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1.Introduction

1.1 Stunting

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Moved to: Stunted growth

Stunting is highly prevalent in low- and middle income countries (LMICs) and has severe consequences including increased risk of infections,[1] mortality[2][3] and loss of human capital.[4][5] The global prevalence of stunting decreased from 33% to 23% between 2000 and 2016.[6] Meanwhile, 37% of children in South Asia are stunted, and due to a large population size, the region bears about 40% of the global burden of stunting.[7] In Nepal, stunting has decreased from 57% in 2001 to 36% in 2016, with lower prevalence in urban than in rural settings.[8] The causes of stunting are complex and include infection and inadequate diet at the individual level, inadequate quality of care for children and women and food insecurity at the household level, poor accessibility to health services and clean water and sanitation at the community level and finally inadequate political and economic structures at the national level (Adapted from UNICEF framework, Fig.1).

A recent risk assessment analysis for 137 developing countries found that the leading risk factors for stunting were fetal growth restriction (birth weight <10th centile) followed by unimproved sanitation and diarrhea. It was estimated that 22% of stunting cases were attributable to environmental factors while 14% were attributable to child nutrition.[9] In addition, looking at trends from 1970 to 2012 for 116 countries, women’s education, gender equality and finally quantity and quality of foods available at the country level have been instrumental in reducing stunting rates, while income growth and governance have played facilitating roles.[10] Finally, in Nepal short maternal stature,[11] low maternal education,[12][13] poor access to health services[14] and poverty[15][16] are strong determinants for stunting.

Almost all stunting occurs within the first 1000 days from conception to 2 years of age,[17][18] which constitutes a window of opportunity for growth promotion.[19] The recognition of pre-natal factors underlines the inter-generational aspects of growth,[20] and the need for early interventions.

Maternal undernutrition increases the risk of stunting at 2 years age.[21] Based on data from 19 birth cohorts from LMICs, 20% of stunting is attributed to being born small-for-gestational-age (SGA).[22] Further, estimated stunting at 2 years attributed to fetal growth restriction and preterm birth in 2011 was 33% in all developing countries and 41% in South Asia.[23] Restricted pre- and postnatal growth are in turn important determinants of short adult height,[24] increasing the likelihood of the next generation also being stunted.[25]

Balanced protein–energy supplementation in pregnancy seem to improve birth weight of children, with greater effects in undernourished women.[26] Meanwhile, micronutrient supplements and lipid based nutrient supplements (LNS) (providing both macro-and micronutrients) during pregnancy have shown mixed effects on birth weight and -length.[27][28] Similarly, studies supplementing LNS to mothers during pregnancy and lactation and their children during the complementary feeding period show heterogeneous results for stunting.[29][30]

1.2 Nature of growth

1.2.1 Growth patterns in early childhood

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A child’s growth results from a complex interaction between genetic and environmental factors.[31] The growth potential of an individual is genetically determined[32] and deviations from expected growth indicate unfavorable environments.[33] The 2006 World Health Organization (WHO) growth charts are based on anthropometric measurements of children in 6 sites in different regions of the world who were exclusively or predominantly breastfed for 4 months, introduced to complementary food by 6 months and who continued breastfeeding until at least 12 months of age.[34] Based on a study comparing growth to WHO standards in 54 LMICs, length/height for age is close to the WHO standard at birth and falters dramatically until 24 months,[35] after which mean values tend to remain between 1.5 and 2 z-scores below the reference.[36] In the South East Asian region, the monthly decline in z-scores between 3 and 24 months age is 0.08.[37] The linear growth rate is highest during the first months of life with decelerating rates as the child ages,[38] and appears to stabilize between 18 and 24 months.[39] Faster growth requires more energy and nutrients.[40] Older children may thus be less responsive to insults on growth than rapidly growing infants.[41][42] Meanwhile, growth is saltatory with no growth occurring during 90-95% of the time from birth to 24 months.[43] Also, deviations from expected growth patterns are common. Weight faltering due to illness may precede linear growth faltering. Catch-up growth will occur if the illness is resolved and conditions for growth otherwise favorable.[44] Frequent illness, however, limits the periods with faster growth and stunting may result.[45][46] Linear catch-up growth can also occur in stunted children independent of illness.[47] To capture any deviations from expected growth pattern including the saltatory nature of growth, it is argued that growth to the extent possible should be assessed by longitudinal charts such as a velocity or increment reference[48][49] instead of cross-sectional measures (HAZ).

