1453
Lillioja S, Esposito-Del Puente A, et al. Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ. Am J Physiol 1990; 259: E650-57. 19. Swinborn BA, Nyomba BL, Saad MF, et al. Insulin resistance associated with lower rates of weight gain in Pima Indians. J Clin Invest 1991; 88: 18. Zurlo F,
In lean individuals, insulin resistance might also indicate weight maintenance. An exception could be exercisetraining; yet, the maintenance of insulin sensitivity of trained indivduals may merely be a response to the glycogen depletion that results from muscular activity.22 During exercise, respiratory quotient falls and fatty-acid oxidation is preferential to carbohydrate oxidation.23 Moreover, the respiratory quotient also tends to be lower during the post-exercise period.24 Therefore, exercise-training may induce an insulin-resistant state more than previously thought, with the maintenance of insulin sensitivity being dependent on whether fuel replenishment is needed. Indeed, the hypoglycaemic response to insulin is only slightly affected by the level of training.25 For others, insulin resistance is an adaptation to maintenance of obesity. Herein, however, there are consequences-ie, the presence of cardiovascular risk factors and a greater incidence of cardiovascular disease, especially for obese subjects with an excess of adipose tissue in the ab.>men.26 Although these sequelae imply that insulin resistance creates an adverse metabolic environment, my hypothesis is that insulin resistance is a necessary adaptation for preventing further weight gain in the obese subject, in an environment wherein excess food intake coupled with inactivity are becoming
168-73. 20. Knowler WC, Pettitt PJ, Savage PJ, Bennett PH. Diabetes incidence in Pima Indians: contributions of obesity and parental diabetes. Am J Epidemiol 1981; 113: 144-56. 21. UK Prospective Study of Therapies of Maturity Onset Diabetes. I, Effect of diet, sulphonylurea, insulin or biguanide therapy on fasting plasma glucose and body weight over one year. Diabetologia 1983; 24: 404-11. 22. Flatt JP. Dietary fat, carbohydrate balance, and weight maintenance: effects of exercise. Am J Clin Nutr 1987; 45: 296-306. 23. Holloszy JO, Coyle EF. Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. J Appl Physiol 1984; 56: 831-38. 24. Bielinski R, Schutz Y, Jequier E. Energy metabolism during the postexercise recovery in man. Am J Clin Nutr 1985; 42: 69-82. 25. LeBlanc J, Nadeau A, Richard D, Tremblay A. Variations in plasma glucose, insulin, growth hormone and catecholamines in response to insulin in trained and non-trained subjects. Metabolism 1982; 31: 453-56. 26. Donahue RP, Abbot RD, Bloom E, Reed DM, Yano K. Central obesity and coronary heart disease in men. Lancet 1987; i: 821-24.
increasingly common.
VIEWPOINT REFERENCES
1. Buchanan TA, Metzger BE, Freinkel N, Bergman RN. Insulin sensitivity and B-cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes. Am J Obstet Gynecol 1990; 162: 1008-14. 2. Bloch CA, Clemons P, Sperling MA. Puberty decreases insulin sensitivity. J Pediatr 1987; 110: 481-87. 3. Newman WP, Brodows RG. Insulin action during acute starvation: evidence for selective insulin resistance in normal man. Metabolism 1983; 32: 590-96. 4. Haffner SM, Stem MP, Hazuda HP, Mitchell BD, Patterson JK, Ferrannini E. Parental history of diabetes is associated with increased cardiovascular risk factors. Arteriosclerosis 1989; 9: 928-33. 5. Hollenbeck CB, Chen N, Chen Y-DI, Reaven GM. Relationship between the plasma insulin response to oral glucose and insulinstimulated glucose utilization in normal subjects. Diabetes 1984; 33: 460-63. 6. Kadowaki T, Bevins CL, Cama A, et al. Two mutant alleles of the insulin receptor gene in a patient with extreme insulin resistance. Science 1988; 240: 787-90. 7. Rossini A. Lipoatrophic diabetes. In: Marble A, Krall LP, Bradley RF, Christlieb AR, Soeldner JS, eds. Joslin’s diabetes mellitus, 12th ed. Philadelphia: Lea and Febiger, 1985: 834-42. 8. Reaven GM. Barting lecture 1988: role of insulin resistance in human disease. Diabetes 1988; 37: 1595-607. 9. Kolterman OG, Gray RS, Griffin J, et al. Receptor and postreceptor defects contribute to the insulin resistance in non-insulin-dependent diabetes mellitus. J Clin Invest 1981; 68: 957-69. 10. Wigand JP, Blackard WG. Down-regulation of insulin receptors in obese men. Diabetes 1979; 28: 207-91. 11.Randle PJ, Garland PB, Hales CN, Newsholme EA. The glucose fatty-acid cycle: its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet 1963; i: 785-89. 12. Olefsky JM, Reaven GM, Farquhar JW. Effects of weight reduction in obesity: studies of lipid and carbohydrate metablism in normal and hyperlipoproteinemic subjects. J Clin Invest 1974; 53:64-76. 13. Eckel RH. Lipoprotein lipase: a multifunctional enzyme relevant to common metabolic diseases. N Engl J Med 1989; 320: 1060-68. 14. Farese RV Jr, Yost TJ, Eckel RH. Tissue-specific regulation of lipoprotein lipase activity by insulin/glucose in normal-weight humans. Metabolism 1991; 40: 214-16. 15. Eckel RH, Yost TJ. Weight reduction increases adipose tissue lipoprotein lipase responsiveness in obese women. J Clin Invest 1987; 80: 992-97. 16. Kramer FM, Jeffrey RW, Forster HL, Snell MK. Long-term follow-up of behavioral treatment for obesity: patterns of weight regain among men and women. Int J Obesity 1989; 13: 123-36. 17. Ravussin E, Lillioja S, Knowler WC, et al. Reduced rate of energy expenditure as a risk factor for body weight gain. N Engl J Med 1988; 318: 467-72.
