moore, Roderick McKenzie: On the Comparative Mortality Among Assured Lives of Abstainers and Non-Abstainers from Alcoholic Beverages. Transactions of the Institute of Actuaries, 1913, XXXVIII, pp. 248–272.
[8] Report of Medico-Actuarial Mortality Investigation, IV, pp. 11–13.
[9] Statistical Abstract for the United Kingdom, Sixty-first Number, 1809–1913 (Wyman & Sons), London, 1914, p. 173; Statistical Abstract for the Principal and Other Foreign Countries, 1901–1912, Thirty-ninth Number, pp. 505, 506, 507; Statistical Abstract of the United States, Thirty-sixth Number, 1913, p. 516.
[10] Kraepelin, Emil: Ueber die Beeinflussung einfacher psychischer Vorgänge durch einige Arzneimittel, Verlag von Gustav Fisher, Jena, 1892; Aschaffenburg, Gustav: Praktische Arbeit unter Alkoholwirkung, Psychologische Arbeiten, 1896, I, pp. 608–626; Kurz, Ernest, and Kraepelin, Emil: Ueber die Beeinflussung psychischer Vorgänge durch regelmässigen Alkoholgenuss, Psychologische Arbeiten, 1901, III, pp. 417–457; Mayer, Martin: Ueber die Beeinflussung der Schrift durch den Alkohol, Psychologische Arbeiten, 1901, III, pp. 535–586; Rudin, Ernst: Ueber die Dauer der psychischen Alkoholwirkung, Psychologische Arbeiten, IV, pp. 1–44.
[11] Vogt, R.: Om virkningen af 15–50 cm3 koncentrert spiritus paa erindringsevnen, Norsk. Mag. f. Laegevidensh., 1910, LXXI, pp. 605–626; The Lancet (London), 1910, II, p. 1040.
[12] Aschaffenburg, Gustav: Crime and Its Repression, Little, Brown & Company, Boston, 1913, p. 84.
[13] Schnyder, L.: Alkohol und Muskelkraft, Archiv für Physiologie, 1902–3, XCIII, p. 451.
[14] Hellsten, A. F.: Ueber den Einfluss von Alkohol, Zucker und Thee auf die Leistungsfähigkeit des Muskels, Munchen Med. Wchnschr., 1914, LI, pp. 18–94.
[15] Bastedo, Walter A.: Materia Medica Pharmacology and Therapeutics, W. B. Saunders Company, Philadelphia and London, 1913, p. 333.
[16] Laitinen, T.: The Norman Kerr Lecture on The Influence of Alcohol on Immunity, Med. Rec., LXXVI, 1909, pp. 445–446. Read before the Twelfth International Anti-Alcoholic Congress, held in London, July, 1909; Uber die Einwirkung der kleinsten Alkoholengen auf die Widerstandsfähigkeit des tierischen Organismus mit besonderer Berücksichtigung der Nachkommenschaft, Ztschr. f. Hyg. u. Infections-krankheiten, LVIII, 1907–8, p. 139.
[17] Rubin, George: The Influence of Alcohol, Ether, and Chloroform on Natural Immunity in its Relation to Leucocytosis and Phagocytosis, Jour. Infct. Dis., 1904, I, pp. 425–444.
[18] Stewart, Chas. E.: The Influence of Alcohol on the Opsonic Power of the Blood, Mod. Med., 1907, XVI, pp. 241–246. Read before the American Society for the Study of Alcohol and Drug Neuroses, Atlantic City, June 4, 1907, and published in the Jour. of Inebriety.
[19] Craig, Chas. F., and Nichols, Henry J.: The Effect of the Ingestion of Alcohol on the Result of the Complement Fixation Test in Syphilis, Jour. A. M. A., 1911, LVII, pp. 474–76.
[20] Fillinger, F. V.: Weitere Mitteilungen über Resistenzverminderung der Erythrozyten nach Alkoholgenuss, Deutsch. Med. Wchnschr., 1912, XXXVIII, p. 999.
[21] Weinburg, W. W.: The Lowering of Stability of Erythrocytes in Alcoholic Intoxication, Russky Vratch, 1912, II, p. 1324; New York Med. Jour., 1912, XCVI, p. 1040.
