- Email: [email protected]
Managed care and education
Letters to the Editor
4.
5.
6.
7.
8.
9.
10.
Minocycline-related lupus. Lancet. 1992; 340:1553. Scott MA, Kauh YC, Luscombe HA. Acquired cutis laxa associated with multiple myeloma. Arch Dermatol. 1976;112:853– 855. Newton JA. Cutis laxa associated with amyloidosis. Clin Exper Dermatol. 1986; 11:87–91. O’Brien JP. Is actinic (solar) damage the provoking cause of “post-inflammatory elastolysis and cutis laxa”? Br J Dermatol. 1976;95:105–106. Gebhart W, Bardach H. The lumpybumpy elastic fiber: a marker of long-term administration of penicillamine. Am J Dermatopathol. 1981;3:33–39. Kerl H, Burg G, Hashimoto K. Fatal, penicillin-induced, generalized, postinflammatory elastolysis (cutis laxa). Am J Dermatopathol. 1993;5:267–276. Koch SE, Williams ML. Acquired cutis laxa: case report and review of disorders of elastolysis. Pediatr Dermatol. 1985;2:282– 288. Lewis P, Hood A, Barnett N, Holbrook KA. Postinflammatory elastolysis and cutis laxa. J Am Acad Dermatol. 1990;22:40 – 48.
THE EFFECTS OF RAMADAN FASTING ON BLOOD LIPID LEVELS To the Editor: The Islamic ritual of fasting during the month of Ramadan requires Muslims to abstain from food and drink
during daylight hours in an effort to achieve better self-control. After sundown, they eat a late supper and midnight breakfast for which there are no dietary restrictions. The time from sunrise to sunset varies, depending on the geographic location and the season, and can be as long as 20 hours. Thus, fasting during Ramadan provides an opportunity to study experimental hunger. We investigated the influence of Ramadan fasting on lipid metabolism. On the first and last days of Ramadan, venous blood samples were taken from 52 healthy volunteers (27 women, mean [⫾ SD] age 33 ⫾ 10 years) after 16 hours of fasting. Serum levels of triglyceride, glucose, and total, low-density lipoprotein (LDL), very low density lipoprotein (VLDL), and high-density lipoprotein (HDL) cholesterol were measured. After fasting, serum total cholesterol, LDL cholesterol, VLDL cholesterol, and triglyceride levels were decreased; however, HDL cholesterol levels were not changed significantly (Table 1). The decreases in blood lipid levels were greater in women. Previous studies have suggested a correlation between loss of weight and decrease in total cholesterol levels (1–3); how-
ever, the women in our study did not lose considerable weight. Studies in laboratory animals have observed the effects of changing eating patterns on metabolic activity. For example, rats developed two important metabolic adaptations when their eating pattern was shifted from their natural nibbling pattern to a single large meal (4,5): they developed an increasing net flux of free fatty acids from fat deposits and an increased gluconeogenesis (6,7). Adaptations such as these may also occur in humans. During short-term hunger, glucose need is supplied by gluconeogenesis (8). Insulin is the principal hormone involved in regulating this initial process of adaptation to fasting, and a reduction in insulin levels increases serum cholesterol levels, probably by changes in the activity of lipoprotein lipase (9). Free fatty acids and amino acids, substrates for gluconeogenesis, are used for the energy supply rather than cholesterol synthesis (10). Our results suggest the possibility that increased blood glucose levels at the end of Ramadan may be related to increased gluconeogenesis. Growth hormone and cortisol also affect gluconeogenesis (11), and these hormones have a circadian rhythm
