Fructose malabsorption may be gender dependent and fails to show compensation by colonic adaptation.

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.

The effect of lactose maldigestion on the relationship between dairy food intake and colorectal cancer: a systematic review.

Dairy food consumption has been inconsistently shown to protect against colorectal cancer (CRC) in case-based studies, and no clear benefits against recurrent colonic polyps (CRP) have been reported. Based on population-based studies we have hypothesized that dairy food intake may have anti-CRC effects at both low intake lactase non-persistent (LNP) populations and at high intake lactase persistent (LP) subjects. We separately analyse existing case-based studies and divide origins into high LNP (>or= 80% LNP prevalence), low LNP (prevalence

Evaluation of relationships among national colorectal cancer mortality rates, genetic lactase non-persistence status, and per capita yearly milk and milk product consumption.

Colorectal cancer (CRC) is one of the leading causes of mortality in Western countries. Its putative pathogenesis revolves around genetic and environmental factors, particularly diet. One of the most studied dietary factors, dairy product intake, is still debated as a protective agent. The role of lactose as a candidate prebiotic (stimulating lactic acid bacteria) and its relation to genetic lactase non-persistence (LNP) status has not been evaluated. We undertook a review and analysis of national per capita dairy product consumption, national LNP prevalence, and national CRC mortality rates (CRCM) to determine whether relationships existed among these variables. Data on these three items were obtained from the available literature. A negative binomial regression model was used to compare national LNP status with national CRCM rates for three time periods. Pearson correlation was used to compare national per capita dairy food intake with national CRCM rates for the approximate midpoint time period of reviewed articles. We found that there was a significant positive correlation between per capita dairy food intake and CRCM rates. However, there was also a significant negative correlation between national LNP prevalence and CRCM rates. Population-based studies supported the suggestion that in both homogeneous high and homogeneous low prevalence LNP countries characterized by low and high dairy food intake respectively, dairy food consumption exerted a protective effect against CRC and CRCM rate. Because some population studies contradict the hypotheses that dairy food intake promotes CRC or that LNP status protects against CRC, we hypothesize that dairy food consumption may operate by two distinct mechanisms--one that operates at low doses in LNP subjects and another in high doses in non-LNP subjects.

Inverse dose effect of pretest dietary lactose intake on breath hydrogen results and symptoms in lactase nonpersistent subjects.

The aim of this study was to determine a relationship between pretest intake of lactose and outcome of lactose breath hydrogen test. Patients presented at a testing laboratory participated in the study. A 3-hour breath hydrogen, 50-g lactose challenge was carried out. Results were tabulated and patients completed a 3-day recall diet questionnaire. Daily lactose intake was independently calculated and was associated with breath hydrogen and total symptom score. Statistical analysis used Spearman's correlation, Mann-Whitney U-test and chi2 or Fisher exact test. Of 118 patients, 50% were lactose maldigesters. In these patients, measured breath hydrogen and symptom scores were significantly higher in the lowest intake group (< 5 g/d) than in the highest intake group (> 20 g/d) (P < .05). In the presumed lactose digesters, 59% experienced some symptoms during testing for unclear reasons. Pretest dietary intake of lactose inversely affects results of breath hydrogen.

Deadaption and readaptation with lactose, but no cross-adaptation to lactulose: a case of occult colonic bacterial adaptation.

The standard 3 h breath hydrogen (3hBH2) test distinguishes lactose maldigesters from lactose digesters. However, multiple factors impact on BH2 and care is needed to exclude a priori variables. When these factors are controlled, a negative BH2 test implies lactase persistent status or lactase nonpersistent status with colonic adaptation. A case of a Sicilian man who tested negative (lactase persistent status confirmed) on an initial 50 g lactose challenge is described. It was observed that he consumed 28.1 g lactose/day before testing. He subsequently underwent five additional challenge tests in the course of the next 10 months. In four tests the dose intake of lactose was varied upon instruction, and in the fifth test a 30 g lactulose challenge was carried out. It was demonstrated that on radically decreasing lactose intake, a full lactase nonpersistent status was unmasked. Output of 3hBH2 varied inversely with daily lactose intake. Finally, at a time when he was readapted to lactose, there was no discernible adaptation to lactulose challenge. It was concluded that 'occult' colonically adapted subjects may contribute to negative BH2 tests. There is a relationship between variation in lactose intake and the results of BH2 testing. Finally, there was no cross-adaptation to lactulose challenge when lactose was used as the adapting sugar.