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Complementary Starch Feeding of the Young Child

2018; Lippincott Williams & Wilkins; Volume: 66; Issue: S3 Linguagem: Inglês

10.1097/mpg.0000000000001972

1536-4801

Buford L. Nichols, William J. Klish,

Child Nutrition and Water Access

“And malt does more than Milton can to justify God's ways to man” LXII, A.E. Housman For human infants, supplementation of maternal nursing is called complementary feeding or beikost. The German word beikost translates as “infant foods other than milk or formula.” Starchy foods are the first offered in most cultures. The introduction of beikost begins the weaning process and introduces environmental vectors stressing the maternal-infant dyad. The presently recommended age for introduction of complementary feedings to the suckling infant is six months. One argument offered by learned committees for this recommendation is that amylase production and secretion in normal infants is physiologically delayed. Pediatricians worldwide, however, know that many mothers begin offering solids in the first months of life and that this common practice is usually rewarded by positive infant behavior. On the other hand, it is believed that in developing countries, stunting of infant growth might be due to nutritional quality and environmental contamination of complementary feedings. Studies of starch feeding show that both whole cereal starch and maltodextrin are digested and absorbed by the young infant. Feeding studies of nursing infants in some, but not all, settings suggest that complementary foods amplify energy intakes and growth. Starch feeding marks a transition of microbiome development. Proximal disorders of starch digestion may contribute to dysbiosis and clinical intolerances.FIGURE 1: Starch Digestion Consortium Workshop Group Picture. Fourth row: Wikrom Karnsakul, David Rose, Antone Opekum, Mark Gilger, Mohammet Chegeni. Third row: Bill Dupere, Marcia Chaudet, Rick Guan, Don Nwose, Ryan Carvalho, Chen Chen, Toshinao Goda, Byung-Hoo Lee, Zihua Ao, Marwa El-Hindaway, Nardo Nava, Amy Lin. Second row: Brandi Rabon, Thammasin Ingviya, Anne Boney, Jongbin Lim, Stan Cohen, Manu Goyal, Bill Klish, Frank Greer, Satish Kalhan, Peter Zimmer. Front row: Mark Manary, Roseland Klein, Fatimata Cisse’, Bruce Hamaker, Robert Pryor, Buford Nichols, Hassan Naim, Michael Lentze, Nancy Butte, Claudia Robayo-Torres, John Watkins. Missing from Picture: Bruno Chumpitazi, Rob Shulman, Jim Versalovic, Derick Cooper.FEEDING COMPLEMENTARY STARCHES In newborn nutrition, glucose is supplied from lactose ingestion and gluconeogenesis. In the fasting state gluconeogenesis predominates. In infant weaning, the adult diet is usually first introduced by the feeding of plant-derived carbohydrates. The nutritional rational for complimentary starch feeding is partially based on the infant's digestive capacity. Complexity of infant starch digestion is increased by a physiologic delay in mature amylase activity. Amylase insufficiency alters digestion of all botanical starches and starch products. Amylase-deficient digestion of starch to absorbable glucose is driven by the mucosal maltases present from birth. The maltase measured in clinical small intestine biopsies is comprised of four activities expressed from two genes; sucrase-isomaltase and maltase-glucoamylase (1,2). Glucoamylase produces glucose at a high rate. After maturation of amylase activity, the products of starch hydrolysis, including maltotriose, inhibit glucoamylase, but not slower sucrase-isomaltase, in the adult pattern of glucogenesis. The history and contemporary practice of complementary starch bikost were reviewed (3,4) by the workshop participants on Figure 1. All starches are shown resistant to full glucogenesis in the small intestine, each with variable enzyme efficiency and specificity. Slowly digested starch fractions are claimed by the distal microbiome. Reduced glucogenesis from starch requires increased gluconeogenesis from other energetic substrates (5). The infant and toddler's brain requirements for glucose provide a rationale for early feeding of complimentary starch (6). GLUCOSE PRODUCTION FROM STARCHES BY MALTASE ACTIVITIES The word malt appears to be derived from an ancient root defining sweet taste. The term malted is used to describe the sweeter taste of grains after sprouting. The chemical description of maltose was determined by O'Sullivan, and the small intestinal enzyme, maltase, by Brown, both English brew-masters. Dahlqvist and Semenza discovered that small intestinal maltase activities in all tested species could be fractionated into multiple components. The terms for these maltase fractions are not yet standardized and those used by Dahlqvist and Semenza, and the authors in this workshop are classified as follows (summarized in Table 1): Dahlqvist labeled isomaltase as Mla, sucrase as Mlb, maltase as Mlll, and glucoamylase as Mll. Moving forward in time, in this Supplement, Rose labeled isomaltase as Nt-Sl, sucrase as Ct-Sl, maltase as Nt-MGAM, and glucoamylase as Ct-MGAM. Naim labeled the enzymes with the following abbreviations, isomaltase as IM, sucrase as SUC, maltase as MAL, and glucoamylase as GAM. Finally, the enzymes labeled by Lee are: isomaltase as small 1,4 and 1,6; sucrase as short 1,4; maltase as large 1,6 short 1,4; and glucoamylase as long 1,4. Because the Dahlqvist biopsy assays measure only total activities using maltose as the substrate, the more fundamental clinical defects in genetic, cellular, and molecular function remain unclear, and a new classification of primary and secondary maltase deficiencies is presented (2).TABLE 1: Maltase (M) fractions characterized in this SupplementCARBOHYDRATE INTOLERANCE DISORDERS Carbohydrate intolerances initiated the clinical work in Gastroenterology and Nutrition in the Pediatric Department of Baylor College of Medicine. The disorder was associated with villous atrophy, reduced disaccharidase activity, poor glucose absorption and clinical dysbiosis presenting in malnourished infants after acute gastroenteritis. Carbohydrate intolerance and dysbiosis was also observed in infants after major intestinal resections (7,8). The contemporary classification of environmental enteropathy may include these infants with acquired mucosal atrophy. Acquired monosaccharide intolerance (AMI) management led to group awareness of mucosal histological defects and carbohydrate intolerance symptoms. The universal failure of the breath hydrogen test in AMI, due to dysbiosis, led to development of alternate 13C-substrate breath tests (9). An early recognition that low disaccharidase activities could contribute to recurrent chronic abdominal pain in children led to a large review of clinical biopsy assays without clinical information (2). Of 30,000 duodenal biopsies, 45% had low assay activities. The largest group (32%) had low lactase activities. The second largest group (9%) had a pandisaccharidase deficiency (PDD). Isolated maltase deficiencies (PMD) were next, with (2%) and without coexisting lactase deficiency (1%). Isolated sucrase deficiencies followed with normal lactase ln congenital sucrase-isomaltase deficiency (CSID) (0.5%). A hypothesis was presented that pandisaccharidase deficiency can be a form of CSID with developmental non-persistent lactase deficiency. Two groups tested this hypothesis in different clinical locations; using different assay labs; different histopathologists; and different electronic record systems (10,11). The hypothesis that pandisaccharidase deficiency can be a form of CSID presenting as recurrent abdominal pain in children appears supported, but could not be differentiated by symptomology. The role of maltase deficiency in PDD and CSID in clinical symptoms of children may extend to the microbiome (12) and remains a frontier for further pediatric research.