Table 1. Changes in Body Mass Index and Serum Glucose and Lipid Levels by Sex Men First Day
Last Day
Women P Value
First Day
Mean ⫾ SD Body mass index (kg/m2) Glucose level (mg/dL) Total cholesterol level (mg/dL) Triglyceride level (mg/dL) HDL cholesterol level (mg/dL) LDL cholesterol level (mg/dL) VLDL cholesterol level (mg/dL)
Last Day
P Value
Mean ⫾ SD
24.3 ⫾ 2.4
23.0 ⫾ 2.5
0.05
23.6 ⫾ 4.2
23.6 ⫾ 4.2
0.05
77.7 ⫾ 8.7
91.9 ⫾ 9.6
0.001
75.8 ⫾ 11.1
92.6 ⫾ 7.6
0.001
198.7 ⫾ 24.6
183.5 ⫾ 26.3
0.01
193.3 ⫾ 29.0
173.9 ⫾ 37.2
0.001
150.6 ⫾ 77.4
121.8 ⫾ 57.9
0.05
92.8 ⫾ 34.6
66.2 ⫾ 36.1
0.01
53.3 ⫾ 5.7
54.7 ⫾ 5.8
0.05
53.7 ⫾ 6.7
54.8 ⫾ 6.0
0.05
114.9 ⫾ 22.5
102.3 ⫾ 25.4
0.05
121.0 ⫾ 32.1
106.4 ⫾ 39.8
0.01
29.8 ⫾ 16.0
24.6 ⫾ 11.5
0.05
18.6 ⫾ 6.9
13.1 ⫾ 7.2
0.01
HDL ⫽ high-density lipoprotein; LDL ⫽ low-density lipoprotein; VLDL ⫽ very-low-density lipoprotein. September 2000
THE AMERICAN JOURNAL OF MEDICINE威
Volume 109 341
Letters to the Editor
(12). During Ramadan, Muslims disrupt their sleep with midnight breakfast. Given this changing regimen, the diurnal profiles of these hormones change, and secretion of adrenocorticotropic hormone and growth hormone increases (12), leading to greater gluconeogenesis. Self-disciplinary Ramadan fasting is different from other instances of shortterm hunger. Because of its voluntary nature, neurogenic signals causing the cephalic phase of gastric secretion may be reduced during fasting. In conclusion, Ramadan fasting reduces serum total cholesterol, LDL cholesterol, VLDL cholesterol, and triglyceride levels without a considerable loss of weight. Ahmet Temizhan, MD Department of Cardiology Izzet Tandogan, MD ¨ mer Do¨nderici, MD O Berrin Demirbas, MD Department of Internal Medicine Numune Education and Research Hospital Ankara, Turkey 1. Fedail SS, Murphy D, Salih SY, et al. Changes in certain blood constituents during Ramadan. Am J Clin Nutr. 1982;36: 350 –353. 2. Hallak MH, Nomani MZA. Body weight loss and changes in blood lipid levels in normal men on hypocaloric diets during Ramadan fasting. Am J Clin Nutr. 1988;48: 1197–1210. 3. Follick MJ, Abrams DB, Smith TW, et al. Contrasting short- and long-term effects of weight loss on lipoprotein levels. Arch Intern Med. 1984;144:1571–1574. 4. Gwinup G, Byron RC, Roush WH, et al. Effect of nibbling versus gorging on serum lipids in man. Am J Clin Nutr. 1963;13: 209 –213. 5. Fabry P, Tepperman J. Meal frequency—a possible factor in human pathology. Am J Clin Nutr. 1970;23:1059 –1068. 6. Ashmore J, Weber G. The role of glucose6-phosphatase in the regulation of carbohydrate metabolism. In: Harris RS, ed. Vitamins and Hormones. New York: Academic Press; 1959:17. 7. Mokrosch LC, Davidson WD, McGilvery RW. The response to glycogenic stress of fructose-1, 6-diphosphatase in rabbit liver. J Biol Chem. 1956;222:170. 8. Bray GA. Protein and/or calorie deficiency. In: Sodeman WA, Sodeman TM, 342
September 2000
9.
10.
11.
12.
eds. Pathologic Physiology: Mechanisms of Disease. Philadelphia: WB Saunders; 1985: 972–976. Guyton AC. Lipid metabolism. In: Wonsiewicz MJ, ed. Textbook of Medical Physiology. Philadelphia: WB Saunders; 1991: 754 –765. Kraus-Friedmann N. Hormonal regulation of hepatic gluconeogenesis. Physiol Rev. 1984;64:170. Guyton AC. Insulin, glucagon, and diabetes mellitus. In: Wonsiewicz MJ, ed. Textbook of Medical Physiology. Philadelphia: WB Saunders; 1991:855– 868. Weitzman ED. Circadian rhythms and episodic hormone secretion in man. Annu Rev Med. 1976;27:225–243.
