Historically, policies and programs focused on economic growth have impacted health outcomes through increased access to health services and improved quality of health services. More generally, economic growth, if equitable, leads to greater household purchasing power. Over time, stunting prevalence from 1985 to 2011 across 141 countries showed an overall decline in stunting as economic indicators improved (13). However, an overall analysis of GDP per capita found no significant relationship with reductions in stunting or other nutrition outcomes (14). Again, the increases in wealth at a country level need to be equitable and investments in health and nutrition are needed in order to impact the nutrition status of the most vulnerable households. Furthermore, the level of wealth at the household level has been shown as an indicator for increased risk of stunting (15). There is also an association between increased risk of stunting and lack of basic infrastructure, which includes water, sanitation, electricity, and shelter (16). A similar association between decreased risk of stunting and increased household wealth and improved community resources, specifically health centers, has also been presented in the Young Life Study (17).

Beyond economic and political factors, cultural factors can play an important role in child growth. The cultural factors, which have been shown to be important to the prevalence of stunting, are women’s autonomy and fertility practices. In Indian households, a woman’s status is related to the birth order of either herself or her husband, which can determine the quantity and quality of resources devoted to both the mother and child (18). Additionally, the distribution of resource among children within the same family can differ. In a secondary analysis on prevalence of stunting and birth order, the data showed that sub-Saharan African countries as a whole had a more constant rate of stunting across birth orders compared to India, where higher birth order (i.e., having more older siblings) was associated with an increasing risk of stunting (19). In addition to the birth order of both parents and children, gender can also have a significant influence on growth. In Pakistan, due to the cultural context of feeding and care practice, female children are often considered secondary to male children and were three times as likely to be stunted (20). While cultural factors play an important role in children’s growth and development, the impact of cultural factors on stunting should be considered as being confined to specific geographic areas and ethnic groups rather than as uniform assumptions.

There are certain types of shocks that can cause disruptions in resources and livelihoods, leading to static or worsening prevalence of stunting. Such shocks, including droughts or civil conflicts, lead to increases in stunting in children, particularly in children 12–24 months and in children from poorer households (21). Different types of shocks can impact different cohorts within a population through different mechanisms. A study of conflict and crop failure in Rwanda found that the impact of these events can lead to sustained growth failure, even after the event had ended (22). Climate events and changes to the natural system can affect the prevalence of stunting through both increases in human morbidity and degradation to the local food system and resources. Exposure to droughts and floods in India was shown to have increased the risk of stunting by 7% (23). Exposure to these types of events can be associated with malnutrition through the impact on the quality and quantity of food or can indirectly be associated through the impact on the economy, political systems, public infrastructure, and water systems.

The underlying causes of malnutrition, found at the community level, impact the ability of the household and individual to obtain proper nutrition. One underlying cause of malnutrition is inadequate household food security. Food security is characterized by having the combination of available food, access to nutritious foods, and proper utilization of food and can be caused by shocks at the household or community levels either in singular, cyclical, or continuous intervals. At the household level, food insecurity relates more to the household economy and contextual determinants of how food is used and consumed. These determinants include maternal knowledge of care and feeding practices, maternal chores or livelihoods, and family eating behaviors (e.g., who eats first, the size of individual rations, etc.) (24). A study on household food security effects on pre-school children showed that household food insecurity has an effect on the prevalence of diarrhea, which leads to a dose–response effect of diarrhea on the prevalence of stunting (25). At the community level in Bangladesh, food insecurity caused by the monsoon season was associated with wasting, but not with stunting, through decreased dietary diversity and lower household income (26). Furthermore, seasonality has not been shown to affect prevalence of stunting unless seasonality directly affects the disease environment (15). On the other hand, increased prevalence of stunting has been linked to repeat instances of food insecurity through the accumulation of bouts of wasting leading to linear growth failure (27). The biological mechanism behind this is based on the manifestation of wasting causing the body to consume fat and tissue leading to the point when no more fat and tissue can be consumed and there is an interruption of linear growth (28). There are key components that make up a sustainable food system and are closely linked to food security. These components include household income, market prices, gender dynamics, dietary diversity, and household and individual behavior (29). Furthermore, the agricultural systems and environmental components of agriculture systems, such as soil, water, and agrobiodiversity, have an impact on food security through both the quantity of available food and the quality of available food, being both diverse and culturally acceptable (30).

