[PHNUTR-L] Arbor Clinical Nutrition Update #260: Heartburn,
chocolate, coffee and spices
Kathrynne Holden, MS, RD
fivestar at nutritionucanlivewith.com
Wed Sep 6 07:12:21 PDT 2006
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Arbor Clinical Nutrition Update #260: Heartburn, chocolate, coffee and
NUTRITION RESEARCH REVIEW
Study 1: Obesity and gastroesophageal reflux
A new analysis from the Nurses Health study looks at the relationship
between weight and GI reflux.
Subjects and method: 10,545 female nurses completed a questionnaire on
gastroesophageal reflux disease (GERD) symptoms. This was compared with
their BMI as measured 2 yrs earlier.
Results: There was a steady rise in the likelihood of having frequent
GERD symptoms across the entire weight spectrum, from BMI below 20
through to obesity. This was also true in relation to the severity of
GERD symptoms - see Graph (in Acrobat version).
Ref.: N Engl J Med. 2006 Jun 1;354(22):2340-8.
Study 2: Meta-analysis confirms link
A meta-analysis has recently been published of studies on the
association between BMI and GERD, oesophagitis and other related GIT
Subjects and method: From a total of 9 observational studies (involving
nearly 63,000 subjects, including 7,372 cases) six studies found an
association between BMI and GERD symptoms. The combined odds ratio for
GERD in 8 studies was 1.43 (95% CI: 1.16-1.77) for overweight (BMI
25-30) and 1.94 (1.47-2.57) for obese (BMI > 30). Overweight and obesity
were also associated with higher risk of oesophageal carcinoma (OR=1.52
and 2.78 respectively).
Ref.: Ann Intern Med. 2005 Aug 2;143(3):199-211.
Study 3: Timing of meals is important
Japanese researchers looked at whether the timing of meals affects the
risk of having GERD symptoms.
Subjects and method: Case-control study of 147 GERD patients and 294
Results: The interval between dinner and bed-time was strongly
associated with the likelihood of having GERD. With an interval of < 3
hrs, the odds ratio was 7.45 (95% CI: 3.38-16.4) compared with an
interval of at least 4 hrs.
Ref.: Am J Gastroenterol. 2005 Dec;100(12):2633-6.
Symptoms of gastroesophageal reflux disease (GERD), such as heartburn
and indigestion, are extremely common, and not just in Western societies
(ref.1, 2). A recent Swedish study reported GERD symptoms in 40% of a
large adult population, 15% of whom had objective reflux on duodenoscopy
(ref.1). Apart from its impact on quality of life (ref.3), GERD may lead
to oesophagitis and predispose to oesophageal cancer (ref.4).
The possible causes of GERD are many, and amongst them are certainly
nutritional factors. Excessive weight is often mentioned in lay circles
(e.g. ref.5), though not so often in medical textbooks (e.g. 6). As new
Studies 1 and 2 show, it should be mentioned more often. Indeed, Study 1
found a more or less continuous rise in GERD risk from light to
seriously obese BMI.
An interesting refinement to this association was reported in a new
Spanish study showing that recent weight gain (> 5 kg over the
preceding 12 months) is associated with a 50% increase in the risk of
new GERD symptoms over that time period (ref.7). Although this cannot
substitute for a lack of RCTs, these observational results do suggest
cause-and-effect is at play in the overweight-GERD relationship.
Mechanisms for such an effect are not hard to guess. Obesity increases
intra-abdominal pressure and obese patients may have disturbances of GI
motility (ref.8, 9). However, whether overweight is linked to all
aspects and types of GERD is another matter. For example, one study
found obesity was not associated with the laryngeal manifestations of
On the other hand, there is evidence that GERD patients who are
overweight are more likely than those who are not to be admitted to
hospital for GERD-related reasons and to have oesophagitis, including
the pre-cancerous Barrett’s oesophagus (ref.11, 12). If weight loss
could not only reduce the symptoms of GERD, such as heartburn, but also
lower the risk of GIT cancer associated with the condition, this would
be big news.
But that is still speculation. The fact is that, for the moment, the
advice often given to GERD patients to “lose weight (if overweight)”
(ref.13) is not supported by the hard evidence of RCTs demonstrating this.
Other dietary approaches commonly recommended by doctors for GERD
emphasise avoidance of aggravating factors: fatty foods, chocolate,
spices, peppermint, coffee, alcohol, and `acidic foods’ (ref.13).
Patients themselves appear to believe that these foods are involved, and
may add `food allergy’ to the mix (ref.14).
Fat restriction has some rationale because fat slows gastric emptying
and increases lower oesophageal sphincter pressure 13. It could also be
a confounder in the observational relationship of obesity and GERD.
However, some epidemiological data shows that obesity is an independent
risk factor not linked with fat intake 11. Some trials have shown fat
can increase reflux, but more found that it does not (ref.15-17). Total
calorie intake was found to be more important than fat intake in
relation to GERD symptoms in one feeding study (ref.18).