1.2.2 Physiology of growth

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Moved section to: Development of the human body

Linear growth takes place in the epiphyseal growth plates (EGP) of long bones.[50] In the growth plate, chondrocytes proliferate, hypertrophy and secrete cartilage extracellular matrix. New cartilage is subsequently remodeled into bone tissue, causing bones to grow longer.[51] Linear growth is a complex process regulated by the growth hormone (GH) - insulin-like growth factor-1 (IGF-1) axis, the thyroxine/triiodothyronine axis, androgens, estrogens, vitamin D, glucocorticoids and possibly leptin.[52] GH is secreted by the anterior pituitary gland in response to hypothalamic, pituitary and circulating factors. It affects growth by binding to receptors in the EGP,[53] and inducing production and release of IGF-1 by the liver.[54] IGF-1 has six binding proteins (IGFBPs), exhibiting different effects on body tissues, where IGFBP-3 is most abundant in human circulation.[55] IGF-1 initiates growth through differentiation and maturation of osteoblasts, and regulates release of GH from the pituitary through feedback mechanisms.[56] The GH/IGF-1 axis is responsive to dietary intake and infections. The endocrine system seems to allow for rapid growth only when the organism is able to consume sufficient amounts of nutrients and signaling from key nutrients such as amino acids and zinc to induce production of IGF-1 is present.[57] At the same time inflammation and increased production of pro-inflammatory cytokines may cause GH resistance and a decrease in circulating IGF-1 and IGFBP-3 which in turn reduces endochondrial ossification and growth.[58][59] However, the EGP appears to conserve much growth capacity to allow for catch-up growth.[60] Concerns have been raised about associations between catch-up growth and increased risk of non-communicable diseases in adulthood.[61] In a large study based on 5 birth cohorts in Brazil, Guatemala, India, the Philippines and South Africa, faster linear growth at 0-2 years was associated with improvements in adult stature and school performance, but also an increased likelihood of overweight (mainly related to lean mass) and a slightly elevated blood pressure in young adulthood.[62]

1.3 Nutrition

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1.3.1 Nutrient intake and growth

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The energy and nutrient requirements that will allow moderately malnourished children to have catch-up growth, strengthened immune function and normalized mental, physical and metabolic development are high.[63] A system classifying nutrients as type 1 or type 2 nutrients depending on the body’s response to their deficiency has been proposed by Golden. Type 1 nutrients (i.e Vitamin A, B-vitamins and iron) are needed for particular biochemical functions in the body. In case of deficiency clinical signs will develop and the child will be susceptible to stress and infection. Type II nutrients (i.e protein, potassium, sodium, magnesium, phosphorous and zinc) are building blocks of tissue and essential for child growth. Given the role of these nutrients in mitosis, cells with rapid turnover, such as intestinal and immune cells, are most vulnerable to insufficiency.[64]

It is generally believed that the protein density of complementary food in LMICs is adequate.[65] Meanwhile, an ecological study from 116 countries underlined the importance of protein quality when assessing risk of protein inadequacy, especially in poorer countries in Africa and Asia.[66] The quality of a protein depends on its ability to meet requirements for 9 essential amino acids,[67] and will depend on the food matrix in which the protein is consumed and the demands of the consumer which is influenced by age, health status and energy balance.[68] It is presently unclear whether current recommendations for essential amino acids are sufficient in settings with a high burden of infectious disease and a substantial need for catch-up growth, but low levels of circulating essential fatty acids have been observed in stunted children.[69] Sulfur-containing amino acids should be used preferentially in stunted populations since sulfate is required for cartilage synthesis[70] which is essential for growth.[71]

Apart from protein, zinc is the only type II nutrient which has been thoroughly investigated in relation to growth. Modest long-term zinc deprivation results in detectable differences in growth and development,[72] while preventive zinc supplementation slightly improves linear growth.[73][74] Zinc deficiency induces anorexia with cyclical food intake and tissue catabolism and breakdown in murine models.[75] Similar responses to insufficiency as for zinc are likely for other type II nutrients for which there are no body stores.[76] In support of this, previous micronutrient supplementation studies where type II nutrients have not been provided have shown little or no effect on growth.[77][78] Malnourished children will likely suffer from multiple nutrient deficiencies,[79] underlining the need to improve whole diets through improved complementary feeding practices.