[22] Parkinson, P. R.: The Relation of Alcohol to Immunity, The Lancet (London), 1909, VII, pp. 1580–82.
[23] Brooks, Clyde: The Action of Alcohol on the Normal Intact Unanesthetized Animal, Jour. A. M. A., 1910, LV, pp. 372–73. Read in the Section on Pathology and Physiology of the A. M. A. at the Sixty-first Session, St. Louis, June, 1910.
[24] Crile, George W.: Blood Pressure in Surgery, J. B. Lippincott Company, Philadelphia, 1903. Cartwright Prize of the Alumni Ass’n of the College of Physicians and Surgeons, New York City.
[25] Cabot, Richard C.: Studies of the Action of Alcohol in Disease, Especially upon the Circulation, Med. News, LXXXIII, 1903, pp. 145–153. Read before the Association of American Physicians, May 13, 1903.
[26] Dennig, Hindelang und Grünbaum: Uber den Einfluss des Alkohols auf den Blutdruck und die Herzarbeit in pathologischen Zuständen, Namentlich beim Fieber, Deutsch. Arch. f. klin. Med., 1909, XCVI, pp. 153–162.
[27] Alexandroff, Emilie: Ueber die analeptische Wirkung des Alkohols bei pathologischen Zuständen, Cor. Bl. f. schweiz. Aerzte., 1910, XL, pp. 465–475; Action of Alcohol During Febrile and other Pathologic Conditions, Jour. A. M. A., 1910, LV, p. 174.
[28] Atwater, W. A., and Benedict, F. G.: An Experimental Inquiry Regarding the Nutritive Value of Alcohol, National Academy of Science, 1902, Sixth Memoir.
[29] Beebe, L. B.: The Effect of Alcohol and Alcoholic Fluids Upon the Excretion of Uric Acid in Man, Amer. Jour. Physiol., 1904, XII, pp. 13–37.
[30] Mendel, L. B., and Hilditch, Warren W.: The Influence of Alcohol Upon Nitrogenous Metabolism in Men and Animals, Amer. Jour. Physiol., 1910, XXVII, pp. 1–23.
[31] Aschaffenburg, Ibid.
[32] Stockard, C. R.: A Study of Further Generations of Mammals from Ancestors Treated with Alcohol, Proc. Soc. Exper. Biol. and Med., 1914, XI, p. 136.
[33] Quensel, Ulrik: The Alcohol Question from a Medical Viewpoint—Studies in the Pathology of Alcoholism, Year Book, United States Brewers’ Association, 1914, p. 168.
Bastedo, Walter A.: Materiel Medico, Pharmacology and Therapeutics, W. B. Saunders Company, Philadelphia and London, 1913, p. 318.
Bertillon, Jacques: On Mortality and the Causes of Death According to Occupations, Proceedings of the Fifteenth International Congress on Hygiene and Demography, Washington, 1912, I, p. 345.
Boos, William F.: The Relation of Alcohol to Industrial Accidents and to Occupational Diseases, Proceedings of the Fifteenth International Congress on Hygiene and Demography, Washington, 1912, I, p. 829.
Cabot, Richard C.: The Consumption of Alcohol and of Other Medicines at the Massachusetts General Hospital, Boston Med. Jour., CLX, 1909, pp. 480–81.
Dixon, W. E.: Alcohol in Relation to Life, The Nineteenth Century, 1910, LXVII, pp. 516, 523.
“Ethyl Alcohol,” The Dispensatory of the United States of America, J. B. Lippincott & Company, Philadelphia, 19th edition, p. 102.
Ewald: Alcohol in Relation to Infectious Diseases, Med. Rec., 1913, LXXXIV, p. 75. Read before the Fourth National Congress on Physiotherapy, Berlin, March 26, 1913.
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.
There 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.
[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.
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 high authorities have shown the presence of nicotin in tobacco smoke, and when we reflect that there is sometimes sufficient nicotin in an ordinary cigar to kill two men, it is not strange that enough of it may be absorbed from the smoke passing over the mucous membranes of the nose, throat and lungs to produce a distinct physiological effect.