John Bostock, hay fever, and the mechanism of allergy
John Bostock was a physician at the Royal Infirmary in Liverpool for 20 years until he moved to London in 1817 and gave up the practice of medicine. He then devoted himself to academic pursuits, wrote the first textbook of physiology in the English language, was appointed lecturer in chemistry at Guy’s Hospital, and ultimately became a vice-president of the Royal Society.1 Bostock had suffered since the age of eight years with what was at that time an unusual affliction. Each year at the beginning of June he developed a cold which lasted for about two months and was associated with a profuse nasal discharge, repeated paroxysms of sneezing, itching of the eyes, difficulty in breathing, and severe malaise. He recognised that these features represented a syndrome which was distinct from the common cold and recorded his own case history in 1819. This is now generally accepted as the first complete description of hay fever. After publication of the paper contemporary observers noted that hay fever was an uncommon conditionand it took Bostock 9 years to collect another 28 cases for a second article.4 Since then, hay fever has become much more common and current estimates suggest a prevalence of about 10% in Europe and the United States.s Emanuel6 has surveyed the published work and concludes that, before 1800, descriptions of hay fever were extremely rare and incomplete; in biblical, Greek, or Roman writings there are none at all. Heberden described a summer cold but did not comment on the itching of the eyes, the long duration of illness, or the associated lethargy which are so ADDRESS: Medical Unit, Royal Liverpool Liverpool L7 8XP, UK (Dr R Finn, FRCP).
University Hospital,
1454
characteristic of severe hay fever. There were also descriptions of the "rose cold", which was regarded as a rarity. Since hay fever is so obviously different from the common cold, it is highly unlikely to have been missed by earlier physicians. We cannot completely exclude the possibility that hay fever was present before the 19th century but had simply not been recognised; there is, however, strong objective evidence that it was much less common in the 19th century than it is now. Hay fever was not mentioned in the Edinburgh Medical and Physical Dictionary (1807). Bostock’s report of his own case was of sufficient interest to merit presentation to a medical society. Bostock commented in 1828 that "one of the most remarkable circumstances respecting this complaint is its not being noticed as a specific affection, until within the last 10 or 12 years". Public dispensary records where the poor were given free medicines showed a decrease in "cattarhus" in the summer months rather than an increase, as would be expected with hay fever.6 Elliotson, in lectures to medical students at St Thomas’, stated that it was a very "extraordinary affection" and he had only seen 2 cases.3 We may therefore accept Emanuel’s conclusion that hay fever is a new disease.6 Today it is so common that television and the newspapers provide us with pollen counts during the summer months. Bostock did not relate his condition to pollen but believed that its seasonal incidence was due to physical factors, possibly temperature. Charles Blackley, a physician in Manchester who also suffered from hay fever, collected some grass pollen in the summer and stored it in a bottle until the middle of the winter. He then removed the top of the bottle and inhaled the pollen. This immediately caused an acute attack with streaming eyes, running nose, and sneezing. This simple and elegant exeriment proved that hay fever was a sensitivity to pollen.7 These historical facts raise the question as to why the first accounts of hay fever and its mechanism came from two physicians from the north-west of England-which was at that time very far removed from the centres of medical excellence and academia such as London, Edinburgh, Paris, and Berlin. To this may be added the question as to why hay fever first appeared at the beginning of the 19th century. The most likely answer to both these questions relates to a third question-was there anything special about the north of England at the beginning of the 19th century? The obvious answer is the Industrial Revolution which began in this area and led to massive chemical pollution for the first time in human history. Chronic chemical damage to the nasal mucosa would facilitate the entry of pollen antigens, leading to immunological sensitisation. According to our current understanding hay fever is due to an allergy to pollen in sensitive subjects. The allergic or sensitivity state is manifested by a high IgE which is probably inherited as an autosomal dominant on chromosome llq.11 This explanation does not, however, explain the rarity of the condition before 1800 or its greatly increased prevalence since; grass has been a feature of the landscape for many thousands of years. A genetic mutation leading to a raised IgE could not be the explanation because a mutation in 1800 could not spread to 10% of the population in less than 200 years. This paradox only becomes explicable if chemical pollution is entered into the equation, coincident with the Industrial Revolution in about 1800. Work in laboratory animals points to an interaction between allergens and pollutants such as S02’ N02, 03, and