MANAGED CARE AND EDUCATION To the Editor: In their discussion of innovative approaches to education in the era of managed care, Lee et al (1) cited the Association of American Medical Colleges’ (AAMC) program of mission-based management as a strategy to identify “the true costs of medical education” so that the crucial financing issues could be addressed by funders “allocating the necessary resources.” As a faculty member at a school that is a pioneer of mission-based management, I recognize the need for such cost-accounting programs. But being pioneers means experiencing hardships as we blaze the trails that push back the frontiers of medical education. Internists, in particular, have noticed the rough-hewn edges of mission-based management. In the pioneering version of mission-based management, faculty members did not receive credit for teaching or for clinical, research, or administrative work at Department of Veterans Affairs (VA) medical centers. This omission is surprising considering the importance of VA medical centers in internal medicine training programs. Readers of The Green Journal will be especially surprised, given the Letter to the Editor in the same issue as the article by Lee et al that dis-
THE AMERICAN JOURNAL OF MEDICINE威
Volume 109
cussed the implementation of guidelines in the VA (2). Mission-based management seeks to document faculty time required for education, but the path it has chosen is one with limitations. The worthwhile goals of determining the time required to prepare an hour of lecture and the time during rounds that is devoted to teaching, rather than patient care, are pursued through consensus estimates of time. This reliance on estimates has not been refined to reflect current research in medical education, as published in the AAMC’s own journal, which shows that estimates correspond poorly to observations of time allocation (3). Mission-based management leadership has been enthusiastic and supportive, and it believes that the record-keeping and reporting for mission-based management requires only minimal additional effort. However, conversations with secretaries and administrative assistants—the people who actually do those chores— convey the opposite impression. Lee et al were correct to highlight the value that cost accounting can bring to decisions about medical education funding. But for internal medicine, unfortunately, the mission-based management pioneers— even with insightful, hardworking leadership— have many miles to travel before they bridge the gaps of questionable assumptions and smooth the bureaucratic bumps out of the trail. Marvin J. Bittner, MD Medical Department VA Medical Center Departments of Medical Microbiology and Immunology and Internal Medicine Creighton University School of Medicine Omaha, Nebraska 1. Lee MY, Phillips RR, Halpern R. Managed care and education: seizing the opportunities. Am J Med. 2000;108:355–358. 2. Kizer KW, Sawin CT. Increased use of beta-
4.
5.
6.
7.
8.
9.
10.
Minocycline-related lupus. Lancet. 1992; 340:1553. Scott MA, Kauh YC, Luscombe HA. Acquired cutis laxa associated with multiple myeloma. Arch Dermatol. 1976;112:853– 855. Newton JA. Cutis laxa associated with amyloidosis. Clin Exper Dermatol. 1986; 11:87–91. O’Brien JP. Is actinic (solar) damage the provoking cause of “post-inflammatory elastolysis and cutis laxa”? Br J Dermatol. 1976;95:105–106. Gebhart W, Bardach H. The lumpybumpy elastic fiber: a marker of long-term administration of penicillamine. Am J Dermatopathol. 1981;3:33–39. Kerl H, Burg G, Hashimoto K. Fatal, penicillin-induced, generalized, postinflammatory elastolysis (cutis laxa). Am J Dermatopathol. 1993;5:267–276. Koch SE, Williams ML. Acquired cutis laxa: case report and review of disorders of elastolysis. Pediatr Dermatol. 1985;2:282– 288. Lewis P, Hood A, Barnett N, Holbrook KA. Postinflammatory elastolysis and cutis laxa. J Am Acad Dermatol. 1990;22:40 – 48.
