editor:
comments
Diet Donald
and 0.
the
Castell,’
lower
CA PT,
MC,
esophageal
The
American
Journal
H. Floch,
M.D.
in gastroenterology
sphincter
USN
Clinicians have recognized for many years that heartburn often occurs after eating, and is most likely to develop after the ingestion of specific kinds of foods in different individuals. This well-known relationship between ingestion of various foods and the development of symptoms of gastroesophageal reflux has been supported by recent physiologic studies. By the use of precise esophageal manometric techniques clear associations have been documented between food ingestion and changes in lower esophageal sphincter (LES) pressure. In addition, the importance of LES pressure in preventing reflux symptoms after food ingestion has been emphasized by a survey recently performed in our laboratory. In this evaluation the number of foods precipitating heartburn was found to be greater in patients with decreased resting sphincter pressures, and a significant inverse correlation was present between [ES pressure and number of heartburn-causing foods. In the normal human esophagus the LES maintains a high pressure zone of approximately 15-- 20 mm Hg above the pressure within the stomach (1). Failure to maintain this normal pressure barrier results in regurgitation of acid gastric contents into the esophagus and the common symptom of heartburn. Control of normal [ES pressure is maintained by a complex interplay of neural, hormonal and mechanical factors, many of which are only now being elucidated (2). The potential actions of gastrointestinal hormones such as gastrin, secretin, and cholecystokinin in regulation of sphincter pressure would appear to have important relationships with the effect of various foods on pressure changes in this region. The observation that exogenous administration of the hormone gastrin resulted in dramatic increases in [ES pressure aroused 1296
Marlin
of Clinical
Nutrition
Downloaded from https://academic.oup.com/ajcn/article-abstract/28/11/1296/4732875 by Washington University in St. Louis user on 23 May 2018
interest on the potential role of this and other gastrointestinal hormones in maintaining sphincter tone, particularly during certain physiologic conditions (3). Subsequently, the effects of secretin and cholecystokinin in decreasing [ES pressure were demonstrated (4, 5). Since these, and other, hormones are believed to be released following ingestion of meals, studies on food effects on the sphincter seemed quite appropriate. It was not surprising that high protein meals, well-known releasers ofgastrin, increased [ES pressure (6). However, of more importance to the clinician has been the observation that ingestion of a fatty meal causes dramatic decreases in LES pressure, and tends to result in reflux symptoms even in usually asymptomatic volunteer subjects (6). In fact, it seems likely that gastric acid reflux resulting from fat-induced lowering of sphincter pressure accounts for a large number of patients with fatty food intolerance. The mechanism by which fat decreases sphincter pressure would appear to be at least partially through the release of cholecystokinin from the small intestinal mucosa, since this peptide is released primarily in response to fat ingestion. Another common foodstuff that has recently been shown to have a deleterious effect on normal [ES pressure is chocolate (7). Although the chocolate lowering of [ES pressure was originally considered due to the high fat content of most chocolate preparations, the use of a defatted chocolate syrup has indicated that chocolate itself decreases sphincter pressure. The mechanism of action is most likely explained by the high content of methyl xanthines (caffeine and theobromine) in chocolate, and their inhibition of phospho-
tional
Chairman, Naval
28: NOVEMBER
Department Medical Center,
1975,
pp.
of Internal Bethesda,
1296-1298.
Medicine, Maryland
Printed
Na20014
in U.S.A.