1.3.2 Complementary feeding

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WHO recommends exclusive breastfeeding until the child is 6 months after which breast milk becomes insufficient, especially in iron and zinc, and complementary food should be provided.[80] High nutrient needs to support growth and development and small quantities of complementary foods consumed implies that nutrient density must be high.[81] Yet the opposite is often true in resource poor settings, where children are primarily fed bulky cereal-based porridges with low energy density[82] and low bioavailability of iron and zinc due to high levels of phytate.[83] Studies from diverse LMIC settings show that even in best case scenarios children are unable to meet their requirements, especially of iron, zinc and calcium, from family foods.[84][85]

Complementary feeding should be timely (starting at 6 months), adequate (providing the appropriate amount of nutrients in addition to breastmilk) and appropriate (diverse with appropriate texture and fed in appropriate quantities).[86] This is reflected in the WHO Infant and young child feeding (IYCF) indicators[87] which were constructed to assess and monitor child feeding practices within and between populations.[88] The indicators include breastfeeding practices, timely introduction of solid, semi-solid or soft foods, minimum dietary diversity (MDD), minimum meal frequency (MMF) and minimum acceptable diet (MAD; MDD and MMF combined).[89] Out of these, timely introduction[90] and dietary diversity[91][92][93] have been associated with linear growth, while meal frequency in most studies is associated with weight.[94][95] For DDS and linear growth, associations are consistent across populations and in studies using different methodologies suggesting that they are robust.[96] Meanwhile, associations between complementary feeding practices and length increments seem less convincing, likely because tracking of good feeding practices and a cumulative positive effect is needed for a change in HAZ to occur.[97] Also, the indicators were not designed to be used separately,[98] and a complementary feeding index encompassing more than one aspect of IYCF has been proposed for studies assessing complementary feeding practices and growth.[99]

Specific food groups associated with improved linear growth are animal source foods,[100][101] and milk in particular.[102] Data from 39 Demographic and Health Surveys (DHS) showed that children who consumed no animal source foods (ASF) the previous day had a 1.44 higher odds of being stunted than children consuming all three types of ASF (egg, meat and dairy).[103] In support of this, since 1970, it is estimated that 18% of stunting reduction may be attributed to per capita dietary energy supply on a national level, while 15% is attributed to the share of energy consumed from non-staple foods.[104] The most recent estimates for South Asia showed that MDD and MAD was achieved by 33 and 21 percent, respectively. Grains were the main complementary food, with 1/3 of children 6-23 months being fed a vitamin-A rich fruit or vegetable and only 17% being fed animal source foods the previous day.[105] Acceptability, availability and affordability seem to limit improvements in dietary quality, especially consumption of animal source foods.[106][107]

1.3.3 Interventions to prevent stunting

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Moved to: Stunted growth

Previous interventions to reduce stunting have shown modest effects. Multiple micronutrient supplementation shows only small benefits for linear growth[108] and results from studies supplementing LNS to children are inconclusive.[109][110] Educational interventions to improve complementary feeding may achieve behavioral change but have no or small effects on growth.[111][112] Further, studies on the effect of micronutrient fortification, increased availability of key nutrients or increased energy density of complementary foods on stunting also show heterogenous results.[113] It is estimated that education interventions, if optimally designed and implemented, could reduce stunting by 0.6 z-scores while food-based interventions could reduce stunting by 0.5 z-scores,[114] which is moderate compared to the average global growth deficit.[115] Finally, the Lancet-series on maternal and child nutrition estimated that the impact of all existing interventions designed to improve nutrition and prevent related diseases in mothers and children, could reduce stunting at 3 years by merely 36%.[116] Hence, factors explaining the shortfall in observed associations between child feeding practices and nutrient intake and linear growth, have increasingly been the focus of scientific interest.[117]

1.4 Environmental enteric dysfunction (EED)

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Crossed out text moved to Environmental enteropathy

1.4.1 Intestinal inflammation and the role of the microbiota

Diarrhea has long been recognized as a main risk factor for child stunting,[118][119] with rotavirus, norovirus, cryptosporidum, shigella, campylobacter and E-coli among the most prevalent causative agents.[120][121]

Meanwhile, studies from the early 1990s in the Gambia showed that children presented with abnormal intestinal architecture and function also in the absence of overt diarrhea.[122] The condition was histologically similar to the tropical enteropathy described since the 1960s in American military and Peace-corps personnel returning from work in Thailand.[123] The name was later changed to environmental enteropathy (EE), and more recently EED, recognizing the importance of environmental risk factors, particularly hygiene and sanitation[124] in the development of EED.

