FÆCAL FAT LOSSES AND COW'S MILK LACTOSE
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207 obtained and the fact that the medicine had been dispensed in such a large quantity in a simple screw-top bottle suggests the need for stricter control of such poisons. No other cytotoxic agent can be bought freely without prescription. Children’s Department, Newcastle General Hospital, Newcastle upon Tyne NE4 6BE A. N. CAMPBELL FÆCAL FAT LOSSES AND COW’S MILK LACTOSE SIR,—The incidence of small-bowel mucosal abnormalities and secondary lactase deficiency is high in Australian Abori- ginal children.1,2 In two studies’ we have observed signifi- cantly lower average weight gains in Aboriginal children receiving normal cow’s milk compared with weight gains dur- ing feeding with a cow’s milk in which the lactose had been hydrolysed. However, we need to know if the lactose in normal milk induces incomplete utilisation of other nutrients in milk. We have done other studies to determine whether fsecal fat losses are higher in Aboriginal children during normal cow’s milk feeding than they are in children taking lactose-hydro- lysed (LH) milk. In a controlled study, children under 3 years of age (mean 1.3 years) from a community known to have a high incidence of secondary hypolactasia,5 were randomly allocated to receive either normal milk or LH milk containing less than 2-5 g/1 of lactose (’Digestelact’; Sharpe Laboratories, Australia) on admission to hospital. Most children were admitted with diarrhoea and/or respiratory-tract infection. Children with known previous hypolactasia by earlier mucosal disaccharidase assay and those with fluid stools containing reducing sub- stances by ’Clinitest’6 were excluded from the trial and fed "declared" LH milk. A high proportion of the children remaining in the trial were suspected of having lactose intoler- ence. 3-day stool collections were obtained during 22 admis- sions, 14 on normal milk and 8 on LH milk. Early discharge of 4 children allocated LH milk accounted for the distribution discrepancy. The children fed normal milk were found to excrete more fat in 24 h (mean 3-4 g, range 1.6-6.5) than those fed LH milk (mean 1.9 g, range 0-5-2-7). This differ- ence was statistically significant at the 0.05 level (one-tailed Mann-Whitney U test). In a one-way crossover trial of a further 12 children who were younger (mean age 0.8 years) and significantly under- nourished (mean % standardised weight for age, 77), 3-day faecal fat excretion was higher during normal milk feeding (mean 3-6 g in 24 h, range 0-6-9-2) than during the preceding period on LH milk (mean 2-7 g, range 0-8-5-6). A difference was significant at the 0.05 level using the Wilcoxon matched- pair signed-ranks test (one-tailed). 8 children excreted more fat on normal milk, one distinctly the reverse, and the remaining 3 excreted similar amounts on both milks. In both the controlled and the crossover trial stool frequency (mean±SE 2.6±0-2 and 3-8±0-5, respectively) as well as stool wet weight were similar on both milk regimens. The milks were identical except that hydrolysis had con- verted most of the lactose to glucose and galactose in the LH milk. The hydrolysis step is unlikely to modify fat bioavailabil- ity or protein antigenicity. 1. Walker-Smith JA, Reye RDK. Small intestinal morphology in Aboriginal children. Aust NZ J Med 1971; 4: 377-84. 2. Harris MJ, Duffy BJ, Beveridge J. Studies on the small bowel of a group of New South Wales Aboriginal children. Med J Aust 1970; i: 356-59. 3. Mitchell JD, Brand J, Halbisch J. Weight gain inhibition by lactose in Aus- tralian Aboriginal children. Lancet 1977; i: 500-02. 4. Brand JC, Miller JJ, Vorbach EA, Edwards RA. A trial of lactose hydrolysed milk in Australian Aboriginal children. Med J Aust 1977; ii: suppl 10-13. 5. Mitchell JD, Duffy BJ. Lactase deficiency and malnutrition amongst children of an Australian Aboriginal community. Proceedings of the 5th Asian-Pacific Congress of Gastroenterology, 1976: 603. 