Re:Fructose Intolerance (malabsorption) & poor response to GF Diet

[Guest guest]

Great stuff Kathy - finally got a chance to read this! Thanks

Jan

In a message dated 12/14/2007 5:33:25 P.M. Mountain Standard Time,

kshattler@... writes:

Jan A pubmed search from 06-07 revealed some of the following that may

interest you:

Dig Dis Sci. 2007 Nov;52(11):2999-Dig Dis Sci. 2007 Nov;52(11)

Division of Gastroenterology, Department of Medicine, Sir Mortimer B.

Jewish General Hospital, McGill University, Montreal, Quebec, Canada.

_aszilagy@...@gaas_ (mailto:aszilagy@...)

Fructose malabsorption is linked to gastrointestinal and other unusual

symptoms. Polymers of fructose are also recognized prebiotics. While some

prebiotics can self-adapt when consumed regularly (resulting in decreased

breath

hydrogen and symptoms), we wondered whether self-adaptation occurs with basic

fructose. We evaluated 90 subjects (61 females). Each completed a diet

questionnaire and underwent a fructose challenge. Breath hydrogen and

quantified

symptom scores were recorded. Group comparisons for sum of breath hydrogen and

total symptom scores were evaluated with the Mann-Whitney U test. Spearman's

correlation coefficient and chi(2) or Fisher's exact test were used as

appropriate. Malabsorption occurred in 29 patients (32.2%) and low-grade

symptoms

without malabsorption in 30 (33%). Women complained of symptoms more frequently

(p = 0.04) and exhibited more fructose malabsorption (p = 0.0527). Breath

hydrogen correlated with symptoms (r = 0.516, p = 0.0037). Adaptation with

increasing pretest fructose intake was absent. We conclude that gender may

influence fructose malabsorption and there is no adaptation to regular

consumption.

Aliment Pharmacol Ther. 2007 Feb 15;25(4):349-Aliment Pharmacol Ther. 2

Department of Gastroenterology and Monash University Department of Medicine,

Box Hill Hospital, , Australia. _peter.gibson@...._

(mailto:peter.gibson@...)

Fructose is found widely in the diet as a free hexose, as the disaccharide,

sucrose and in a polymerized form (fructans). Free fructose has limited

absorption in the small intestine, with up to one half of the population unable

to

completely absorb a load of 25 g. Average daily intake of fructose varies

from 11 to 54 g around the world. Fructans are not hydrolysed or absorbed in

the small intestine. The physiological consequences of their malabsorption

include increasing osmotic load, providing substrate for rapid bacterial

fermentation, changing gastrointestinal motility, promoting mucosal biofilm and

altering the profile of bacteria. These effects are additive with other

short-chain poorly absorbed carbohydrates such as sorbitol. The clinical

significance

of these events depends upon the response of the bowel to such changes; they

have a higher chance of inducing symptoms in patients with functional gut

disorders than asymptomatic subjects. Restricting dietary intake of free

fructose

and/or fructans may have durable symptomatic benefits in a high proportion

of patients with functional gut disorders, but high quality evidence is

lacking. It is proposed that confusion over the clinical relevance of fructose

malabsorption may be reduced by regarding it not as an abnormality but as a

physiological process offering an opportunity to improve functional

gastrointestinal symptoms by dietary change.

Gastrointest Endosc Clin N Am. 2006 Apr;16(2):317-Gast

Department of Medicine I (Gastroenterology, Hepatology, Pneumonology and

Endocrinology)Department of Medicine I (Gastroenterology, Hepatology,

Pneum_Norbert.Krauss@..._

(mailto:Norbert.Krauss@...)

Because of the wide variations in the clinical presentation of celiac

disease and because treatment exists that is effective in most cases, screening

of

the general population for celiac disease has been considered. There is still

no evidence that patients who have symptom-free celiac disease are at

increased risk of small intestinal lymphoma or other complications. Prevention

of

osteoporosis seems to be the strongest indicator for widespread screening

today [22].The major cause of failure to respond to a gluten-free diet is

continuing ingestion of gluten, but other underlying diseases must be

considered.Many different drugs (eg, anti-tumor necrosis factor [TNF]-alpha)

have been

used in patients who have RCD [23]. Steroid treatment has been reported to be

effective even in patients who have underlying early EATL.Histologic recovery

in patients who have celiac disease usually takes several months but can take

up to 1 year, even if the patient remains on a strict gluten-free diet. Some

patients report celiac-related symptoms for months after a single gluten

intake.The definitions for RCD in literature vary. The authors consider the

definition give by Daum and colleagues [24] suitable. They defined true RCD as

villous atrophy with crypt hyperplasia and increased IELs persisting for more

than 12 months in spite of a strict gluten-free diet.If a patient is not

responding well to a gluten-free diet, three considerations are necessary: (1)