vehicle exhausts.9 Thus exposure of guineapigs to ozone at 5 parts per million increases the likelihood of sensitisation and anaphylaxis after inhalation of an albumen aerosol." Intraperitoneal sensitisation of mice to Japanese cedar pollen occurs with concurrent administration of diesel exhaust particles but not without." Blackley originally noted that hay fever was more common in the town than the country, and the incidence of red cedar hay fever in Japan is directly related to the level of pollutants." Thus it is widely accepted that irritant damage to mucous membranes acts as an aggravating factor in allergic disease. The historical data relating to hay fever suggest something very different-namely, that chemical damage to the mucous membrane of the nose is a primary event, and without such damage hay fever would not occur or would occur only very rarely. Primary sensitisation through an intact nasal mucous membrane would be unlikely. The nasal mucosa has evolved to prevent the entry of antigens, but the sudden onset of massive chemical pollution has overwhelmed the natural resistance of the nasal mucous membrane. Throughout his career both in Liverpool and later in London, Bostock was an active chemist and wrote several papers on the chemical composition of body fluids including urine.13 He was later to work with Richard Bright at Guy’s, and can be regarded as the first English chemical pathologist. Might his laboratory work, which brought him into regular contact with irritant chemicals, have exacerbated his undoubtedly severe seasonal rhinitis? Bostock gave a paper14 to the Literary and Philosophical Society in Liverpool in 1817 entitled "The best means of obviating the nuisance arising from the smoke of steam engines". Unfortunately the text of this paper has not survived, but Bostock was almost certainly aware of the dangers of chemical pollution. This could have been one of the earliest papers on the effects of chemical pollution, since the steam engine was the major cause of pollution consequent on the Industrial Revolution. The immune system has evolved over millions of years and must have developed powerful homoeostatic mechanisms; spontaneous dysregulation of the immune system, as in allergy, would be an unlikely primary event. Thus, allergies will tend to occur only as a result of external chemical damage predisposing to sensitisation. This could act either by damage to mucosal surfaces with consequent entry of large amounts of antigen, or by direct damage to the immune system leading to destabilisation. This historical analysis suggests that certain allergies are diseases of civilisation, and that the current high incidence of allergic diseases might be reduced by control of chemical
pollution.
REFERENCES 1. Obituary. Dr J. Bostock. Lancet 1846; ii: 222. 2. Bostock J. Case of a periodical affection of the eyes and chest.
Medico-Chirurg Trans 1819; 10: 161-62. 3. Elliotson J. On hay fever. Lancet 1830; ii: 370-73. 4. Bostock J. On the cattarhus aestivus or summer catarrh. Medico-Chirurg Trans 1828; 14: 437-46. 5. Fleming DM, Crombie DL. Prevalence of asthma and hay fever in England and Wales. BMJ 1987; 296: 279-83. 6. Emanuel MB. Hay fever, a post industrial revolution epidemic: a history of its growth during the 19th century. Clin Allergy 1988; 18: 295-304. 7. Blackley CH. Experimental researches on the causes and nature of cattarhus aestivus (hay fever or hay asthma) London. Baillière, Tindall and Cox, 1873.
1455
8. Cookson WOCM, Young RP, Sandford AJ, et al. Maternal inheritance of atopic IgE resposiveness on chromosome 11q. Lancet 1992; 340: 381-84. 9. Molfino NA, Slutsky AS, Zamel N. The effects of air pollution on allergic bronchial responsiveness. Clin Exp Allergy 1992; 22: 667-72. 10. Matsumara Y. The effects of ozone, nitrogen dioxide, and sulphur dioxide on the experimentally induced allergic respiratory disorder in guinea pigs 1. The effect on sensitisation with albumin through the airway. Am Rev Respir Dis 1970; 102: 430-37. 11. Murawaka M, Suzuki S, Koizumi K, et al. Adjuvant activity of diesel exhaust particulates for the production of IgE antibodies in mice. J Allergy Clin Immunol 1986; 77: 616-23.