THE EFFECTS OF RAMADAN FASTING ON BLOOD LIPID LEVELS To the Editor: The Islamic ritual of fasting during the month of Ramadan requires Muslims to abstain from food and drink
during daylight hours in an effort to achieve better self-control. After sundown, they eat a late supper and midnight breakfast for which there are no dietary restrictions. The time from sunrise to sunset varies, depending on the geographic location and the season, and can be as long as 20 hours. Thus, fasting during Ramadan provides an opportunity to study experimental hunger. We investigated the influence of Ramadan fasting on lipid metabolism. On the first and last days of Ramadan, venous blood samples were taken from 52 healthy volunteers (27 women, mean [⫾ SD] age 33 ⫾ 10 years) after 16 hours of fasting. Serum levels of triglyceride, glucose, and total, low-density lipoprotein (LDL), very low density lipoprotein (VLDL), and high-density lipoprotein (HDL) cholesterol were measured. After fasting, serum total cholesterol, LDL cholesterol, VLDL cholesterol, and triglyceride levels were decreased; however, HDL cholesterol levels were not changed significantly (Table 1). The decreases in blood lipid levels were greater in women. Previous studies have suggested a correlation between loss of weight and decrease in total cholesterol levels (1–3); how-
ever, the women in our study did not lose considerable weight. Studies in laboratory animals have observed the effects of changing eating patterns on metabolic activity. For example, rats developed two important metabolic adaptations when their eating pattern was shifted from their natural nibbling pattern to a single large meal (4,5): they developed an increasing net flux of free fatty acids from fat deposits and an increased gluconeogenesis (6,7). Adaptations such as these may also occur in humans. During short-term hunger, glucose need is supplied by gluconeogenesis (8). Insulin is the principal hormone involved in regulating this initial process of adaptation to fasting, and a reduction in insulin levels increases serum cholesterol levels, probably by changes in the activity of lipoprotein lipase (9). Free fatty acids and amino acids, substrates for gluconeogenesis, are used for the energy supply rather than cholesterol synthesis (10). Our results suggest the possibility that increased blood glucose levels at the end of Ramadan may be related to increased gluconeogenesis. Growth hormone and cortisol also affect gluconeogenesis (11), and these hormones have a circadian rhythm
Table 1. Changes in Body Mass Index and Serum Glucose and Lipid Levels by Sex Men First Day
Last Day
Women P Value
First Day
Mean ⫾ SD Body mass index (kg/m2) Glucose level (mg/dL) Total cholesterol level (mg/dL) Triglyceride level (mg/dL) HDL cholesterol level (mg/dL) LDL cholesterol level (mg/dL) VLDL cholesterol level (mg/dL)
Last Day
P Value
Mean ⫾ SD
24.3 ⫾ 2.4
23.0 ⫾ 2.5
0.05
23.6 ⫾ 4.2
23.6 ⫾ 4.2
0.05
77.7 ⫾ 8.7
91.9 ⫾ 9.6
0.001
75.8 ⫾ 11.1
92.6 ⫾ 7.6
0.001
198.7 ⫾ 24.6
183.5 ⫾ 26.3
0.01
193.3 ⫾ 29.0
173.9 ⫾ 37.2
0.001
150.6 ⫾ 77.4
121.8 ⫾ 57.9
0.05
92.8 ⫾ 34.6
66.2 ⫾ 36.1
0.01
53.3 ⫾ 5.7
54.7 ⫾ 5.8
0.05
53.7 ⫾ 6.7
54.8 ⫾ 6.0
0.05
114.9 ⫾ 22.5
102.3 ⫾ 25.4
0.05
121.0 ⫾ 32.1
106.4 ⫾ 39.8
0.01
29.8 ⫾ 16.0
24.6 ⫾ 11.5
0.05
18.6 ⫾ 6.9
13.1 ⫾ 7.2
0.01
HDL ⫽ high-density lipoprotein; LDL ⫽ low-density lipoprotein; VLDL ⫽ very-low-density lipoprotein. September 2000
THE AMERICAN JOURNAL OF MEDICINE威
Volume 109 341
Letters to the Editor
(12). During Ramadan, Muslims disrupt their sleep with midnight breakfast. Given this changing regimen, the diurnal profiles of these hormones change, and secretion of adrenocorticotropic hormone and growth hormone increases (12), leading to greater gluconeogenesis. Self-disciplinary Ramadan fasting is different from other instances of shortterm hunger. Because of its voluntary nature, neurogenic signals causing the cephalic phase of gastric secretion may be reduced during fasting. In conclusion, Ramadan fasting reduces serum total cholesterol, LDL cholesterol, VLDL cholesterol, and triglyceride levels without a considerable loss of weight. Ahmet Temizhan, MD Department of Cardiology Izzet Tandogan, MD ¨ mer Do¨nderici, MD O Berrin Demirbas, MD Department of Internal Medicine Numune Education and Research Hospital Ankara, Turkey 1. Fedail SS, Murphy D, Salih SY, et al. Changes in certain blood constituents during Ramadan. Am J Clin Nutr. 1982;36: 350 –353. 2. Hallak MH, Nomani MZA. Body weight loss and changes in blood lipid levels in normal men on hypocaloric diets during Ramadan fasting. Am J Clin Nutr. 1988;48: 1197–1210. 3. Follick MJ, Abrams DB, Smith TW, et al. Contrasting short- and long-term effects of weight loss on lipoprotein levels. Arch Intern Med. 1984;144:1571–1574. 4. Gwinup G, Byron RC, Roush WH, et al. Effect of nibbling versus gorging on serum lipids in man. Am J Clin Nutr. 1963;13: 209 –213. 5. Fabry P, Tepperman J. Meal frequency—a possible factor in human pathology. Am J Clin Nutr. 1970;23:1059 –1068. 6. Ashmore J, Weber G. The role of glucose6-phosphatase in the regulation of carbohydrate metabolism. In: Harris RS, ed. Vitamins and Hormones. New York: Academic Press; 1959:17. 7. Mokrosch LC, Davidson WD, McGilvery RW. The response to glycogenic stress of fructose-1, 6-diphosphatase in rabbit liver. J Biol Chem. 1956;222:170. 8. Bray GA. Protein and/or calorie deficiency. In: Sodeman WA, Sodeman TM, 342
September 2000
9.
