What Is Known
- Infants commonly are fed starches in the first few months of life.
- Pancreatic amylase activity increases very slowly over the first year of life.
What Is New
- Starch digestion in young infants depends primarily on the activity of maltase-glucoamylase.
- Starch digestive capacity also is a critical factor in deciding when to begin cereal feeding in infants.
The introduction of complementary (solid) feeding, such as cereal, to infants is not recommended until 6 months of age (1,2). Despite these recommendations, 30% to 40% of infants in the United States are fed cereal before this time (3,4). Some reasons for early introduction of cereal by parents or caretakers relate to the perception that the infant is not satisfied with formula and/or breast milk or that early introduction of cereal will reduce fussiness or improve sleep (5,6).
Considerations for when cereal should be introduced into the diet include the physical ability of the infant to swallow solids, the allergic potential of the components in the cereal, and the risk for the development of later allergies (7–9). An often-overlooked issue is the ability of the young infant to digest and absorb cereal.
The primary component of dietary cereal provided to infants is starch, with protein a much smaller component. Although amylase is present in saliva, in infants it is present at very low levels and is inactivated in an acidic milieu (10,11). Pancreatic amylase is the primary enzyme responsible for starch digestion in the lumen of the intestine (12). Its presence and activity are at very low, and in some cases, undetectable levels in duodenal fluid until 4 to 6 months of age, and even at 1 year of age remain well below that in children (11,13–18). Consequently, one would anticipate that the ability of young infants to digest, and ultimately, to absorb dietary cereal would be impaired whenever compared with that in older infants and children. The colonic microbiota are capable of salvaging some amount of malabsorbed dietary carbohydrate (including starch) by converting it to short-chain fatty acids, which then are absorbed and can be utilized as energy by the infant (11–16,19). Starch digestibility also is dependent on the type of starch and the degree to which it is cooked (20).
Breast milk contains amylase activity, which is greatest in colostrum and declines thereafter, but does not decrease significantly after 6 months of lactation (21–23). There is small intraindividual variation in breast milk amylase activity but great interindividual variation (21,23). Evidence suggests that depending on the amount of amylase activity present, some activity is capable of surviving passage through the stomach and remaining active in the duodenum (22,24). That said, whether breast-fed infants are able to digest starches to a greater degree than formula-fed infants, to our knowledge, remains to be determined.
The use of stable isotopes has enabled starch (cereal) digestibility studies to be carried out in young infants. Feeding maize (corn) flour naturally enriched in the stable isotope 13C to infants (n = 10; mean age 11 months, range 7–16), Weaver et al (25) demonstrated that the addition of a small quantity of amylase-rich flour resulted in a 33% greater recovery of 13C in breath compared with that of corn flour alone, implying better digestion and absorption. Importantly, the recovery of 13C with the amylase-rich flour was inversely correlated with age suggesting that younger infants received an advantage related to lower pancreatic amylase levels (25). Christian et al (26) studied infants (n = 13; mean age 12 months, range 8–23) who were fed 13C-enriched wheat flour. Using mathematical modeling, they attempted to separate the 13CO2 excreted in breath from digestion and absorption of the wheat starch from that produced from the metabolism of the short-chain fatty acids produced by colonic microbial fermentation (26). They estimated that up to 20% of the starch ingested was digested in the colon (26).
A more direct and quantitative method to assess the digestibility of cereal, both in terms of the starch component and the minor protein component, is through use of fecal measurement. The recovery of 13C in stool following the feeding of 13C-enriched cereal quantitatively measures cereal digestibility (27). In a proof of concept study, it was shown that 1-month-old infants (n = 4) could digest and absorb 3.7% to 13.1% of a 1 g/kg feeding of corn cereal (27). Importantly, there were no differences in the recovery of 13CO2 in breath following feeding of the cereal and an equal dose of glucose polymers or glucose (n = 16), demonstrating the difficulty of quantifying cereal digestion through breath testing (27).
