Here’s some evidence¹ that you’re not imagining what has been the cause of the problem. It’s only a couple of case reports, so that’s marginally better than anecdotal evidence, but still:

Severe Weight Loss Caused by Chewing Gum
Juergen Bauditz, consultant¹, Kristina Norman, nutrition scientist¹, Henrik Biering, junior doctor¹, Herbert Lochs, head of department¹, Matthias Pirlich, consultant^1
1 Department of Gastroenterology, Hepatology, and Endocrinology, Charité Universitätsmedizin, 10117 Berlin, Germany
Correspondence to:J Bauditz juergen.bauditz@charite.de

Sorbitol intake should be considered in patients with bowel problems, chronic diarrhoea, and weight loss.

About 10-20% of adults and adolescents are estimated to have symptoms related to functional bowel disorders, resulting in high healthcare costs.¹ We report two cases of chronic diarrhoea and substantial weight loss in which extensive investigations had been performed previously.

However, final diagnosis was only established after precise evaluation of eating habits, which showed habitual ingestion of sorbitol, a widely used sweetener in food products which has laxative properties.

CASE REPORTS

Case 1

A 21 year old woman had experienced diarrhoea and diffuse abdominal pain for eight months. She had four to 12 bowel movements with watery stools daily. She was initially suspected to have infectious colitis. However, as clinical investigation suggested no clear diagnosis and diarrhoea persisted, she was transferred to our department for further evaluation. At that time she had lost 11 kg and weighed 40.8 kg (body mass index 16.6). Laboratory analysis showed hypoalbuminaemia (albumin 30.7, normal range 33-50 g/l; total protein 64.3, 66-87 g/l). Further laboratory investigations (including antigastrin antibodies, antigliadin antibodies, endomysial antibodies, stool pancreatic elastase, and stool cultures) were normal. The colon had a normal macroscopic appearance on colonoscopy; histology showed no specific changes (single lymphocytes and plasma cells, no granulocytes, normal mucosal architecture) and no evidence of microscopic colitis. Findings of gastroscopy with deep duodenal biopsy, abdominal ultrasound, and computed tomography were normal. Stool collection showed that the patient produced large amounts stool—up to 1900 g daily (normal <250 g). Stool electrolytes were 71 mmol/l of sodium and 34 mmol/l of potassium. Using the formula, osmotic gap = 290–2([Na]+[K]) (x 2 to account for anions), we found the osmotic gap to be 80 mmol/l (normal <50 mmol/l), raising the suspicion of an osmotic purgative. When we questioned the patient further, we found that she chewed large amounts of sugar-free gum, accounting for a total daily dose of 18-20 g sorbitol (one stick contains about 1.25 g sorbitol). After she started a sorbitol-free diet her diarrhoea subsided—with one formed bowel movement daily on discharge from hospital. One year later she still had normal bowel movements (one or two formed stools daily) and had gained 7 kg (body mass index 19.5).

Case 2

A 46 year old man was admitted to our hospital because of diarrhoea and a weight loss of 22 kg within the past year. Extensive diagnostic procedures had been performed previously: Blood and stool investigations (including albumin, protein, antigastrin antibodies, antigliadin antibodies, endomysial antibodies, stool pancreatic elastase, and stool cultures) and endoscopic and radiological examinations (gastroscopy with distal duodenal biopsy, colonoscopy, abdominal ultrasound, and computed tomography) were normal. Histology of colon biopsies showed an intact mucosal architecture with single lymphocytes, no infiltrating granulocytes, and no evidence of microscopic colitis.

On admission he weighed 79.9 kg (body mass index 25.8) and reported abdominal gas, bloating, and seven to 10 watery stools daily. Apart from slight abdominal tenderness his physical examination was normal. Thorough evaluation of the patients’ history with detailed analysis of eating habits suggested that he might have sorbitol induced diarrhoea—he reported chewing 20 sticks of sugar-free gum and eating up to 200 g of sweets each day, which together contained around 30 g sorbitol. We therefore evaluated his stool electrolytes, which were 54 mmol/l for sodium and 33 mmol/l for potassium, resulting in a stool osmotic gap of 116 mmol/l. During a 24 h fast with intravenous fluid substitution diarrhoea stopped, also consistent with osmotic diarrhoea. The patient was then asked to resume his normal diet. Within one day he had four watery stools. After he started a sorbitol-free diet, diarrhoea completely subsided, with one bowel movement daily. Six months later he had gained 5 kg (body mass index 27.4) and had normal stool frequency (one formed stool daily).

