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Lactose intolerance and gastrointestinal cow’s milk allergy in infants and children – common misconceptions revisited

Lactose intolerance and gastrointestinal cow’s milk allergy in infants and children – common misconceptions revisited

This summary is adapted from Lactose intolerance and gastrointestinal cow’s milk allergy in infants and children – common misconceptions revisited

Lactose intolerance develops in approximately 70% of the world’s population after weaning1. It is caused by an inability to digest and absorb dietary lactose, due to insufficient levels of the biological molecule (enzyme) called lactase. Lactase is responsible for breaking down lactose into component parts which can be processed by the body. Lactose intolerance develops due to a gradual, genetically programmed decline in lactase after the weaning period. This is referred to as lactase non-persistence. It occurs due to evolutionary reasons, as cow’s milk started to be consumed by adults relatively late into human evolution and did not occur simultaneously in all human populations. Symptoms of lactose intolerance usually include abdominal pain, flatulence and diarrhoea.

Primary lactose intolerance rarely occurs in children under 5 years, however gastrointestinal symptoms in this age group can sometimes still be confused as lactose intolerance by parents and occasionally healthcare professionals. For this reason, infants can be inappropriately fed with lactose-free formula. The aim of the paper summarised here was to provide an overview of lactose intolerance and address common misconceptions associated with lactose intolerance in infants and young children.

Those who have lactose intolerance absorb between 42 and 77% of consumed lactose, whereas individuals without absorb 95%. Due to genetic factors, lactose intolerance varies by population. People of Northern European, West African, or Middle Eastern background have lower levels of lactose intolerance (2-5%)2. This rises to about 50% in South America and Africa, and to 90-100% in Southeast Asia2. Rates in Northern America vary based on ethnicity, from 21-79%3.

Lactose in human breast milk is important to provide adequate energy intake for breastfed infants, as it is a form of sugar molecule. It is also thought to increase the absorption of calcium, aiding in preventing the effects of deficiency. Young infants do not absorb all of the lactose present in breast milk, but that which is not absorbed acts as a prebiotic in the infant gut, encouraging the growth of healthy bacteria which may have a beneficial effect on immune development in the infant.

There are four main types of lactase intolerance. Congenital lactase deficiency is a rare and severe genetic disorder where newborn infants develop severe diarrhoea when breast feeding is commenced, due to a complete absence of lactase. These infants generally cannot sustain breastfeeding and should be switched to lactose-free infant formula. This can result in normal growth and development. Developmental lactase deficiency is seen in premature infants, and improves with time. Lactase non-persistence is by far the most common form, as described above. Secondary lactose intolerance may occur as a consequence of various gastrointestinal disorders such as Crohn’s disease.

Diagnosis of lactose intolerance can be difficult, relying on the identification of gastrointestinal symptoms after consuming lactose-containing foods. Some additional laboratory tests can also be run, but they are not conclusive. Cow’s milk allergy is often confused for lactose intolerance as both cause gastrointestinal symptoms. Extensively hydrolyzed formula is the effective treatment for this, and lactose-free formula will not show a benefit. Most infants with cow’s milk allergy can tolerate lactose without a problem.

In infants diagnosed with lactose intolerance, breast-feeding should be continued. If the infant is formula fed, a limited trial of lactose-free formula may be recommended. Reintroduction of lactose-containing formula or foods should be attempted after 2-4 weeks. In infants with some digestion problems such as celiac disease, a lactose free formula may also be required until the underlying disease can be treated. Lactose free infant formula is only encouraged when absolutely necessary, due to the benefits obtained from lactose in the infant. In recent times there has been a sharp decline in the consumption of cow’s milk in the community and this is reflected in infant formulas. Avoidance of dairy products can lead to rickets in young children, and even low bone mineral density and increased fracture risk later in life4.

In conclusion, lactose intolerance is rare in children under 5 years and symptoms of cow’s milk allergy and other gut conditions can be wrongly attributed to lactose intolerance. In these cases, lactose restriction is only required until the underlying disease has been treated or resolved. This also goes for cow’s milk allergy, as lactose can usually still be tolerated and added to EHF to give all the benefits associated with its consumption such as prebiotic effects. Educational initiatives will help increase knowledge around lactose intolerance and cow’s milk allergy in the community.

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References

  1. Harvey CB, Hollox EJ, Poulter M, Wang Y, Rossi M, Auricchio S, Iqbal TH, Cooper BT, Barton R, Sarner M, Korpela R, Swallow DM. Lactase haplotype frequencies in Caucasians: association with the lactase persistence/non-persistence polymorphism. Ann Hum Genet. 1998;62:215–223. doi: 10.1046/j.1469-1809.1998.6230215.x.
  2. Itan Y, Jones BL, Ingram CJ, Swallow DM, Thomas MG. A worldwide correlation of lactase persistence phenotype and genotypes. BMC Evol Biol. 2010;10:36. doi: 10.1186/1471-2148-10-36.
  3. Welsh JD, Poley JR, Bhatia M, Stevenson DE. Intestinal disaccharidase activities in relation to age, race, and mucosal damage. Gastroenterology. 1978;75:847–855.
  4. Doulgeraki AE, Manousakis EM, Papadopoulos NG. Bone health assessment of food allergic children on restrictive diets: a practical guide. J Pediatr Endocrinol Metab. 2017;30:133–139. doi: 10.1515/jpem-2016-0162.

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