See Dubinsky MC et al on page 1105 in CGH;See editorial on page 1038. Background & Aims:Childhood-onset inflammatory bowel disease (IBD) might be etiologically different from adult-onset IBD. We analyzed disease phenotypes and progression of childhood-onset disease and compared them with characteristics of adult-onset disease in patients in Scotland. ; 43% vs 3%; P < .0001; OR, 23.36; 95% CI, 13.45-40.59) with less isolated ileal (L1; 2% vs 31%; P < .0001; OR, 0.06; 95% CI, 0.03-0.12) or colonic disease (L2; 15% vs 36%; P < .0001; OR, 0.31; 95% CI, 0.21-0.46). UC was extensive in 82% of the children at diagnosis, versus 48% of adults (P < .0001; OR, 5.08; 95% CI, 2.73-9.45); 46% of the children progressed to develop extensive colitis during followup. Forty-six percent of children with CD and 35% with UC required immunomodulatory therapy within 12 months of diagnosis. The median time to first surgery was longer in childhood-onset than adult-onset patients with CD (13.7 vs 7.8 years; P < .001); the reverse was true

Objective: To test the efficacy in terms of birth weight and infant survival of a diet supplement programme in pregnant African women through a primary healthcare system. Design: 5 year controlled trial of all pregnant women in 28 villages randomised to daily supplementation with high energy groundnut biscuits (4.3MJ/day) for about 20 weeks before delivery (intervention) or after delivery (control). Setting: Rural Gambia. Subjects: Chronically undernourished women (twin bearers excluded), yielding 2047 singleton live births and 35 stillbirths. Main outcome measures: Birth weight; prevalence of low birth weight ( < 2500 g); head circumference; birth length; gestational age; prevalence of stillbirths; neonatal and postneonatal mortality. Results: Supplementation increased weight gain in pregnancy and significantly increased birth weight, particularly during the nutritionally debilitating hungry season (June to October). Weight gain increased by 201 g (P < 0.001) in the hungry season, by 94 g (P < 0.01) in the harvest season (November to May), and by 136 g (P < 0.001) over the whole year. The odds ratio for low birthweight babies in supplemented women was 0.61 (95% confidence interval 0.47 to 0.79, P < 0.001). Head circumference was significantly increased (P < 0.01), but by only 3.1 mm. Birth length and duration of gestation were not affected. Supplementation significantly reduced perinatal mortality: the odds ratio was 0.47 (0.23 to 0.99, P < 0.05) for stillbirths and 0.54 (0.35 to 0.85, P < 0.01) for all deaths in first week of life. Mortality after 7 days was unaffected. Conclusion: Prenatal dietary supplementation reduced retardation in intrauterine growth when effectively targeted at genuinely at-risk mothers. This was associated with a substantial reduction in the prevalence of stillbirths and in early neonatal mortality. The intervention can be successfully delivered through a primary healthcare system.

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SUMMARY Passive intestinal permeability in 33 newborn babies was studied using feeds containing lactulose and mannitol. Each marker is thought to pass across the gut wall by a different route; lactulose by a paracellular and mannitol by a transcellular pathway. Neither is metabolised and both are wholly and solely excreted by the kidney; urinary recovery is a measure of the intestinal uptake. Babies born before 34 weeks' gestation exhibited a higher intestinal permeability to lactulose than more mature babies, and all preterm babies showed an appreciable decline in lactulose absorption during the first week of oral feeds. Babies of 34 to 37 weeks' gestation achieved a 'mature' intestinal permeability to lactulose within four days of starting oral feeds. These findings may reflect the immaturity of the gut of the preterm baby rather than a process essential to adaptation to enteral nutrition.One of the major challenges faced by the newborn baby is the abrupt transition from parenteral to enteral nutrition. By the third trimester of pregnancy the gut seems to be anatomically prepared,1 but after oral feeding begins, considerable physiological and morphological changes take place.2 These adaptations to extrauterine nutrition all contribute to the major function of the gut-absorption. Presented with food for the first time, however, the gut must distinguish the essential from the harmful, and balance selection with exclusion.

In 2 prospective randomized trials, we showed that a nutrient-enriched diet in infancy increased fat mass later in childhood. These experimental data support a causal link between faster early weight gain and a later risk of obesity, have important implications for the management of infants born small for gestational age, and suggest that the primary prevention of obesity could begin in infancy.

Changes in small intestinal structure, cytokinetics, and function are dynamic ways in which the gut adapts to diet, disease, and damage. Adequate length provides a static 'reserve' permitting an immediate response to pathophysiological changes. The length of the small intestine from conception to adulthood using data taken from eight published reports of necropsy measurement of 1010 guts is described. Mean The lengths of 1010 specimens were plotted against the lengths or heights of the subjects. All length measurements were converted to cm. To establish the relation between intestinal length and body length or height, the data were fitted by cubic spline regression." To deal with the mixture of individual and grouped data in the sample, each point in the analysis was given a weighting corresponding to the number of individuals contained in it: 1 for individuals and n for groups of size n. The spline curve was fitted to both the original data and to the log transformed data. In the latter case, the slope of the regression curve indicated the power relation between small intestinal length and body length. The small intestine is the major site of nutrient and water absorption. To ensure an adequate surface area to meet the nutritional requirements of the organism, it is a long coiled organ whose epithelial surface is increased many times by circular folds, villi, and microvilli.'For most mammals there is a direct relation between the gross surface area of the small intestine and body size. This is related to the diet eaten by each species, and for man it conforms with that of other members of the superfamily (Fig 1).Growth in intestinal length continued during early postnatal life, but from about 1 year (75 cm body length) onwards it slowed and remained linear with increasing age to adulthood. From birth there was a wide range in intestinal lengths reported, with 100% variation from early childhood onwards. The coefficient of variation of small intestinal length postnatally was 24%, sixfold greater than for body length. Figure 2 shows the corresponding results and spline curve obtained after log transformation of the data. The pre-and perinatal acceleration in length is clearly seen. In proportional terms, prenatal growth in small intestinal length was consistently faster than that of body length, increasing as the power law small intestinal length a body length to the power 4/3. After birth there was a noticeable deceleration in small intestinal length growth, so that it was less than 1321 on 12 May 2018 by guest. Protected by copyright.