DISCUSSION

Valid data on the prevalence of laxative misuse in unselected patients are lacking, but such misuse is thought to be the leading cause of chronic diarrhoea of unknown origin in patients studied prospectively.² A cost-benefit analysis showed that it was cheaper to screen for laxatives than to use diagnostic procedures in patients with laxative misuse.³

Both our patients consumed large amounts of sorbitol, which belongs to the family of polyalcohol sugars, like mannitol and xylitol, some of which are regularly used as laxatives.⁴ However, sorbitol is also used as a sweetener in many sugar-free foods and drug products.⁵ People with diabetes often eat dietetic foods containing sorbitol.⁶ In addition, sugar-free or low sugar foods are increasingly eaten in Western countries by people without diabetes because they are low in calories and are less likely than sugar to cause caries.⁷ As possible side effects are usually found only within the small print on foods containing sorbitol, consumers may be unaware of its laxative effects and fail to recognise a link with their gastrointestinal problems.

As sorbitol is poorly absorbed by the small intestine it acts as an osmotic agent. Ingestion of relatively small amounts (5-20 g) causes gastrointestinal symptoms like gas, bloating, and abdominal cramps in a dose dependent manner. Higher doses (20-50 g) may cause osmotic diarrhoea,^{8 9} as in our patients, in whom prolonged use of sugar-free gum and sweets had led to substantial weight loss; in one of the cases it even led to hypoalbuminaemia as a result of malabsorption. These symptoms fulfil the criteria of severe nutritional risk according to the recently published guidelines of the European Society for Clinical Nutrition and Metabolism (ESPEN).¹⁰ Consumption of just 20 g produces diarrhoea in about half of normal people.¹¹ When we questioned our patients closely, we found that they replaced the gum sticks frequently, which accounts for the high doses of sorbitol ingested. Such habits could partly explain why only a minority of people who chew gum develop diarrhoea. In addition to the osmotic effects, habitual use of chewing gum might also influence stool frequency by stimulating saliva, gastric juices, and intestinal juices and by increasing intestinal motility. Sorbitol consumption is also associated with irritable bowel syndrome.¹²

Analysis of stool composition is a simple and reliable way to clarify diarrhoea of uncertain origin.¹³ In contrast to secretory diarrhoea, stools in osmotic diarrhoea have a large osmotic gap (>50 mmol/l) as a result of the unabsorbed solute. In addition, osmotic diarrhoea responds to fasting whereas secretory diarrhoea does not. Although extensive diagnostic procedures had been performed before, only a careful dietary history and the finding of an abnormally high osmotic gap led to the final diagnosis in both our patients.

In conclusion, our cases show that sorbitol consumption can cause not only chronic diarrhoea and functional bowel problems but also considerable unintended weight loss (about 20% of usual body weight). Thus, the investigation of unexplained weight loss should include detailed dietary history with regard to foods containing sorbitol.

Competing interests: None declared.

Provenance and peer review: Not commissioned; externally peer reviewed.

REFERENCES

Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC. Functional bowel disorders. Gastroenterology 2006;130:1480-91.

Read NW, Krejs GJ, Read MG, Santa Ana CA, Morawski SG, Fordtran JS. Chronic diarrhoea of unknown origin. Gastroenterology 1980;78:264-71.

Bytzer P, Stokholm M, Andersen I, Klitgaard NA, Schaffalitzky deMuckadell OB. Prevalence of surreptitious laxative abuse in patients with diarrhoea of uncertain origin: a cost benefit analysis of a screening procedure. Gut 1989;30:1379-84.