the

initial diagnosis of celiac disease must be reassessed;(Because of the wide

variations in the clinical presentation of celiac disease and because

treatment exists that is effective in most cases, screening of the general

population for celiac disease has been considered. There is still no evidence

that

patients who have symptom-free celiac disease are at increased risk of small

intestinal lymphoma or other complications. Prevention of osteoporosis seems

Because of the wide variations in the clinical presentation of celiac disease

and because treatment exists that is effective in most cases, screening of the

general population for celiac disease has been consBecause of the wide

variations in the clinical presentation of celiac disease and because treatment

exists that is effective in most cases, screening of the general population for

celiac disease has been considered. There is still no evidence that patients

who have symptom-free celiac disease are at increased risk of small

intestinal lymphoma or other complications. Prevention of osteoporosis seems to

be

the strongest indicator for widespread screening today [22].The major cause of

failure to respond to a gluten-free diet is continuing ingestion of gluten,

but other underlying diseases must be considered.Many different drugs (eg,

anti-tumor necrosis factor [TNF]-alpha) have been used in patients who have RCD

[23]. Steroid treatment has been reported to be effective even in patients

who have underlying early EATL.Histologic recovery in patients a gluten-free

diet.Eleven patients (7.0%) with persisting (partial) villous atrophy were

considered to have RCD; 5 of them developed EATL [27].RCD type I is

characterized

by normal expression of T-cell antigens and polyclonal TCR gene

rearrangement.a gluten-free diet.Eleven patients (7.0%) with persisting

(partial) villous

atrophy were considered to have RCD; 5 of them developed EATL [27].RCD type

I is characterized by normal expression of T-cell antigens and polyclonal TCR

gene rearrangement.<WBR>RCD type II is characterized by an abnormal IEL

phenotype with the expression of intracytoplasmic CD3e, surface CD103, and the

lack of classic surface T-cell markers such as CD8, CD4, and TCR-alpha/beta.

This clonal IEL population can be considered crypt IEL [24]. RCD II has a poor

prognosis, which is a problem for therapy.Clonal TCR gene rearrangements and

loss of T-cell antigens such as CD8 and TCR-beta in IELs may indicate the

development of an EATL in patients who have RCD.The markers for an overt EATL

are a positive stool blood test, increased lactate dehydrogenase, or

beta2-microglobulin [24]. If an overt lymphoma is suspected, upper and lower

endoscopy,

an ear, nose, and throat work-up, CT scan, capsule endoscopy, and possibly

double-balloon enteroscopy should be performed.Most reports of the

difficulties in treating pa tients who have true RCE are casereports.

and

colleagues [28] reported on an induction of remission by useof the

anti-TNF-alpha

antibody infliximab and maintenance with prednisoloneand azathioprine. Olaussen

and coa gluten-free diet.Eleven patients (7.0%) with persisting (partial)

villous atrophy were considered to have RCD; 5 of them developed EATL [27].RCD

type I is characterized by normal expression of T-cell antigens and polyclonal

TCR gene rearrangement.<WBR>RCD type II is characterized by an abnormal IEL

phenotype with the expression of intracytoplasmic CD3e, surface CD103, and

the lack of classic surface T-cell markers such as CD8, CD4, and

TCR-alpha/beta. This clonal IEL population can be considered crypt IEL [24].

RCD II has a

poor prognosis, which is a problem for therapy.Clonal TCR gene rearrangements

and loss of T-cell antigens such as CD8 and TCR-beta in IELs may indicate the

development of an EATL in patients who have RCD.The markers for an overt

EATL are a positive stool blood test, increased lactate dehydrogenase, or

beta2-microglobulin [24]. If an overt lymphoma is suspected, upper and lower

endoscopy, an ear, nose

Clin Nutr. 2006 Oct;25(5):824-Clin Nutr. 2006 Oct;25(5):

CONCLUSIONS: Sugar malabsorption and intolerance seem to be frequent in

patients with functional abdominal bloating and gas-related complaints. A

malabsorbed sugar-free diet might be a long-term effective therapy in a high

percentage of patients. Further controlled clinical trials are warranted

K.athy J. Shattler, M.S.,RD

Director of Nutrition Services, CEU4U.COM

_Http://www.ceu4u.Htt_ (http://www.ceu4u.com/)

_kshattler@..._ (mailto:kshattler@...)

Virtual Continuing Education University

[Non-text portions of this message have been removed]

Jan Patenaude, RD

Director of Medical Nutrition

Signet Diagnostic Corporation

(Mountain Time)

(toll free)

Fax:

DineRight4@...

Mediator Release Testing and LEAP Diet Protocol for Irritable Bowel

Syndrome, Migraine, Fibromyalgia and more, caused by food sensitivity

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