12. Ishizaki
T, Koizumi K, Ikemori R, et al. Studies of prevalence of Japanese cedar pollinosis among the residents in a densely cultivated area. Ann Allergy 1987; 58: 265-70. 13. Bostock J. On the nature of animal fluids. Medico-Chirurg Trans 1813; 4: 53-88. 14. Bostock J. The best means of obviating the nuisances arising from the smoke of steam engines. Minutes of the Literary and Philosophical Society of Liverpool 1812-1817. Liverpool City Archives 060 LIT.
1/1. 15. Sears MR.
Epidemiology of asthma. In: O’Byrne PM, ed. Asthma as an inflammatory disease. New York: Dekker, 1990: 15-48.
BOOK SHELF Principles and Practice of Surgery for the Colon, Rectum, and Anus Edited by Philip H. Gordon, Santhat Nivatvongs. St Louis: Quality Medical Publishing. 1992. Pp 1097. 195. ISBN 0-942219104.
Philip Gordon and Santhat Nivatvongs have produced a "must" for every colorectal surgeon. The text is profusely illustrated in colour and the book is a positive pleasure to read. Its authors are up-to-the-minute performers from the North American colorectal seminar circuit. Their written accounts of individual conditions reflect all the views, prejudices, and talking points that are current across the USA and Canada. Phil Gordon from Montreal is a regular and popular presenter of basic surgical science lectures to surgeons. The first two chapters on surgical anatomy and physiology are therefore especially splendid. Some of the arterial anatomy is oversimplified and I would like to have seen more extensive coverage of the difficult area of autonomic nerve anatomy in the pelvis. I applaud their philosophy of careful identification and preservation of the nerve plexuses as a basic principle of colorectal surgery. Curiously, however, for a book so well illustrated there were few surgeon-friendly illustrations to assist this process. A further area that will especially suit the surgeon is the discussion about the awkward interface between basic physiology and anorectal manometry, electromyography, etc, and the clinical applications of these techniques. A physiology chapter of 35 pages equips the surgeon with the facts necessary to understand often incomprehensible modem symposia, whilst the 160 references permit complete immersion for the real enthusiast. In the field of diagnostic imaging, I would have preferred more about the potential of computed tomography, magnetic resonance imaging, and endorectal ultrasound. Anorectal disorders are well done with clear comprehensible drawings among 275 pages of excellent writing. When I turned to rectal carcinoma-a controversial subject of particular interest to me-it would be surprising if some points of disagreement did not emerge. Most of the pictures of stapling machines add nothing and the discussion about high ligation omits its only real value: that of releasing the splenic flexure for a low anastomosis. Scant mention is accorded to irrigation of the rectal stump below a clamp. This is a serious mistake because it is likely to lead younger readers to omit this simple precaution against preventable local recurrence. Exclusion from a clinical trial of adjuvant therapy because the rectal stump is washed out with water verges on the absurd and, in my view, conveys
incorrect priorities. My criticisms are few. The book’s name is similar to the "bible" of our specialty: Surgery of the Anus, Rectum and Colon by Professor J. C. Goligher, whose achievement still remains unsurpassed. But Phil Gordon and Sandy Nivatvong’s effort certainly deserves a place on the shelf beside it. Colorectal Research Unit, Basingstoke District Hospital, Basingstoke RG24 9NA, UK
Atlas of
R.
J. HEALD
Transvaginal Surgery
S. Raz. London: Saunders. 1992. 0-721624316.
Pp
288.
78. ISBN
Dr Raz and his publishers have produced a wellpresented description of transvaginal surgery. But why transvaginal surgery? Because so much can be done by this route rather than an abdominal approach, and with far less morbidity and upset to the patient. And gynaecologists are accustomed to doing most of their operative work from the sitting position! I found the diagrams of the various operations for stress incontinence valuable. A helpful addition would have been the 3/0 coated vicryl round-bodied 22 mm J-shaped needle. This suture is useful in repair of vesico-vaginal fistulae, reconstruction of the urethra, and anterior colporrhaphy. Three cheers for Indigo Carmine, which is still available in the USA. Anyone will tell you that it is much better than methylene blue, which we in the UK are obliged to use. In the description of posterior vaginal repair, interrupted rather than continuous sutures are best adopted to prevent shortening of the posterior vaginal wall. The author admits that the timing of surgery is a controversial issue in repair of vesico-vaginal fistulae and he advocates a short waiting period of only 2-3 weeks in some cases. While this approach will undoubtedly appeal to patients, the truth is that by operating early one will include some unnecessary procedures because at least 4% heal spontaneously. In advocating retention of the fistulous tract, it would be helpful to have had the evidence that it "provides a ring of protection against post-surgical bladder spasms." Is excision of Bartholin’s cyst ever justified? Surely marsupialisation is the operation of choice to prevent recurrence.