The main cause of EED is likely repeated exposure to enteric pathogens through fecal contamination.[125][126][127]

The key histological features are villous flattening, crypt hyperplasia and inflammation in the epithelium and lamina propria.[128][129]

Intestinal inflammation interacts strongly with age,[130] and in the MAL-ED study appears to peak at about 9-12 months.[131][132] This likely in part reflects intestinal immunologic maturation, where some degree of self-limiting inflammatory response is protective against enteric pathogens.[133] Gut microbiota assembly and maturation (towards increased diversity) occur in the same age span as intestinal immunologic maturation[134] and microbiota containing low diversity is less resistant to enteropathogens.[135] Maturation of the microbiota and the intestinal immune system therefore likely interact in a reciprocal manner to promote healthy gut development.[136] The intestinal mucosa is essential for nutrient absorption and acts as a barrier between the body and the environment.[137] The intestinal barrier function consists of a mechanical barrier formed by a single layer of epithelial cells joined by adherens and tight junctions, an antimicrobial barrier composed of defensins, immunoglobulins and mucins, an immunological barrier made up of immune cells in the sub-epithelial layer and finally an ecological barrier created by the gut microbiota which destroys pathogens.[138] Meanwhile, chronic T-cell mediated inflammation[139] seen in EED may pave the way for intestinal permeability with microbial translocation (MT), resulting in systemic inflammation.[140]

EED is described as a reversible[141][142] condition which is probabilistically associated with poor development, but is neither a necessary nor a sufficient cause and may lead to no observable clinical outcomes.[143] This contributes to difficulties encountered when assessing EED.

1.4.2. Markers of EED

One main challenge in studies assessing EED is the lack of validated biomarkers.[144][145] Biopsies are used to diagnose diseases with similar pathological changes such as celiac disease.[146] However, biopsies are considered invasive in children without clinical illness,[147] unfeasible in endemic settings, and the sample collected may not be representative of the whole intestine.[148] A range of biomarkers measured in stool, urine or blood have therefore come into use to diagnose EED. These represent intestinal absorptive function (of various sugars, for instance lactulose and mannitol), intestinal barrier function (i.e alpha-1-antitrypsin (AAT) and claudins), microbial translocation (i.e lipopolysaccharide (LPS), IgA and IgG anti-LPS and zonulin), intestinal inflammation (i.e myeloperoxidase (MPO), calprotectin, neopterin (NEO), lactoferrin and Reg1A), systemic inflammation (i.e acid glycoprotein (AGP), interleukins, TNFα, EndoCab and C-reactive Protein (CRP)) and finally metabolites/growth markers such as Tryptophan, Citrulline , IGFBP-3 and IGF-1.[149] The biomarkers have been found to correlate weakly with each other,[150][151] likely due to the diverse functions assessed and distinct physiological processes described. Further, the biomarkers show varying specificity for EED-induced growth faltering, with heterogeneous results among studies using the same biomarker.[152]

The lactulose:mannitol (L:M) ratio, measured in urine, has been most commonly used to assess EED in previous studies.[153] The test builds on the assumption that while mannitol is passively absorbed proportional to intestinal absorptive capacity, lactulose is a disaccharide which is not absorbed by the healthy intestine. Increased L:M ratio thus indicates reduced absorptive capacity and increased permeability.[154] EED is shown by numerous studies to be highly prevalent in LMICs,[155] but studies often lack reference values for diagnostic markers on which they base their findings.[156] Assignment of reference values is challenging because they may change with physiologic maturation. Also, a response to environmental exposures may initially reflect adaptive rather than pathologic processes.[157] Reference values for L:M ratio have usually been based on UK childhood values [158][159] or presumed norms for children in LMICs.[160][161] Most previous studies have applied 0.12 as reference.[162]

Compared to the L:M test, fecal markers are more readily collectible, and may be more feasible for surveillance of EED. MPO is a marker of neutrophil activity in the lamina propria[163] and has been correlated with disease activity and severity in inflammatory bowel disease.[164] MPO is a preferred biomarker in breastfed children since it is not elevated in breastmilk as are lactoferrin and calprotectin.[165] Neopterin is produced by macrophages and dendritic cells upon stimulation with inferferon-gamma (IFN-γ) produced by activated T helper cells. It is thus a marker of TH1 stimulation[166] and has been linked to disease activity in celiac disease.[167] Finally, alpha-1-antitrypsin is a serum trypsin inhibitor which is excreted intact into stool.[168] It is thus a marker of intestinal permeability and protein losing enteropathies.[169] Due to large molecular polar surface area,[170] AAT is an indicator of relatively severe gut barrier disruption.[171] The level of fecal markers appear to be directly associated with the number of pathogens in stool,[172][173] and most strongly with pathogens that are enteroinvasive or cause mucosal disruption.[174]