DIET
AND
THE
LOWER
ESOPHAGEAL
diesterase, resulting in accumulation of cyclic AMP. Clinically, chocolate is a well-known “bad actor” in patients with heartburn symptoms. The effect of coffee or caffeine on [ES pressure is of particular interest. Although this methyl xanthine does not have the marked sphincter lowering effect of chocolate, it does result in slight decreases in pressure even in the dose range commonly encountered in one to two cups of coffee (8). More importantly, the slight decreases in sphincter pressure occur during the first 30 to 45 mm after caffeine ingestion, at the same time that maximal increases in gastric acid secretion have been documented after caffeine. Thus while lowering sphincter pressure concurrent with stimulation of gastric acid, coffee or caffeine have a dual role in the potential production of increased acid reflux and heartburn. Alcohol produces indigestion in many normal individuals and there are a variety of reasons for the development of such symptoms. A reduction in [ES pressure and resuIting acid reflux is also quite likely after the ingestion of alcohol (9). Recent studies have demonstrated that alcohol ingestion will decrease LES pressure and concurrently result in disordered motility of esophagus. These events should make the reflux of acid and the delayed clearing of acid from the esophagus likely, and thereby contribute to development of heartburn. Other common foods which are often incriminated by heartburn sufferers as aggravating their symptoms include citrus juices and “spicy” foods. Systematic study of the
TABLE I Effects of common sphincter pressure
foods on lower esophageal in normal subjects Mean maximal
Effect
(6)’
Increase Decrease
+8 -8
20-30 5-10
Chocolate(7) Caffeine(8) Alcohol (9) Smoking(lO)
Decrease Decrease Decrease Decrease
Peppermint(lI)
Decrease
-10 -5 -8 -8 ND’
5-10 30 ND’ 5 5
Protein Fat(6)
a
Reference
num ben from
pressure change. mm Hg
Onset
Food
text.
‘
Not
of
effect, (mm)
documented.
Downloaded from https://academic.oup.com/ajcn/article-abstract/28/11/1296/4732875 by Washington University in St. Louis user on 23 May 2018
SPHINCTER
1297
effects of such agents have failed to reveal persistent decreases in [ES pressure, with only transient lowering of pressure noted immediately following ingestion (7). However, orange juice has been shown to result in disordered motility in the lower segment of the esophagus. These observations suggest that this mildly acid substance may result in symptomatology due to a more direct irritating effect on the lower esophagus, particularly in patients with an already inflamed esophagus secondary to chronic acid reflux. Although the content of spicy foods varies tremendously, one common factor is a tomato base. Like orange juice, tomato products tend to have a somewhat acidic pH, and might be irritating to the inflamed esophagus. Our studies have documented that tomato juice will also cause some degree of disordered motility in the distal portion of the esophagus, again suggesting that spicy foods containing tomato products may exert their symptomatology more through direct irritation than through a predominant sphincter lowering action. Another particular “bad actor” in production of heartburn symptoms in susceptible patients is cigarette smoking. Cigarettes result in very dramatic and rapid decreases in [ES pressure, which are sustained during the period of smoking, and then quickly return toward normal (10). Although the exact mechanism by which cigarette smoking lowers sphincter pressure is not clear, recent studies indicate that nicotine itself has a strong action in decreasing [ES pressure. The mechanism of this effect would appear to be through the action of nicotine on the neural controls of normal [ES pressure. Other food substances which have been shown to result in decreased [ES pressure and apparent reflux are carminatives ( I I). These volatile oils, including peppermint and spearmint, which are often included in foods and after dinner liqueurs, may provide another explanation for postprandial heartburn. Although the foods which are likely to produce heartburn symptoms in susceptible patients are many and varied, and not all have been systematically studied in the physiology laboratory, the mechanisms by which some of the more common heartburn producers exert their effect are becoming more clearly defined. Most patients note exacerbation of
1298
CASTELL
their symptoms after fatty foods, spicy foods, alcohol, or chocolate ingestion. In addition, smoking also is a frequent promoter of increasing heartburn, particularly when combined in the usual after-dinner cigarette and cup ofcoffee. The implication ofthese clinical observations with their recent physiologic support is important in the practice of clinical medicine. Certainly the patient with regular reflux symptoms is well-advised to avoid the use of any or all of the items listed in the above discussion. El
4.
References
9.