Birmingham Maternity Hospital, Queen Elizabeth Medical Centre, Birmingham B15 2TG, UK
JOHN KELLY
Lillioja S, Esposito-Del Puente A, et al. Low ratio of fat to carbohydrate oxidation as predictor of weight gain: study of 24-h RQ. Am J Physiol 1990; 259: E650-57. 19. Swinborn BA, Nyomba BL, Saad MF, et al. Insulin resistance associated with lower rates of weight gain in Pima Indians. J Clin Invest 1991; 88: 18. Zurlo F,
In lean individuals, insulin resistance might also indicate weight maintenance. An exception could be exercisetraining; yet, the maintenance of insulin sensitivity of trained indivduals may merely be a response to the glycogen depletion that results from muscular activity.22 During exercise, respiratory quotient falls and fatty-acid oxidation is preferential to carbohydrate oxidation.23 Moreover, the respiratory quotient also tends to be lower during the post-exercise period.24 Therefore, exercise-training may induce an insulin-resistant state more than previously thought, with the maintenance of insulin sensitivity being dependent on whether fuel replenishment is needed. Indeed, the hypoglycaemic response to insulin is only slightly affected by the level of training.25 For others, insulin resistance is an adaptation to maintenance of obesity. Herein, however, there are consequences-ie, the presence of cardiovascular risk factors and a greater incidence of cardiovascular disease, especially for obese subjects with an excess of adipose tissue in the ab.>men.26 Although these sequelae imply that insulin resistance creates an adverse metabolic environment, my hypothesis is that insulin resistance is a necessary adaptation for preventing further weight gain in the obese subject, in an environment wherein excess food intake coupled with inactivity are becoming
168-73. 20. Knowler WC, Pettitt PJ, Savage PJ, Bennett PH. Diabetes incidence in Pima Indians: contributions of obesity and parental diabetes. Am J Epidemiol 1981; 113: 144-56. 21. UK Prospective Study of Therapies of Maturity Onset Diabetes. I, Effect of diet, sulphonylurea, insulin or biguanide therapy on fasting plasma glucose and body weight over one year. Diabetologia 1983; 24: 404-11. 22. Flatt JP. Dietary fat, carbohydrate balance, and weight maintenance: effects of exercise. Am J Clin Nutr 1987; 45: 296-306. 23. Holloszy JO, Coyle EF. Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. J Appl Physiol 1984; 56: 831-38. 24. Bielinski R, Schutz Y, Jequier E. Energy metabolism during the postexercise recovery in man. Am J Clin Nutr 1985; 42: 69-82. 25. LeBlanc J, Nadeau A, Richard D, Tremblay A. Variations in plasma glucose, insulin, growth hormone and catecholamines in response to insulin in trained and non-trained subjects. Metabolism 1982; 31: 453-56. 26. Donahue RP, Abbot RD, Bloom E, Reed DM, Yano K. Central obesity and coronary heart disease in men. Lancet 1987; i: 821-24.
increasingly common.
VIEWPOINT REFERENCES
1. Buchanan TA, Metzger BE, Freinkel N, Bergman RN. Insulin sensitivity and B-cell responsiveness to glucose during late pregnancy in lean and moderately obese women with normal glucose tolerance or mild gestational diabetes. Am J Obstet Gynecol 1990; 162: 1008-14. 2. Bloch CA, Clemons P, Sperling MA. Puberty decreases insulin sensitivity. J Pediatr 1987; 110: 481-87. 3. Newman WP, Brodows RG. Insulin action during acute starvation: evidence for selective insulin resistance in normal man. Metabolism 1983; 32: 590-96. 4. Haffner SM, Stem MP, Hazuda HP, Mitchell BD, Patterson JK, Ferrannini E. Parental history of diabetes is associated with increased cardiovascular risk factors. Arteriosclerosis 1989; 9: 928-33. 5. Hollenbeck CB, Chen N, Chen Y-DI, Reaven GM. Relationship between the plasma insulin response to oral glucose and insulinstimulated glucose utilization in normal subjects. Diabetes 1984; 33: 460-63. 6. Kadowaki T, Bevins CL, Cama A, et al. Two mutant alleles of the insulin receptor gene in a patient with extreme insulin resistance. Science 1988; 240: 787-90. 7. Rossini A. Lipoatrophic diabetes. In: Marble A, Krall LP, Bradley RF, Christlieb AR, Soeldner JS, eds. Joslin’s diabetes mellitus, 12th ed. Philadelphia: Lea and Febiger, 1985: 834-42. 8. Reaven GM. Barting lecture 1988: role of insulin resistance in human disease. Diabetes 1988; 37: 1595-607. 9. Kolterman OG, Gray RS, Griffin J, et al. Receptor and postreceptor defects contribute to the insulin resistance in non-insulin-dependent diabetes mellitus. J Clin Invest 1981; 68: 957-69. 10. Wigand JP, Blackard WG. Down-regulation of insulin receptors in obese men. Diabetes 1979; 28: 207-91. 11.Randle PJ, Garland PB, Hales CN, Newsholme EA. The glucose fatty-acid cycle: its role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Lancet 1963; i: 785-89. 12. Olefsky JM, Reaven GM, Farquhar JW. Effects of weight reduction in obesity: studies of lipid and carbohydrate metablism in normal and hyperlipoproteinemic subjects. J Clin Invest 1974; 53:64-76. 13. Eckel RH. Lipoprotein lipase: a multifunctional enzyme relevant to common metabolic diseases. N Engl J Med 1989; 320: 1060-68. 14. Farese RV Jr, Yost TJ, Eckel RH. Tissue-specific regulation of lipoprotein lipase activity by insulin/glucose in normal-weight humans. Metabolism 1991; 40: 214-16. 15. Eckel RH, Yost TJ. Weight reduction increases adipose tissue lipoprotein lipase responsiveness in obese women. J Clin Invest 1987; 80: 992-97. 16. Kramer FM, Jeffrey RW, Forster HL, Snell MK. Long-term follow-up of behavioral treatment for obesity: patterns of weight regain among men and women. Int J Obesity 1989; 13: 123-36. 17. Ravussin E, Lillioja S, Knowler WC, et al. Reduced rate of energy expenditure as a risk factor for body weight gain. N Engl J Med 1988; 318: 467-72.