1.4.3 Dietary intake and EED
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Crossed out text moved to Environmental enteropathy

The role of nutrition in EED is increasingly being recognized.[175] EED is likely associated with energy deficiency and underweight. Mice fed a moderately energy- and protein deficient diet who are exposed to intestinal pathogens show traits similar to EED.[176]

Further, weight gain in malnourished children is shown to improve EED.[177] Severe malnourishment is also likely associated with microbiota immaturity,[178] which might increase EED.[179] The intestinal mucosa turnover is dynamic, nutrient-dependent and rapid,[180] and malnourished children have rate-limiting stores for repairing mucosal damage.[181]

The nutrients known to contribute to intestinal regeneration and improved barrier function are sulphur containing amino acids, [182] glutamine, vitamin A and zinc.[183][184] Meanwhile, studies investigating associations between glutamine[185] or vitamin A supplementation,[186][187] serum retinol[188][189] or zinc supplementation either alone,[190] in combination with vitamin A[191] or with micronutrients and antibiotics[192] and EED show mixed results.

Gut barrier repair and gut function may also be improved by a reduction in the inflammatory response. Short-chain fatty acids (SCFA) result from fermentation of non starch polysaccharides in the colon.[193] It is likely that short-chain fatty acids in addition to zinc[194] and polyunsaturated fatty acids (PUFAs)[195] may reduce gastrointestinal inflammation. Although neither fibre nor polyunsaturated fatty acids provided as supplements improved L:M ratio or inflammation in intervention trials,[196][197] an increased protein and fibre intake from legumes as complementary food, might improve EED.[198][199] Cessation of breastfeeding and introduction of complementary foods, especially foods with high fibre and protein content, also likely increases microbiota diversity,[200] which might benefit the intestine. As for micronutrient intake and EED, studies from Africa have demonstrated that multiple micronutrient supplementation may improve L:M ratio in adults,[201] and transiently in children.[202] Finally, despite the diverse roles attributed to zinc in EED the effect of supplementation as prophylaxis is uncertain.[203] This may partly be due to the perturbed nutrient metabolism occurring in EED.[204]

1.5 Nutrient intake and nutritional status in EED

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Crossed out text moved to Environmental enteropathy

The relationship between dietary intake and infection is difficult to study since it is reciprocal in nature.[205][206] Further, the gut tissue consumes the nutrients it requires before passage of excess nutrients to the rest of the body.[207][208] The benefits achieved by improved nutrient intake on EED may thus be independent of nutritional status. Nutrient intake during inflammation is usually decreased. Reports of “poor appetite” by caregivers in LMICs,[209] and restriction of complementary foods during illness[210] is common. Appetite may be reduced both by pro-inflammatory cytokines and leptin[211] and low zinc status,[212] and may be continuous in children with EED[213] . Nutrient availability for growth in EED is further limited due to reduced intestinal surface area and loss of enzymatic activity causing malabsorption of nutrients[214][215] and, following microbial translocation, retention of circulating nutrients (i.e vitamin A, zinc and iron) in body tissues in order to starve pathogens.[216] Associations between nutrient intake and biomarkers for nutrient status[217] and nutrient status and growth[218] are thus likely distorted in children with inflammation. The systemic inflammation resulting from microbial translocation will increase basal metabolic rate and nutrient needs by the immune system.[219] At the same time, nutrient losses increase due to intestinal secretion.[220] The associations are thus complex, and further complicated by intestinal host-pathogen-microbiome interactions[221] and the effects of these interactions on intestinal nutrient availability,[222][223] where additional research is needed. Finally, evidence of whether nutrition interventions may be successful in children with repeated episodes of infection or persistent subclinical infection is scant.[224] Meanwhile, there seems to be agreement that successful interventions to improve complementary feeding practices[225] and reduce stunting[226][227] must encompass both immediate and underlying causes.

References

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 This article incorporates text by Marianne Sandsmark Morseth available under the CC BY-SA 3.0 license.

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