Lederle FA, Busch DL, Mattox KM, West MJ, Aske DM. Cost-effective treatment of constipation in the elderly: a randomized double-blind comparison of sorbitol and lactulose. Am J Med 1990;89:597-601.

Johnston KR, Govel LA, Andritz MH. Gastrointestinal effects of sorbitol as an additive in liquid medications. Am J Med 1994;97:185-91.

Badiga MS, Jain NK, Casanova C, Pitchumoni CS. Diarrhoea in diabetics: the role of sorbitol. J Am Coll Nutr 1990;9:578-82.

Dills WL Jr. Sugar alcohols as bulk sweeteners. Ann Rev Nutr 1989;9:161-86.

Ravry MJ. Dietetic food diarrhoea. JAMA 1980;244:270.

Greaves RR, Bown RL, Farthing MJ. An air stewardess with puzzling diarrhoea. Lancet 1996;348:1488.

Lochs H, Allison SP, Meier R, Pirlich M, Kondrup J, Schneider S, et al. Introductory to the ESPEN guidelines on enteral nutrition: terminology, definitions and general topics. Clin Nutr 2006;25:180-6.

Hyams SJ. Sorbitol intolerance: an unappreciated cause of functional gastrointestinal complaints. Gastroenterology 1983;84:30-3.

Goldstein R, Braverman D, Stankiewicz H. Carbohydrate malabsorption and the effect of dietary restriction on symptoms of irritable bowel syndrome and functional bowel complaints. Isr Med Assoc J 2000;2:583-7.

Eherer AJ, Fordtran JS. Fecal osmotic gap and pH in experimental diarrhoea of various causes. Gastroenterology 1992;103:545-51.

1. Bauditz J, Norman K, Biering H, Lochs H, Pirlich M., Severe Weight Loss Caused by Chewng Gum, BMJ. 2008 Jan 12;336(7635):96-7.

© Periapex for Life's Context, 2008. | Permalink | 22 comments |

BMJ, doi:10.1136/bmj.39231.599815.55 (published 29 June 2007)

Mary Hickson, research dietitian¹, Aloysius L D’Souza, research fellow², Nirmala Muthu, research nurse³, Thomas R Rogers, professor of clinical microbiology and honorary consultant (Hammersmith Hospitals NHS Trust)⁴, Susan Want, clinical scientist⁵, Chakravarthi Rajkumar, senior lecturer², Christopher J Bulpitt, professor of geriatric medicine²

¹ Nutrition and Dietetic Research Group, Faculty of Medicine, Imperial College, London W12 0HS, ² Medicine for the Elderly, Faculty of Medicine, Imperial College, London, ³ Hillingdon Hospital, Uxbridge, ⁴ Department of Infectious Diseases and Immunity, Faculty of Medicine, Imperial College School of Medicine, London, ⁵ Microbiology Department, Hammersmith Hospital NHS Trust, London

Correspondence to: M Hickson mhickson@hhnt.nhs.uk

Objective: To determine the efficacy of a probiotic drink containing Lactobacillus for the prevention of any diarrhoea associated with antibiotic use and that caused by Clostridium difficile.

Design: Randomised double blind placebo controlled study.

Participants: 135 hospital patients (mean age 74) taking antibiotics. Exclusions included diarrhoea on admission, bowel pathology that could result in diarrhoea, antibiotic use in the previous four weeks, severe illness, immunosuppression, bowel surgery, artificial heart valves, and history of rheumatic heart disease or infective endocarditis.

Intervention: Consumption of a 100 g (97 ml) drink containing Lactobacillus casei, L bulgaricus, and Streptococcus thermophilus twice a day during a course of antibiotics and for one week after the course finished. The placebo group received a longlife sterile milkshake.

Main outcome measures:

Primary outcome: occurrence of antibiotic associated diarrhoea.

Secondary outcome: presence of  C difficile toxin and diarrhoea.