10.
11.
12.
eds. Pathologic Physiology: Mechanisms of Disease. Philadelphia: WB Saunders; 1985: 972–976. Guyton AC. Lipid metabolism. In: Wonsiewicz MJ, ed. Textbook of Medical Physiology. Philadelphia: WB Saunders; 1991: 754 –765. Kraus-Friedmann N. Hormonal regulation of hepatic gluconeogenesis. Physiol Rev. 1984;64:170. Guyton AC. Insulin, glucagon, and diabetes mellitus. In: Wonsiewicz MJ, ed. Textbook of Medical Physiology. Philadelphia: WB Saunders; 1991:855– 868. Weitzman ED. Circadian rhythms and episodic hormone secretion in man. Annu Rev Med. 1976;27:225–243.
MANAGED CARE AND EDUCATION To the Editor: In their discussion of innovative approaches to education in the era of managed care, Lee et al (1) cited the Association of American Medical Colleges’ (AAMC) program of mission-based management as a strategy to identify “the true costs of medical education” so that the crucial financing issues could be addressed by funders “allocating the necessary resources.” As a faculty member at a school that is a pioneer of mission-based management, I recognize the need for such cost-accounting programs. But being pioneers means experiencing hardships as we blaze the trails that push back the frontiers of medical education. Internists, in particular, have noticed the rough-hewn edges of mission-based management. In the pioneering version of mission-based management, faculty members did not receive credit for teaching or for clinical, research, or administrative work at Department of Veterans Affairs (VA) medical centers. This omission is surprising considering the importance of VA medical centers in internal medicine training programs. Readers of The Green Journal will be especially surprised, given the Letter to the Editor in the same issue as the article by Lee et al that dis-
THE AMERICAN JOURNAL OF MEDICINE威
Volume 109
cussed the implementation of guidelines in the VA (2). Mission-based management seeks to document faculty time required for education, but the path it has chosen is one with limitations. The worthwhile goals of determining the time required to prepare an hour of lecture and the time during rounds that is devoted to teaching, rather than patient care, are pursued through consensus estimates of time. This reliance on estimates has not been refined to reflect current research in medical education, as published in the AAMC’s own journal, which shows that estimates correspond poorly to observations of time allocation (3). Mission-based management leadership has been enthusiastic and supportive, and it believes that the record-keeping and reporting for mission-based management requires only minimal additional effort. However, conversations with secretaries and administrative assistants—the people who actually do those chores— convey the opposite impression. Lee et al were correct to highlight the value that cost accounting can bring to decisions about medical education funding. But for internal medicine, unfortunately, the mission-based management pioneers— even with insightful, hardworking leadership— have many miles to travel before they bridge the gaps of questionable assumptions and smooth the bureaucratic bumps out of the trail. Marvin J. Bittner, MD Medical Department VA Medical Center Departments of Medical Microbiology and Immunology and Internal Medicine Creighton University School of Medicine Omaha, Nebraska 1. Lee MY, Phillips RR, Halpern R. Managed care and education: seizing the opportunities. Am J Med. 2000;108:355–358. 2. Kizer KW, Sawin CT. Increased use of beta-