John Bostock, hay fever, and the mechanism of allergy
John Bostock was a physician at the Royal Infirmary in Liverpool for 20 years until he moved to London in 1817 and gave up the practice of medicine. He then devoted himself to academic pursuits, wrote the first textbook of physiology in the English language, was appointed lecturer in chemistry at Guy’s Hospital, and ultimately became a vice-president of the Royal Society.1 Bostock had suffered since the age of eight years with what was at that time an unusual affliction. Each year at the beginning of June he developed a cold which lasted for about two months and was associated with a profuse nasal discharge, repeated paroxysms of sneezing, itching of the eyes, difficulty in breathing, and severe malaise. He recognised that these features represented a syndrome which was distinct from the common cold and recorded his own case history in 1819. This is now generally accepted as the first complete description of hay fever. After publication of the paper contemporary observers noted that hay fever was an uncommon conditionand it took Bostock 9 years to collect another 28 cases for a second article.4 Since then, hay fever has become much more common and current estimates suggest a prevalence of about 10% in Europe and the United States.s Emanuel6 has surveyed the published work and concludes that, before 1800, descriptions of hay fever were extremely rare and incomplete; in biblical, Greek, or Roman writings there are none at all. Heberden described a summer cold but did not comment on the itching of the eyes, the long duration of illness, or the associated lethargy which are so ADDRESS: Medical Unit, Royal Liverpool Liverpool L7 8XP, UK (Dr R Finn, FRCP).
University Hospital,
1454
characteristic of severe hay fever. There were also descriptions of the "rose cold", which was regarded as a rarity. Since hay fever is so obviously different from the common cold, it is highly unlikely to have been missed by earlier physicians. We cannot completely exclude the possibility that hay fever was present before the 19th century but had simply not been recognised; there is, however, strong objective evidence that it was much less common in the 19th century than it is now. Hay fever was not mentioned in the Edinburgh Medical and Physical Dictionary (1807). Bostock’s report of his own case was of sufficient interest to merit presentation to a medical society. Bostock commented in 1828 that "one of the most remarkable circumstances respecting this complaint is its not being noticed as a specific affection, until within the last 10 or 12 years". Public dispensary records where the poor were given free medicines showed a decrease in "cattarhus" in the summer months rather than an increase, as would be expected with hay fever.6 Elliotson, in lectures to medical students at St Thomas’, stated that it was a very "extraordinary affection" and he had only seen 2 cases.3 We may therefore accept Emanuel’s conclusion that hay fever is a new disease.6 Today it is so common that television and the newspapers provide us with pollen counts during the summer months. Bostock did not relate his condition to pollen but believed that its seasonal incidence was due to physical factors, possibly temperature. Charles Blackley, a physician in Manchester who also suffered from hay fever, collected some grass pollen in the summer and stored it in a bottle until the middle of the winter. He then removed the top of the bottle and inhaled the pollen. This immediately caused an acute attack with streaming eyes, running nose, and sneezing. This simple and elegant exeriment proved that hay fever was a sensitivity to pollen.7 These historical facts raise the question as to why the first accounts of hay fever and its mechanism came from two physicians from the north-west of England-which was at that time very far removed from the centres of medical excellence and academia such as London, Edinburgh, Paris, and Berlin. To this may be added the question as to why hay fever first appeared at the beginning of the 19th century. The most likely answer to both these questions relates to a third question-was there anything special about the north of England at the beginning of the 19th century? The obvious answer is the Industrial Revolution which began in this area and led to massive chemical pollution for the first time in human history. Chronic chemical damage to the nasal mucosa would facilitate the entry of pollen antigens, leading to immunological sensitisation. According to our current understanding hay fever is due to an allergy to pollen in sensitive subjects. The allergic or sensitivity state is manifested by a high IgE which is probably inherited as an autosomal dominant on chromosome llq.11 This explanation does not, however, explain the rarity of the condition before 1800 or its greatly increased prevalence since; grass has been a feature of the landscape for many thousands of years. A genetic mutation leading to a raised IgE could not be the explanation because a mutation in 1800 could not spread to 10% of the population in less than 200 years. This paradox only becomes explicable if chemical pollution is entered into the equation, coincident with the Industrial Revolution in about 1800. Work in laboratory animals points to an interaction between allergens and pollutants such as S02’ N02, 03, and