Results: 7/57 (12%) of the probiotic group developed diarrhoea associated with antibiotic use compared with 19/56 (34%) in the placebo group (P=0.007). Logistic regression to control for other factors gave an odds ratio 0.25 (95% confidence interval 0.07 to 0.85) for use of the probiotic, with low albumin and sodium also increasing the risk of diarrhoea. The absolute risk reduction was 21.6% (6.6% to 36.6%), and the number needed to treat was 5 (3 to 15). No one in the probiotic group and 9/53 (17%) in the placebo group had diarrhoea caused by C difficile (P=0.001). The absolute risk reduction was 17% (7% to 27%), and the number needed to treat was 6 (4 to 14).

Conclusion: Consumption of a probiotic drink containing L casei, L bulgaricus, and S thermophilus can reduce the incidence of antibiotic associated diarrhoea and C difficile associated diarrhoea. This has the potential to decrease morbidity, healthcare costs, and mortality if used routinely in patients aged over 50.  Lactobacillus for the prevention of any diarrhoea associated with antibiotic use and that caused by Clostridium difficile.

Design Randomised double blind placebo controlled study.

Participants 135 hospital patients (mean age 74) taking antibiotics. Exclusions included diarrhoea on admission, bowel pathology that could result in diarrhoea, antibiotic use in the previous four weeks, severe illness, immunosuppression, bowel surgery, artificial heart valves, and history of rheumatic heart disease or infective endocarditis.

Intervention Consumption of a 100 g (97 ml) drink containing Lactobacillus casei, L bulgaricus, and Streptococcus thermophilus twice a day during a course of antibiotics and for one week after the course finished. The placebo group received a longlife sterile milkshake.

Main outcome measures Primary outcome: occurrence of antibiotic associated diarrhoea. Secondary outcome: presence of C difficile toxin and diarrhoea.

Results 7/57 (12%) of the probiotic group developed diarrhoea associated with antibiotic use compared with 19/56 (34%) in the placebo group (P=0.007). Logistic regression to control for other factors gave an odds ratio 0.25 (95% confidence interval 0.07 to 0.85) for use of the probiotic, with low albumin and sodium also increasing the risk of diarrhoea. The absolute risk reduction was 21.6% (6.6% to 36.6%), and the number needed to treat was 5 (3 to 15). No one in the probiotic group and 9/53 (17%) in the placebo group had diarrhoea caused by C difficile (P=0.001). The absolute risk reduction was 17% (7% to 27%), and the number needed to treat was 6 (4 to 14).

Conclusion Consumption of a probiotic drink containing L casei, L bulgaricus, and S thermophilus can reduce the incidence of antibiotic associated diarrhoea and C difficile associated diarrhoea. This has the potential to decrease morbidity, healthcare costs, and mortality if used routinely in patients aged over 50.

© 2007 BMJ Publishing Group Ltd.

© Ameloblast for Life's Context, 2007. | Permalink | 4 comments |

Lots of people are understandably feeling betrayed after having put the time and emotional energy into reading Frey’s memoirs only to find out that he lied. Oprah is no exception.

There’s a part in his book describing his experience of having multiple root canals without anesthetic. This is unrealistic to most people and also probably untrue in his case. Novocaine hasn’t been used in Dentistry for decades (we use other types of local anesthetics such as lidocaine) and most root canal procedures would be excruciating without anesthetic because we’re fiddling directly with nerve tissue. There’s also the issue of the local anesthetic potentiating his drug addiction. That’s untrue because local has no addictive properties. Local anesthetic interrupts nerve conduction rather than binding to receptors in the brain like general anesthetics or narcotics which make you feel stoned enough to not care about pain.

That being said, most endodontists have done some number of cases without anesthetic. For some patients, the fear of the needle outweighs the actual procedure. If you combine this fear with a tooth that is asymptomatic and already dead (no live nerve in it), it is possible to do a root canal without anesthetic. In fact, there are some cases where the tooth is so heavily infected that anesthetic wouldn’t work anyway because of the amount of pus that has gone into the gums. When these teeth are opened up and pus spews out, the patient usually feels substantial immediate relief.