1. WINANS, C. S., AND L. D. HARRIS. Quantitation of lower esophageal sphincter competence. Gastroenterology 52: 773-778, 1967. 2. CASTEI.L, D. 0. The lower esophageal sphincter: physiologic and clinical aspects. Ann. Intern. Med. In press. 3. CASTELL, D. 0., AND L. D. HARRIS. Hormonal control of gastroesophageal sphincter strength. New. EngI. J. Med. 282: 886-889, 1970.
Downloaded from https://academic.oup.com/ajcn/article-abstract/28/11/1296/4732875 by Washington University in St. Louis user on 23 May 2018
COHEN, tion
of
S.,
AND
human
W.
lower
LIPSHUTZ.
Hormonal
esophageal
sphincter
regulastrength.
Invest. 50: 449-454, 1971. H., D. H. STERN, R. A. STURDEVANT, et al. Effect of the C-terminal octapeptide of cholecystokinin on lower esophageal sphincter pressure in man. Gastroenterology 64: 946-949, 1973. NEBEL, 0. T., AND D. 0. CASTELL. Lower esophageal sphincter pressure changes after food ingestion. Gastroentenology 63: 778-783, 1972. BABKA, J. C., AND D. 0. CASTELL On the genesis of heartburn. Am. J. Digest. Diseases 18: 391-397. 1973. DENNISH, G. W., AND D. 0. CASTELL. Caffeine and the lower esophageal sphincter. Am. J. Digest. Diseases 17: 993-996, 1972. HOGAN, W. J., S. R. VIEGAS DE ANDRADE AND D. H . WINSHIP. Ethanol-induced acute esophageal motor dysfunction. J. AppI. Physiol. 32: 755-760, 1972. DENNISH, G. W., AND D. 0. CASTELL. Inhibitory
J. Clin. 5.
6.
7.
8.
10.
RESIN,
effect
II.
of smoking
on the
lower
esophageal
sphincter.
New Engl.J. Med. 284: 1136-1137, 1971. SIGMUND, C. J., AND E. F. MCNALLY. The action of a carminative on the lower esophageal sphincter. Gastroenterology 56: 13-18, 1969.
comments
Diet Donald
and 0.
the
Castell,’
lower
CA PT,
MC,
esophageal
The
American
Journal
H. Floch,
M.D.
in gastroenterology
sphincter
USN
Clinicians have recognized for many years that heartburn often occurs after eating, and is most likely to develop after the ingestion of specific kinds of foods in different individuals. This well-known relationship between ingestion of various foods and the development of symptoms of gastroesophageal reflux has been supported by recent physiologic studies. By the use of precise esophageal manometric techniques clear associations have been documented between food ingestion and changes in lower esophageal sphincter (LES) pressure. In addition, the importance of LES pressure in preventing reflux symptoms after food ingestion has been emphasized by a survey recently performed in our laboratory. In this evaluation the number of foods precipitating heartburn was found to be greater in patients with decreased resting sphincter pressures, and a significant inverse correlation was present between [ES pressure and number of heartburn-causing foods. In the normal human esophagus the LES maintains a high pressure zone of approximately 15-- 20 mm Hg above the pressure within the stomach (1). Failure to maintain this normal pressure barrier results in regurgitation of acid gastric contents into the esophagus and the common symptom of heartburn. Control of normal [ES pressure is maintained by a complex interplay of neural, hormonal and mechanical factors, many of which are only now being elucidated (2). The potential actions of gastrointestinal hormones such as gastrin, secretin, and cholecystokinin in regulation of sphincter pressure would appear to have important relationships with the effect of various foods on pressure changes in this region. The observation that exogenous administration of the hormone gastrin resulted in dramatic increases in [ES pressure aroused 1296
Marlin
of Clinical
Nutrition
Downloaded from https://academic.oup.com/ajcn/article-abstract/28/11/1296/4732875 by Washington University in St. Louis user on 23 May 2018
