[PHNUTR-L] Arbor Clinical Nutrition Update #260: Heartburn, chocolate, coffee and spices

[Kathrynne Holden, MS, RD]

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Arbor Clinical Nutrition Update #260: Heartburn, chocolate,  coffee and 
spices

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                                  NUTRITION RESEARCH REVIEW


Study 1: Obesity and gastroesophageal reflux
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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 
disorders.

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 
non-GERD controls.

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.


COMMENTARY
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 
reflux (ref.10).

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’.

References:
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.
5. http://www.aboutgerd.org/treatment.html
6. The Merck Manual of Diagnosis and Therapy. Chapter 20. 
http://www.merck.com/mrkshared/mmanual/section3/chapter20/20g.jsp
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. 
http://hopkins-gi.nts.jhu.edu/pages/latin/templates/index.cfm?pg=disease4&organ=1&disease=26&lang_id=1
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.
37. http://www.healingdaily.com/conditions/acid-reflux.htm


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