Investigators who claim to show by experiments the absence of nicotin from tobacco smoke must explain why the palpable effects of smoking, in those who have not established a “tolerance,” are those of nicotin poisoning, and why the symptoms produced by chewing tobacco are identical with those following the smoking of tobacco, which are: mild collapse, pallor of the skin, nausea, sweating, and perhaps vomiting, diarrhea, muscular weakness, faintness, dizziness, and rise in blood pressure followed by lowered blood pressure.
Nicotin is undoubtedly decomposed by burning, but it may become volatilized by heat and a certain amount absorbed before decomposition takes place.
Lehmann,[41] in 1908, found in tobacco smoke the following percentages of the nicotin contained in the tobacco:
| Cigaret smoke | 82 | per cent. |
|---|---|---|
| Cigar smoke | 85 to 97 | " " |
The London Lancet[42] (1912) gives the following figures:
| Cigaret smoke | 3.75 to 84 | per cent. |
|---|---|---|
| Pipe mixture smoke, smoked as cigarets | 79 | " " |
| Pipe smoke | 77 to 92 | " " |
| Cigar smoke | 31 to 63 | " " |
The United States Department of Agriculture[43] found in tobacco smoke about 30 per cent. of the nicotin originally present in the tobacco.
Contrary to general opinion, Havana cigars contain less nicotin than the cheaper brands, which augurs ill for the large class of people who cannot afford to smoke higher priced brands. Many of the cheaper grades do, however, show a low percentage of nicotin.
By means of an ingenious apparatus, Zhebrovski,[44] a Russian investigator, compelled rabbits to smoke cigaret tobacco for a period of 6 to 8 hours daily. Some died within a month, and showed changes in the nerve-ganglia of the heart. Others established a tolerance similar to that exhibited by habitual smokers, but upon being killed at the end of five months, degenerative changes similar to those produced by the injection of nicotin were found, viz., hardening of the blood vessels. There is, indeed, no difficulty in producing the characteristic effects of nicotin by administering tobacco smoke, either in man or in animals.[45]
Nicotin causes brief stimulation of brain and spinal cord, followed by depression. There is an increased flow of saliva, followed by a decrease (large doses diminish it at once) and often nausea, vomiting and diarrhea. The heart action is at first slowed and the blood pressure increased. Subsequently there is a depression of the circulation, with rapid heart action and lowered blood pressure. In habitual smokers, this preliminary stimulation may not occur. The stimulating effect on the brain is so brief that tobacco can not properly be termed a stimulant. Its effect is narcotic or deadening. Those who fancy that their thoughts flow more readily under the use of tobacco are in the same case with any other habitué whose thoughts can not flow serenely except under his accustomed indulgence. That a sound healthy man, who has never been accustomed to the use of tobacco, can do better mental or physical work with tobacco than without it has never been shown. Indeed, such experiments as have been made on students and others show to the contrary.[46]
The statistics presented by Prof. Fred. J. Pack are of interest in this connection.
In six educational institutions the students competing for places on the football team were grouped as follows:
| Institution. | Smoker. | Non-smoker. | Institution. | Smoker. | Non-smoker. |
|---|---|---|---|---|---|
| A | 65.2 | 69.8 | G | 74.0 | 75.0 |
| B | 64.7 | 74.6 | H | 75.2 | 79.4 |
| C | 78.8 | 81.1 | I | 81.6 | 88.4 |
| D | 75.8 | 77.6 | J | 78.5 | 81.3 |
| E | 84.6 | 84.8 | K | 74.0 | 84.6 |
| F | 69.6 | 71.3 | L | 77.3 | 77.6 |
The following table shows the relative scholastic standing of smokers and non-smokers:
| Number of Men. |
Total Mark. |
Average Mark. |
|
|---|---|---|---|
| Smokers | 81 | 6,034 | 74.5 |
| Non-smokers | 101 | 8,021 | 79.4 |
Twelve institutions reporting:
| Number of Men. |
Highest Marks. |
Lowest Marks. |
|
|---|---|---|---|
| Smokers | 81 | 4 | 12 |
| Non-smokers | 101 | 11 | 6 |
| Number of Men. |
Highest Marks. |
Lowest Marks. |
|
| 101 non-smokers furnish | 11 | 6 | |
| 101 smokers would furnish | 5 | 15 | |
| Number of Men. |
Total Conditions and Failures. |
Average | |
| Smokers | 82 | 70 | .853 |
| Non-smokers | 98 | 48 | .439 |