As far as chocolate is concerned, there is evidence that ingestion
decreases oesophageal sphincter pressure and acid reflux (ref.19-21).
However no good trials show that avoiding chocolate reduces symptoms
(ref.21). The situation is similar for alcohol (ref.21-23).
The evidence on coffee as a risk factor is also hard to interpret with
certainty. Whilst some observational data shows it is a risk factor for
GERD (ref.24), other researchers found it to be a protective (ref.25).
(They also found, curiously, that regular use of table salt increased
risk). Data on coffee’s impact on oesophageal sphincter pressure have
been inconsistent (ref.26). There are human trials both showing that
coffee increases reflux and that it does not (ref.27, 28). Coffee does
not decrease gastric pH (ref.29) and whether decaffeination makes any
difference to reflux is also unclear (ref.22, 27, 30).
Very little good objective clinical evidence exists on the impact of
spicy food, other than some isolated data that both chilli and capsaican
(a major active ingredient of chilli) can affect heartburn (ref.31, 32).
Fibre intake was protective against GERD in an Egyptian observational
study 33, but adding fibre did not improve reflux in enterally-fed
patients (ref.34). Increasing colonic fermentation through consumption
of indigestible carbohydrate fructooligosaccharides aggravated reflux in
one trial 35. Intolerance for food protein may be relevant to reflux in
infants (ref.36), but we lack clinical studies confirming that food
allergy plays a significant role in adult reflux, as we do on the idea
held in the lay community (e.g. ref.37) that abnormal bowel flora is
involved and probiotics could therefore help.
Despite this lack of convincing evidence of foods aggravating GERD, your
editor’s many years of clinical experience have taught him not to ignore
patients’ observations about what affects their symptoms.
So, along with regular therapy, a `trial- and-error’ food avoidance
approach may be appropriate when a patient notices that some types of
food affect their indigestion or heartburn. If overweight, weight loss
could well be worthwhile. And finally, the observational data from new
Study 3 suggest that increasing the time between dinner and bedtime may
also be worth fitting into such a patient `N of 1 experiment’.
1. Scand J Gastroenterol. 2005 Mar;40(3):275-85.
2. Clin Gastroenterol Hepatol. 2006 Apr;4(4):398-407.
3. Z Gastroenterol. 2003 Dec;41(12):1137-43.
4. J Nutr. 2002 Nov;132(11 Suppl):3467S-3470S.
6. The Merck Manual of Diagnosis and Therapy. Chapter 20.
7. Am J Gastroenterol. 2006 Feb;101(2):229-33.
8. Obes Surg. 2005 Oct;15(9):1225-32.
9. Obes Res. 2004 Nov;12(11):1723-32.
10. Laryngoscope. 2005 Jun;115(6):1042-5.
11. Cancer Epidemiol Biomarkers Prev. 2005 Nov;14(11 Pt 1):2481-6.
12. Ann Epidemiol. 1999 Oct;9(7):424-35.
13. The John Hopkins Medical Institutions. Gastroenterology and
Hepatology Resource Center.
14. J Gastroenterol Hepatol. 2000 Jan;15(1):35-9.
15. Am J Gastroenterol. 1989 Jul;84(7):782-6.
16. Gut. 1998 Mar;42(3):330-3.
17. Am J Gastroenterol. 1999 May;94(5):1192-6.
18. Scand J Gastroenterol. 2002 Jan;37(1):3-5.
19. Am J Dig Dis. 1975 Aug;20(8):703-7.
20. Am J Gastroenterol. 1988 Jun;83(6):633-6.
21. Arch Intern Med. 2006 May 8;166(9):965-71.
22. Gut. 1978 Apr;19(4):336-8.
23. Scand J Gastroenterol. 2003 Aug;38(8):807-11.
24. World J Gastroenterol. 2004 Jun 1;10(11):1647-51.
26. Gut. 2004 Dec;53(12):1730-5.
26. Scand J Gastroenterol Suppl. 1999;230:35-9.
27. Aliment Pharmacol Ther. 1994 Jun;8(3):283-7.
28. Eur J Gastroenterol Hepatol. 1999 Nov;11(11):1271-6.
29. Dig Dis Sci. 1998 Apr;43(4):834-9.
30. Aliment Pharmacol Ther. 1997 Jun;11(3):483-6.
31. Dig Dis Sci. 1998 Mar;43(3):485-90.
32. Aliment Pharmacol Ther. 2000 Jan;14(1):129-34.
33. Gut. 2005 Jan;54(1):11-7.
34. Clin Nutr. 2001 Aug;20(4):307-12.
35. Gastroenterology. 2003 Apr;124(4):894-902.
36. J Pediatr. 2000 May;136(5):641-7.
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