6. Kerry KR, Anderson CM. A ward test for sugar in fæces. Lancet 1964; i: 981-82. These studies indicate that nutrient bioavailability may be reduced by a small, but nutritionally significant, amount by milk feeding of children with mild and clinically occult second- ary lactose intolerance. The findings need to be considered in terms of losses not only of fat but also of other likely nutrients including fat-soluble vitamins. Our firidings should have par- ticular relevance in developing countries, where dietary in- takes are frequently marginal. Only a mild increase in fsecal nutrient and energy losses may then significantly affect growth and nutrition during childhood. Human Nutrition Unit, Department of Biochemistry, University of Sydney, Sydney, New South Wales, Australia JANETTE BRAND Prince of Wales Children’s Hospital, Randwick, New South Wales JOHN D. MITCHELL LACTOSE-FREE FORMULÆ FOR INFANTILE DIARRHŒA SIR,-Rees and Brook’ suggest that children under age 4 years who have been admitted to hospital with acute gastro- enteritis and fed initially with milk are neither sick longer nor kept longer in hospital than are children fed a lactose-free for- mula. The Committee on Nutrition of the American Academy of Pediatrics recommends initial feeding with a lactose-free formula only for malnourished children with severe diarrhoea.2 However, the committee goes on to suggest that further studies on the effect of lactose-free feeding in the management of acute gastroenteritis are needed. Our experience in a regional (refer- ral) hospital is different from that of Rees and Brook and leads us to extend the A.A.P.’s recommendation. DURATION OF DIARRHŒA IN INFANTS ON LACTOSE AND SUCROSE FREE FORMULA OR COW’S MILK We studied 75 children less than 1 year of age, admitted consecutively with acute (less than 1 week) gastroenteritis. 65% had less than 5% dehydration. Oral feedings were rou- tinely discontinued on admission for 6-24 h while intravenous fluids were given. Then one randomly selected group was grad- ually put on cow’s milk while the other received lactose and sucrose free soy formula, supplemented with glucose. The results (table) suggest that cow’s milk as the initial feed- ing regimen in children under 1 year with acute gastroenteritis significantly prolongs the illness. The chief differences between our patients and those studied by Rees and Brook are that ours were younger and that 35% of them were more dehydrated (>5%). We conclude that, at least in severe acute dehydration under 1 year, a non-lactose containing formula is the initial oral regimen of choice. Division of Pædiatrics, Soroka University Medical Centre, Beersheba, Israel R. DAGAN R. GORODISCHER S. MOSES C. MARGOLIS 1. Rees L, Brook CGD. Gradual reintroduction of full-strength milk after acute gastroenteritis in children. Lancet 1979; i: 770. 2. Barness L, ed. Pediatric nutrition handbook. Evanston: American Academy of Pediatrics, 1979: 385.
Transcript of FÆCAL FAT LOSSES AND COW'S MILK LACTOSE
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obtained and the fact that the medicine had been dispensed insuch a large quantity in a simple screw-top bottle suggests theneed for stricter control of such poisons. No other cytotoxicagent can be bought freely without prescription.Children’s Department,Newcastle General Hospital,Newcastle upon Tyne NE4 6BE A. N. CAMPBELL
FÆCAL FAT LOSSES AND COW’S MILK LACTOSE
SIR,—The incidence of small-bowel mucosal abnormalitiesand secondary lactase deficiency is high in Australian Abori-ginal children.1,2 In two studies’ we have observed signifi-cantly lower average weight gains in Aboriginal children
receiving normal cow’s milk compared with weight gains dur-ing feeding with a cow’s milk in which the lactose had beenhydrolysed. However, we need to know if the lactose in normalmilk induces incomplete utilisation of other nutrients in milk.We have done other studies to determine whether fsecal fatlosses are higher in Aboriginal children during normal cow’smilk feeding than they are in children taking lactose-hydro-lysed (LH) milk.
In a controlled study, children under 3 years of age (mean1.3 years) from a community known to have a high incidenceof secondary hypolactasia,5 were randomly allocated to receiveeither normal milk or LH milk containing less than 2-5 g/1 oflactose (’Digestelact’; Sharpe Laboratories, Australia) on
admission to hospital. Most children were admitted withdiarrhoea and/or respiratory-tract infection. Children withknown previous hypolactasia by earlier mucosal disaccharidaseassay and those with fluid stools containing reducing sub-stances by ’Clinitest’6 were excluded from the trial and fed"declared" LH milk. A high proportion of the children
remaining in the trial were suspected of having lactose intoler-ence. 3-day stool collections were obtained during 22 admis-sions, 14 on normal milk and 8 on LH milk. Early dischargeof 4 children allocated LH milk accounted for the distribution
discrepancy. The children fed normal milk were found toexcrete more fat in 24 h (mean 3-4 g, range 1.6-6.5) thanthose fed LH milk (mean 1.9 g, range 0-5-2-7). This differ-ence was statistically significant at the 0.05 level (one-tailedMann-Whitney U test).