Using fecal 13C measurements, the digestibility of rice cereal was quantitated in 1-month-old infants (28). Infants (n = 8) were fed 4 g of rice cereal in formula (an amount commonly used to thicken feedings for infants with gastroesophageal reflux) (28,29). As would be expected, energy and nitrogen intakes were increased whenever rice cereal was added to the formula. Despite this, however, net retention of energy and nitrogen did not increase following cereal feeding (28). Rather, fecal bacterial mass increased almost 7-fold, suggesting that the cereal was nutritionally unavailable to the infant, but was avidly utilized by the colonic microbiota (28). It was estimated that 30% of the cereal reached the colon,12% was recovered in stool, and 18% was fermented by colonic bacteria (28). In contrast to the findings in these 1-month-old infants, older infants (3–5 months of age; n = 9) were able to digest 95% of the nitrogen in the rice cereal (vs 79% in the 1-month-old infants) with no increase in fecal mass, thus, implying improved digestion and absorption of the cereal starch, as well, compared with that in 1-month-old infants (30).
These studies underscore the limited capacity of young infants to digest and absorb cereal (starch), related to the immaturity of pancreatic (amylase) function. Small intestinal mucosal maltase-glucoamylase, however, is capable of hydrolyzing the nonreducing terminal α-1,4 glucose bonds of nonbranched starches, but is most active against short-chain polymers (<10 glucose units) (31–33). Limited data suggest that young infants appear to have measurable maltase-glucoamylase activity (34–36). The digestibility of glucose polymers was measured in 1-month-old infants (n = 12) who were fed 13C-enriched glucose polymers (degree of polymerization [DP] = 3–8 and average DP = 43) (37). The digestion of the short-chain polymers was complete, but 5 of 12 infants had measurable malabsorption (4–19%) of the long-chain polymers (37). No correlation was found between digestibility of the polymers and 13CO2 excretion in breath (37). A study in preterm infants (n = 21, mean weight 2051 g) compared the digestion and absorption of short-chain glucose polymers with that of lactose, using the triple lumen intestinal perfusion method (38). The digestion and absorption of the polymers was greater than that of lactose, underscoring the importance of maltase-glucoamylase in the carbohydrate-related nutrition of preterm infants, in addition to that of older infants (38). Given the limited ability of young infants to digest starch, the argument could be raised that some degree of starch malabsorption could have a prebiotic effect. Data suggest that Bifidobacteria do contain the genes encoding for enzymes capable of degrading starch (39).
In summary, recommendations are underscored for the timing of the introduction of complementary cereal feeding, not only by recognizing the physical ability of the infant to swallow solids, and the possibility of allergy issues, but also by the limited starch digestive capacity of the young infant. The studies reviewed emphasize the great variability among infants in the rate at which pancreatic amylase function develops, and, therefore, the ability of infants to digest starch. One must also consider the potential of cereal feeding to cause poor weight gain and/or diarrhea (40). Conversely, evidence exists suggesting that the feeding of starch can enhance pancreatic amylase activity (16).
1. Kleinman REG, F.R.. Complementary Feeding. American Academy of Pediatrics, Pediatric Nutrition
. Elk Grove Village, IL:2014.
2. Brown KH. WHO/UNICEF review on complementary feeding and suggestions for future research: WHO/UNICEF guidelines on complementary feeding. Pediatrics
3. Briefel RR, Reidy K, Karwe V, et al. Feeding infants and toddlers study: Improvements needed in meeting infant feeding recommendations. J Am Diet Assoc
2004; 104 (1 Suppl 1):s31–s37.
4. Clayton HB, Li R, Perrine CG, et al. Prevalence and reasons for introducing infants early to solid foods: variations by milk feeding type. Pediatrics
5. Wasser H, Bentley M, Borja J, et al. Infants perceived as “fussy” are more likely to receive complementary foods before 4 months. Pediatrics
6. Crocetti M, Dudas R, Krugman S. Parental beliefs and practices regarding early introduction of solid foods to their children. Clin Pediatr (Phila)
7. Fiocchi A, Assa’ad A, Bahna S, et al. Food allergy and the introduction of solid foods to infants: a consensus document. Adverse Reactions to Foods Committee, American College of Allergy, Asthma and Immunology. Ann Allergy Asthma Immunol
8. Grimshaw KE, Maskell J, Oliver EM, et al. Introduction of complementary foods and the relationship to food allergy. Pediatrics
9. Feeding Infants: A Guide for Use in the Child Nutrition Programs. Available at: https://www.fns.usda.gov/tn/feeding-infants-guide-use-child-nutrition-programs
. Accessed November 1, 2017.