interest on the potential role of this and other gastrointestinal hormones in maintaining sphincter tone, particularly during certain physiologic conditions (3). Subsequently, the effects of secretin and cholecystokinin in decreasing [ES pressure were demonstrated (4, 5). Since these, and other, hormones are believed to be released following ingestion of meals, studies on food effects on the sphincter seemed quite appropriate. It was not surprising that high protein meals, well-known releasers ofgastrin, increased [ES pressure (6). However, of more importance to the clinician has been the observation that ingestion of a fatty meal causes dramatic decreases in LES pressure, and tends to result in reflux symptoms even in usually asymptomatic volunteer subjects (6). In fact, it seems likely that gastric acid reflux resulting from fat-induced lowering of sphincter pressure accounts for a large number of patients with fatty food intolerance. The mechanism by which fat decreases sphincter pressure would appear to be at least partially through the release of cholecystokinin from the small intestinal mucosa, since this peptide is released primarily in response to fat ingestion. Another common foodstuff that has recently been shown to have a deleterious effect on normal [ES pressure is chocolate (7). Although the chocolate lowering of [ES pressure was originally considered due to the high fat content of most chocolate preparations, the use of a defatted chocolate syrup has indicated that chocolate itself decreases sphincter pressure. The mechanism of action is most likely explained by the high content of methyl xanthines (caffeine and theobromine) in chocolate, and their inhibition of phospho-
tional
Chairman, Naval
28: NOVEMBER
Department Medical Center,
1975,
pp.
of Internal Bethesda,
1296-1298.
Medicine, Maryland
Printed
Na20014
in U.S.A.
DIET
AND
THE
LOWER
ESOPHAGEAL
diesterase, resulting in accumulation of cyclic AMP. Clinically, chocolate is a well-known “bad actor” in patients with heartburn symptoms. The effect of coffee or caffeine on [ES pressure is of particular interest. Although this methyl xanthine does not have the marked sphincter lowering effect of chocolate, it does result in slight decreases in pressure even in the dose range commonly encountered in one to two cups of coffee (8). More importantly, the slight decreases in sphincter pressure occur during the first 30 to 45 mm after caffeine ingestion, at the same time that maximal increases in gastric acid secretion have been documented after caffeine. Thus while lowering sphincter pressure concurrent with stimulation of gastric acid, coffee or caffeine have a dual role in the potential production of increased acid reflux and heartburn. Alcohol produces indigestion in many normal individuals and there are a variety of reasons for the development of such symptoms. A reduction in [ES pressure and resuIting acid reflux is also quite likely after the ingestion of alcohol (9). Recent studies have demonstrated that alcohol ingestion will decrease LES pressure and concurrently result in disordered motility of esophagus. These events should make the reflux of acid and the delayed clearing of acid from the esophagus likely, and thereby contribute to development of heartburn. Other common foods which are often incriminated by heartburn sufferers as aggravating their symptoms include citrus juices and “spicy” foods. Systematic study of the
TABLE I Effects of common sphincter pressure
foods on lower esophageal in normal subjects Mean maximal
Effect
(6)’
Increase Decrease
+8 -8
20-30 5-10
Chocolate(7) Caffeine(8) Alcohol (9) Smoking(lO)
Decrease Decrease Decrease Decrease
Peppermint(lI)
Decrease
-10 -5 -8 -8 ND’
5-10 30 ND’ 5 5
Protein Fat(6)
a
Reference
num ben from
pressure change. mm Hg
Onset
Food
text.
‘
Not
of
effect, (mm)
documented.