© Periapex for Life's Context, 2006. | Permalink | 11 comments |

Pseudomembranous Colitis is a severe case of (often bloody) diarrhea. The diarrhea is a result of alterations between the balance of “good” bacteria and “bad” bacteria in the colon. Bacteria exist in all of our intestines and live within this equilibrium. The good bacteria help with some digestive processes and also some pharmacologic processes–the birth control pill relies on good bacteria to help its components get absorbed into the body.

Antibiotics either kill bacteria or stop their proliferation. Most antibiotics will significantly alter the proportion of good bacteria in the intestine. This can lead to failure of oral contraception, or as related to this topic, overgrowth of the bad bacteria.

Clostridium Difficile is a common problem in nursing homes and hospitals because of the population of immuno-compromised patients and the fact that this bacterium can be resistant to antibiotics. It is also generally considered the cause of antibiotic-induced pseudomembranous colitis. Overgrowth of this bacterium in the gut produces toxins that lead to bloody diarrhea. Persistent diarrhea that appears for no obvious reason during antibiotic therapy even up to six weeks after cessation of antibiotics can indicate that you have the condition.

Treatment for the diarrhea is the antibiotic Metronidazole, or in resistant cases, Vancomycin. It is interesting to note that Metronidazole itself can cause pseudomembranous colitis, yet it is also a treatment. As long as Metronidazole wasn’t responsible for the original bacterial imbalance, it should be effective at bringing C. Difficile levels back down.

Dental infections have been shown to be polymicrobial in nature and fuel cariogenesis, periodontal, and endodontic pathosis. Endodontic infection is the number one reason for the emergency use of antibiotics in dentistry.

Decades of microbiologic testing have found that certain species of bacteria turn up again and again in endodontic infections. Susceptibility testing by Baumgartner found that Amoxicillin (combined with Clavulinic acid) was 100% effective at killing bacteria within his study sample. Clindamycin was second at 96%¹.

In addition, there is evidence that is suggestive that teeth which have had root canal treatment in the past, and that are either recurrently or persistently infected, contain bacteria that might be better treated with Clindamycin².

With all of this taken into consideration, it is reasonable to assume that dentists will need to prescribe a significant amount of Clindamycin to control tooth abscesses. A good number of patients’ charts in my office have little stickers indicating Penicillin allergy (Amoxicillin is a type of Penicillin). This then leaves Clindamycin as the next logical choice.

To finish up, here’s the final important fact: Both Amoxicillin and Clindamycin (among other antibiotics) have been shown to contribute to the risk of developing Pseudomembranous Colitis.

With the amount of dental infection out there, we have to assume that there’s a lot of Amoxicillin and Clindamycin being prescribed by dentists. For argument sake, say the incidence of Clinda-induced colitis is 1% and there are 1000 prescriptions a week for Clinda. Ten patients a week would have some sort of diarrhea within 6 weeks of taking the antibiotic. An E.R. department would probably not see all of these patients, but they would sure see a good number of them. This then reinforces within the mind of this particular E.R. Doc, of whom I am writing, that Clinda is bad–very bad. I’m sure he doesn’t ask patients if they’ve been taking any other antibiotics, and if he does, he doesn’t realise the link these antibiotics might have to the diarrhea. He just attributes the diarrhea to something else less obvious.

This particular MD vehemently informs patients that the dentist is at fault for giving them Clindamycin and encourages them to seek further action against the dentist. This type of behaviour is unprofessional, has gone on long enough, and is going to result in action on my part.

As an aside; I recently retreated a root canal on a patient who is the husband of a physician in town. He flared up between appointments, so I prescribed Clinda for him. His wife refused to let him take the antibiotic because they had a patient once who got colitis from it. So she gave him something else (probably Clarithromycin) and the infection got worse while he was taking this other antibiotic. A week later, he was no better off. They reconsidered their choice at that time.

1. Baumgartner JC, Xia T. Antibiotic susceptibility of bacteria associated with endodontic abscesses. J Endod. 2003 Jan;29(1):44-7.
2. Molander A, Reit C, Dahlen G, Kvist T. Microbiological status of root-filled teeth with apical periodontitis. Int Endod J. 1998 Jan;31(1):1-7.

© Ameloblast for Life's Context, 2006. | Permalink | One comment |