10. Sevenhuysen GP, Holodinsky C, Dawes C. Development of salivary alpha-amylase in infants from birth to 5 months. Am J Clin Nutr
11. Kamaryt J, Fintajslova O. Development of salivary and pancreatic amylase in children during the 1st year of life. Z Klin Chem Klin Biochem
12. Christian M, Edwards C, Weaver LT. Starch digestion in infancy. J Pediatr Gastroenterol Nutr
13. Hadorn B, Zoppi G, Shmerling DH, et al. Quantitative assessment of exocrine pancreatic function in infants and children. J Pediatr
14. Klumpp TG, Neale AV. The gastric and duodenal contents of normal infants and children. Am J Dis Child
15. Lebenthal E, Lee PC. Development of functional responses in human exocrine pancreas. Pediatrics
16. Zoppi G, Andreotti G, Pajno-Ferrara F, et al. Exocrine pancreas function in premature and full term neonates. Pediatr Res
17. Lucas Keene MF, Hewer EE. Digestive enzymes of the human foetus. Lancet
18. Track NS, Creutzfeldt C, Bokermann M. Enzymatic, functional and ultrastructural development of the exocrine pancreas--II. The human pancreas. Comp Biochem Physiol A Comp Physiol
19. Bach Knudsen KE. Microbial degradation of whole-grain complex carbohydrates and impact on short-chain fatty acids and health. Adv Nutr
20. Dreher ML, Dreher CJ, Berry JW. Starch digestibility of foods: a nutritional perspective. Crit Rev Food Sci Nutr
21. Hegardt P, Lindberg T, Borjesson J, et al. Amylase in human milk from mothers of preterm and term infants. J Pediatr Gastroenterol Nutr
22. Lindberg T, Skude G. Amylase in human milk. Pediatrics
23. Dewit O, Dibba B, Prentice A. Breast-milk amylase activity in English and Gambian mothers: effects of prolonged lactation, maternal parity, and individual variations. Pediatr Res
24. Heitlinger LA, Lee PC, Dillon WP, et al. Mammary amylase: a possible alternate pathway of carbohydrate digestion in infancy. Pediatr Res
25. Weaver LT, Dibba B, Sonko B, et al. Measurement of starch digestion of naturally 13C-enriched weaning foods, before and after partial digestion with amylase-rich flour, using a 13C breath test. Br J Nutr
26. Christian MT, Amarri S, Franchini F, et al. Modeling 13C breath curves to determine site and extent of starch digestion and fermentation in infants. J Pediatr Gastroenterol Nutr
27. Shulman RJ, Wong WW, Irving CS, et al. Utilization of dietary cereal by young infants. J Pediatr
28. Shulman RJ, Boutton TW, Klein PD. Impact of dietary cereal on nutrient absorption and fecal nitrogen loss in formula-fed infants. J Pediatr
29. Orenstein SR, Magill HL, Brooks P. Thickening of infant feedings for therapy of gastroesophageal reflux. J Pediatr
30. Shulman RJ, Gannon N, Reeds PJ. Cereal feeding and its impact on the nitrogen economy of the infant. Am J Clin Nutr
31. Eggermont E. The hydrolysis of the naturally occurring alpha-glucosides by the human intestinal mucosa. Eur J Biochem
32. Nichols BL, Eldering J, Avery S, et al. Human small intestinal maltase-glucoamylase cDNA cloning. Homology to sucrase-isomaltase
. J Biol Chem
33. Kelly JJ, Alpers DH. Properties of human intestinal glucoamylase. Biochim Biophys Acta
34. Lebenthal E, Lee PC. Glucoamylase and disaccharidase activities in normal subjects and in patients with mucosal injury of the small intestine. J Pediatr
35. Lee PC, Werlin S, Trost B, et al. Glucoamylase activity in infants and children: normal values and relationship to symptoms and histological findings. J Pediatr Gastroenterol Nutr
36. Raul F, Lacroix B, Aprahamian M. Longitudinal distribution of brush border hydrolases and morphological maturation in the intestine of the preterm infant. Early Hum Dev
37. Shulman RJ, Kerzner B, Sloan HR, et al. Absorption and oxidation of glucose polymers of different lengths in young infants. Pediatr Res
38. Shulman RJ, Feste A, Ou C. Absorption of lactose, glucose polymers, or combination in premature infants. J Pediatr
39. Liu S, Ren F, Zhao L, et al. Starch and starch hydrolysates are favorable carbon sources for bifidobacteria in the human gut. BMC Microbiol
40. Lilibridge CB, Townes PL. Physiologic deficiency of pancreatic amylase in infancy: a factor in iatrogenic diarrhea. J Pediatr