Downloaded from https://academic.oup.com/ajcn/article-abstract/28/11/1296/4732875 by Washington University in St. Louis user on 23 May 2018
SPHINCTER
1297
effects of such agents have failed to reveal persistent decreases in [ES pressure, with only transient lowering of pressure noted immediately following ingestion (7). However, orange juice has been shown to result in disordered motility in the lower segment of the esophagus. These observations suggest that this mildly acid substance may result in symptomatology due to a more direct irritating effect on the lower esophagus, particularly in patients with an already inflamed esophagus secondary to chronic acid reflux. Although the content of spicy foods varies tremendously, one common factor is a tomato base. Like orange juice, tomato products tend to have a somewhat acidic pH, and might be irritating to the inflamed esophagus. Our studies have documented that tomato juice will also cause some degree of disordered motility in the distal portion of the esophagus, again suggesting that spicy foods containing tomato products may exert their symptomatology more through direct irritation than through a predominant sphincter lowering action. Another particular “bad actor” in production of heartburn symptoms in susceptible patients is cigarette smoking. Cigarettes result in very dramatic and rapid decreases in [ES pressure, which are sustained during the period of smoking, and then quickly return toward normal (10). Although the exact mechanism by which cigarette smoking lowers sphincter pressure is not clear, recent studies indicate that nicotine itself has a strong action in decreasing [ES pressure. The mechanism of this effect would appear to be through the action of nicotine on the neural controls of normal [ES pressure. Other food substances which have been shown to result in decreased [ES pressure and apparent reflux are carminatives ( I I). These volatile oils, including peppermint and spearmint, which are often included in foods and after dinner liqueurs, may provide another explanation for postprandial heartburn. Although the foods which are likely to produce heartburn symptoms in susceptible patients are many and varied, and not all have been systematically studied in the physiology laboratory, the mechanisms by which some of the more common heartburn producers exert their effect are becoming more clearly defined. Most patients note exacerbation of
1298
CASTELL
their symptoms after fatty foods, spicy foods, alcohol, or chocolate ingestion. In addition, smoking also is a frequent promoter of increasing heartburn, particularly when combined in the usual after-dinner cigarette and cup ofcoffee. The implication ofthese clinical observations with their recent physiologic support is important in the practice of clinical medicine. Certainly the patient with regular reflux symptoms is well-advised to avoid the use of any or all of the items listed in the above discussion. El
4.
References
9.
1. WINANS, C. S., AND L. D. HARRIS. Quantitation of lower esophageal sphincter competence. Gastroenterology 52: 773-778, 1967. 2. CASTEI.L, D. 0. The lower esophageal sphincter: physiologic and clinical aspects. Ann. Intern. Med. In press. 3. CASTELL, D. 0., AND L. D. HARRIS. Hormonal control of gastroesophageal sphincter strength. New. EngI. J. Med. 282: 886-889, 1970.
Downloaded from https://academic.oup.com/ajcn/article-abstract/28/11/1296/4732875 by Washington University in St. Louis user on 23 May 2018
COHEN, tion
of
S.,
AND
human
W.
lower
LIPSHUTZ.
Hormonal
esophageal
sphincter
regulastrength.
Invest. 50: 449-454, 1971. H., D. H. STERN, R. A. STURDEVANT, et al. Effect of the C-terminal octapeptide of cholecystokinin on lower esophageal sphincter pressure in man. Gastroenterology 64: 946-949, 1973. NEBEL, 0. T., AND D. 0. CASTELL. Lower esophageal sphincter pressure changes after food ingestion. Gastroentenology 63: 778-783, 1972. BABKA, J. C., AND D. 0. CASTELL On the genesis of heartburn. Am. J. Digest. Diseases 18: 391-397. 1973. DENNISH, G. W., AND D. 0. CASTELL. Caffeine and the lower esophageal sphincter. Am. J. Digest. Diseases 17: 993-996, 1972. HOGAN, W. J., S. R. VIEGAS DE ANDRADE AND D. H . WINSHIP. Ethanol-induced acute esophageal motor dysfunction. J. AppI. Physiol. 32: 755-760, 1972. DENNISH, G. W., AND D. 0. CASTELL. Inhibitory
J. Clin. 5.
6.
7.
8.
10.
RESIN,
effect
II.
of smoking
on the
lower
esophageal
sphincter.
New Engl.J. Med. 284: 1136-1137, 1971. SIGMUND, C. J., AND E. F. MCNALLY. The action of a carminative on the lower esophageal sphincter. Gastroenterology 56: 13-18, 1969.