vehicle exhausts.9 Thus exposure of guineapigs to ozone at 5 parts per million increases the likelihood of sensitisation and anaphylaxis after inhalation of an albumen aerosol." Intraperitoneal sensitisation of mice to Japanese cedar pollen occurs with concurrent administration of diesel exhaust particles but not without." Blackley originally noted that hay fever was more common in the town than the country, and the incidence of red cedar hay fever in Japan is directly related to the level of pollutants." Thus it is widely accepted that irritant damage to mucous membranes acts as an aggravating factor in allergic disease. The historical data relating to hay fever suggest something very different-namely, that chemical damage to the mucous membrane of the nose is a primary event, and without such damage hay fever would not occur or would occur only very rarely. Primary sensitisation through an intact nasal mucous membrane would be unlikely. The nasal mucosa has evolved to prevent the entry of antigens, but the sudden onset of massive chemical pollution has overwhelmed the natural resistance of the nasal mucous membrane. Throughout his career both in Liverpool and later in London, Bostock was an active chemist and wrote several papers on the chemical composition of body fluids including urine.13 He was later to work with Richard Bright at Guy’s, and can be regarded as the first English chemical pathologist. Might his laboratory work, which brought him into regular contact with irritant chemicals, have exacerbated his undoubtedly severe seasonal rhinitis? Bostock gave a paper14 to the Literary and Philosophical Society in Liverpool in 1817 entitled "The best means of obviating the nuisance arising from the smoke of steam engines". Unfortunately the text of this paper has not survived, but Bostock was almost certainly aware of the dangers of chemical pollution. This could have been one of the earliest papers on the effects of chemical pollution, since the steam engine was the major cause of pollution consequent on the Industrial Revolution. The immune system has evolved over millions of years and must have developed powerful homoeostatic mechanisms; spontaneous dysregulation of the immune system, as in allergy, would be an unlikely primary event. Thus, allergies will tend to occur only as a result of external chemical damage predisposing to sensitisation. This could act either by damage to mucosal surfaces with consequent entry of large amounts of antigen, or by direct damage to the immune system leading to destabilisation. This historical analysis suggests that certain allergies are diseases of civilisation, and that the current high incidence of allergic diseases might be reduced by control of chemical
pollution.
REFERENCES 1. Obituary. Dr J. Bostock. Lancet 1846; ii: 222. 2. Bostock J. Case of a periodical affection of the eyes and chest.
Medico-Chirurg Trans 1819; 10: 161-62. 3. Elliotson J. On hay fever. Lancet 1830; ii: 370-73. 4. Bostock J. On the cattarhus aestivus or summer catarrh. Medico-Chirurg Trans 1828; 14: 437-46. 5. Fleming DM, Crombie DL. Prevalence of asthma and hay fever in England and Wales. BMJ 1987; 296: 279-83. 6. Emanuel MB. Hay fever, a post industrial revolution epidemic: a history of its growth during the 19th century. Clin Allergy 1988; 18: 295-304. 7. Blackley CH. Experimental researches on the causes and nature of cattarhus aestivus (hay fever or hay asthma) London. Baillière, Tindall and Cox, 1873.
1455
8. Cookson WOCM, Young RP, Sandford AJ, et al. Maternal inheritance of atopic IgE resposiveness on chromosome 11q. Lancet 1992; 340: 381-84. 9. Molfino NA, Slutsky AS, Zamel N. The effects of air pollution on allergic bronchial responsiveness. Clin Exp Allergy 1992; 22: 667-72. 10. Matsumara Y. The effects of ozone, nitrogen dioxide, and sulphur dioxide on the experimentally induced allergic respiratory disorder in guinea pigs 1. The effect on sensitisation with albumin through the airway. Am Rev Respir Dis 1970; 102: 430-37. 11. Murawaka M, Suzuki S, Koizumi K, et al. Adjuvant activity of diesel exhaust particulates for the production of IgE antibodies in mice. J Allergy Clin Immunol 1986; 77: 616-23.