In a one-way crossover trial of a further 12 children whowere younger (mean age 0.8 years) and significantly under-nourished (mean % standardised weight for age, 77), 3-dayfaecal fat excretion was higher during normal milk feeding(mean 3-6 g in 24 h, range 0-6-9-2) than during the precedingperiod on LH milk (mean 2-7 g, range 0-8-5-6). A differencewas significant at the 0.05 level using the Wilcoxon matched-pair signed-ranks test (one-tailed). 8 children excreted more faton normal milk, one distinctly the reverse, and the remaining3 excreted similar amounts on both milks.
In both the controlled and the crossover trial stool frequency(mean±SE 2.6±0-2 and 3-8±0-5, respectively) as well as stoolwet weight were similar on both milk regimens.The milks were identical except that hydrolysis had con-
verted most of the lactose to glucose and galactose in the LHmilk. The hydrolysis step is unlikely to modify fat bioavailabil-ity or protein antigenicity.
1. Walker-Smith JA, Reye RDK. Small intestinal morphology in Aboriginalchildren. Aust NZ J Med 1971; 4: 377-84.
2. Harris MJ, Duffy BJ, Beveridge J. Studies on the small bowel of a group ofNew South Wales Aboriginal children. Med J Aust 1970; i: 356-59.
3. Mitchell JD, Brand J, Halbisch J. Weight gain inhibition by lactose in Aus-tralian Aboriginal children. Lancet 1977; i: 500-02.
4. Brand JC, Miller JJ, Vorbach EA, Edwards RA. A trial of lactose hydrolysedmilk in Australian Aboriginal children. Med J Aust 1977; ii: suppl 10-13.
5. Mitchell JD, Duffy BJ. Lactase deficiency and malnutrition amongstchildren of an Australian Aboriginal community. Proceedings of the 5thAsian-Pacific Congress of Gastroenterology, 1976: 603.
6. Kerry KR, Anderson CM. A ward test for sugar in fæces. Lancet 1964; i:981-82.
These studies indicate that nutrient bioavailability may bereduced by a small, but nutritionally significant, amount bymilk feeding of children with mild and clinically occult second-ary lactose intolerance. The findings need to be considered interms of losses not only of fat but also of other likely nutrientsincluding fat-soluble vitamins. Our firidings should have par-ticular relevance in developing countries, where dietary in-takes are frequently marginal. Only a mild increase in fsecalnutrient and energy losses may then significantly affect growthand nutrition during childhood.
Human Nutrition Unit,Department of Biochemistry,University of Sydney,Sydney, New South Wales, Australia JANETTE BRANDPrince of Wales Children’s Hospital,Randwick, New South Wales JOHN D. MITCHELL
LACTOSE-FREE FORMULÆ FOR INFANTILEDIARRHŒA
SIR,-Rees and Brook’ suggest that children under age 4years who have been admitted to hospital with acute gastro-enteritis and fed initially with milk are neither sick longer norkept longer in hospital than are children fed a lactose-free for-mula. The Committee on Nutrition of the American Academyof Pediatrics recommends initial feeding with a lactose-freeformula only for malnourished children with severe diarrhoea.2However, the committee goes on to suggest that further studieson the effect of lactose-free feeding in the management of acutegastroenteritis are needed. Our experience in a regional (refer-ral) hospital is different from that of Rees and Brook and leadsus to extend the A.A.P.’s recommendation.
DURATION OF DIARRHŒA IN INFANTS ON LACTOSE AND SUCROSE
FREE FORMULA OR COW’S MILK
We studied 75 children less than 1 year of age, admitted
consecutively with acute (less than 1 week) gastroenteritis.65% had less than 5% dehydration. Oral feedings were rou-tinely discontinued on admission for 6-24 h while intravenousfluids were given. Then one randomly selected group was grad-ually put on cow’s milk while the other received lactose andsucrose free soy formula, supplemented with glucose.The results (table) suggest that cow’s milk as the initial feed-
ing regimen in children under 1 year with acute gastroenteritissignificantly prolongs the illness. The chief differences betweenour patients and those studied by Rees and Brook are that ourswere younger and that 35% of them were more dehydrated(>5%). We conclude that, at least in severe acute dehydrationunder 1 year, a non-lactose containing formula is the initialoral regimen of choice.
Division of Pædiatrics,Soroka University Medical Centre,Beersheba, Israel
R. DAGANR. GORODISCHERS. MOSESC. MARGOLIS
1. Rees L, Brook CGD. Gradual reintroduction of full-strength milk after acutegastroenteritis in children. Lancet 1979; i: 770.
2. Barness L, ed. Pediatric nutrition handbook. Evanston: American Academyof Pediatrics, 1979: 385.