12. Ishizaki
T, Koizumi K, Ikemori R, et al. Studies of prevalence of Japanese cedar pollinosis among the residents in a densely cultivated area. Ann Allergy 1987; 58: 265-70. 13. Bostock J. On the nature of animal fluids. Medico-Chirurg Trans 1813; 4: 53-88. 14. Bostock J. The best means of obviating the nuisances arising from the smoke of steam engines. Minutes of the Literary and Philosophical Society of Liverpool 1812-1817. Liverpool City Archives 060 LIT.
1/1. 15. Sears MR.
Epidemiology of asthma. In: O’Byrne PM, ed. Asthma as an inflammatory disease. New York: Dekker, 1990: 15-48.
BOOK SHELF Principles and Practice of Surgery for the Colon, Rectum, and Anus Edited by Philip H. Gordon, Santhat Nivatvongs. St Louis: Quality Medical Publishing. 1992. Pp 1097. 195. ISBN 0-942219104.
Philip Gordon and Santhat Nivatvongs have produced a "must" for every colorectal surgeon. The text is profusely illustrated in colour and the book is a positive pleasure to read. Its authors are up-to-the-minute performers from the North American colorectal seminar circuit. Their written accounts of individual conditions reflect all the views, prejudices, and talking points that are current across the USA and Canada. Phil Gordon from Montreal is a regular and popular presenter of basic surgical science lectures to surgeons. The first two chapters on surgical anatomy and physiology are therefore especially splendid. Some of the arterial anatomy is oversimplified and I would like to have seen more extensive coverage of the difficult area of autonomic nerve anatomy in the pelvis. I applaud their philosophy of careful identification and preservation of the nerve plexuses as a basic principle of colorectal surgery. Curiously, however, for a book so well illustrated there were few surgeon-friendly illustrations to assist this process. A further area that will especially suit the surgeon is the discussion about the awkward interface between basic physiology and anorectal manometry, electromyography, etc, and the clinical applications of these techniques. A physiology chapter of 35 pages equips the surgeon with the facts necessary to understand often incomprehensible modem symposia, whilst the 160 references permit complete immersion for the real enthusiast. In the field of diagnostic imaging, I would have preferred more about the potential of computed tomography, magnetic resonance imaging, and endorectal ultrasound. Anorectal disorders are well done with clear comprehensible drawings among 275 pages of excellent writing. When I turned to rectal carcinoma-a controversial subject of particular interest to me-it would be surprising if some points of disagreement did not emerge. Most of the pictures of stapling machines add nothing and the discussion about high ligation omits its only real value: that of releasing the splenic flexure for a low anastomosis. Scant mention is accorded to irrigation of the rectal stump below a clamp. This is a serious mistake because it is likely to lead younger readers to omit this simple precaution against preventable local recurrence. Exclusion from a clinical trial of adjuvant therapy because the rectal stump is washed out with water verges on the absurd and, in my view, conveys
incorrect priorities. My criticisms are few. The book’s name is similar to the "bible" of our specialty: Surgery of the Anus, Rectum and Colon by Professor J. C. Goligher, whose achievement still remains unsurpassed. But Phil Gordon and Sandy Nivatvong’s effort certainly deserves a place on the shelf beside it. Colorectal Research Unit, Basingstoke District Hospital, Basingstoke RG24 9NA, UK
Atlas of
R.
J. HEALD
Transvaginal Surgery
S. Raz. London: Saunders. 1992. 0-721624316.
Pp
288.
78. ISBN
Dr Raz and his publishers have produced a wellpresented description of transvaginal surgery. But why transvaginal surgery? Because so much can be done by this route rather than an abdominal approach, and with far less morbidity and upset to the patient. And gynaecologists are accustomed to doing most of their operative work from the sitting position! I found the diagrams of the various operations for stress incontinence valuable. A helpful addition would have been the 3/0 coated vicryl round-bodied 22 mm J-shaped needle. This suture is useful in repair of vesico-vaginal fistulae, reconstruction of the urethra, and anterior colporrhaphy. Three cheers for Indigo Carmine, which is still available in the USA. Anyone will tell you that it is much better than methylene blue, which we in the UK are obliged to use. In the description of posterior vaginal repair, interrupted rather than continuous sutures are best adopted to prevent shortening of the posterior vaginal wall. The author admits that the timing of surgery is a controversial issue in repair of vesico-vaginal fistulae and he advocates a short waiting period of only 2-3 weeks in some cases. While this approach will undoubtedly appeal to patients, the truth is that by operating early one will include some unnecessary procedures because at least 4% heal spontaneously. In advocating retention of the fistulous tract, it would be helpful to have had the evidence that it "provides a ring of protection against post-surgical bladder spasms." Is excision of Bartholin’s cyst ever justified? Surely marsupialisation is the operation of choice to prevent recurrence.
Birmingham Maternity Hospital, Queen Elizabeth Medical Centre, Birmingham B15 2TG, UK
JOHN KELLY