Other underlying causes of malnutrition are inadequate care practices, which include lack of exclusive breastfeeding and poor IYCF practices. Breast milk is important component of an infant’s intake and is key to help build a strong immune system (31). Exclusive breastfeeding for the first 6 months is the UNICEF recommendation (32). Breast milk contains immune-modulating compounds, which are the building blocks to a strong immune system (33). IYCF practices recommend early-initiated and exclusive breastfeeding for the first 6 months, and continued breast-feeding with introduction of adequate solid, semi-solid, and soft food from 6 to 12 months. In a study in Bangladesh of an Integrated Management of Childhood Illnesses (IMCI) strategy, where the IMCI treatment group had a higher prevalence of exclusive breastfeeding for 6 months, exclusive breastfeeding resulted in a 7.3% decrease in the prevalence of stunting (34).

Additional underlying causes of malnutrition are inadequate services and the presence of an unhealthy environment. More specifically, this includes poor access to and quality of health services, water, and sanitation facilities, substandard hygiene practices, and inadequate food preparation, all of which are important in their contribution to the disease environment. A study found that family housing quality was negatively associated with stunting, where housing quality was measured by the type of dwelling, the availability of a safe water supply, the adequacy of sanitation, and garbage collection (35). Poor household environmental conditions were associated with increased infections in children and an increased risk of stunting compared to non-contaminated household environments. (36) There appears to be a positive correlation between water and sanitation hygiene (WASH) and stunting. However, in a literature review of WASH interventions on nutrition status, WASH was only found to be a slightly significant factor in reducing the risk of stunting and was found to increase the average height-for-age z-score by 0.08 standard deviations. (37) The authors noted that more rigorous testing was needed. In an additional study, improved sanitation and a reduction in open defecation by 20% was found to increase the average height-for-age z-score by 0.1 standard deviations (38).

These underlying causes do not affect stunting in isolation of each other. The combination and interaction between them amplify the effect on the overall prevalence of stunting. A study on the Millennium Villages Project attributes a reduction in stunting to the combination and interaction of several factors across multiple sectors (39). However, further studies are needed to assess the impact of multi-sector efforts on reducing stunting.

The immediate causes of the conceptual framework include inadequate food intake and risks posed by the disease environment on the individual. Inadequate food intake refers to both quantity of food and quality of the diet. The nutritional quality of food intake holds importance in driving the biological processes that govern the growth and development of the musculoskeletal and the nervous system. The second part of inadequate food intake is the quality of the food. The quality of a diet is reflected by the dietary diversity and the micronutrient content of the diet. A study in Cambodia showed an association between greater diet diversity and reduction in or lack of stunting (40). A noted key component in this study was the consumption of animal-source foods. Animal-source foods contain vitamin A, vitamin B₁₂, riboflavin, calcium, iron, and zinc as well as higher amounts of protein, energy, and fat compared with plant food sources.

The lack of essential vitamins and minerals within the diet is also known as the “hidden hunger.” Deficiency of certain vitamins and nutrients can lead to specific conditions but the deficiency in even just one can be a limiting factor for growth. It is also important to acknowledge that when there is one micronutrient deficiency there is a high likelihood that there are multiple micronutrient deficiencies (7). Research is needed to look at the effect of micronutrient deficiencies on stunting. Furthermore, there are many challenges in diagnosing specific micronutrient deficiencies in low-resource settings, since laboratory testing is often required.

The second immediate cause in the conceptual framework is disease. Disease can be a cause and consequence of malnutrition. Common childhood infections and diarrheal diseases can lead to poor absorption or ability to retain nutrients. The risk of a child being stunted at 2 years of age increases with the incidence of diarrhea (41). The incidence of diarrhea in children has a dose–response effect on stunting; as the incidence of diarrhea increases, the risk of becoming stunted also increases (25). The dose–response effect is part of a downward spiral interaction between poor nutrition and disease.

Children may not only be at risk of stunting due to diarrheal disease but also due to environmental enteropathy. Humphrey proposes environmental enteropathy as a hypothesis, defining environmental enteropathy as a subclinical disease caused by ingestion of fecal material and the subsequent intestinal inflammation and enteric infection (42). There have been few studies examining environmental enteropathy and the link with stunting. Tests for environmental enteropathy include collecting intestinal biopsies and biomarkers to examine the nutrient absorptive capacity of the intestine due to morphological changes in the lining that may take place due to chronic enteric infection (43). A study of Gambian children found no significant association of linear growth with adequate diet or diarrhea but did find an association between poor intestinal absorption and growth faltering (44). There have been few other studies that support the hypothesis of the impact of environmental enteropathy on stunting (45, 46).

Both diarrhea and environmental enteropathy are related to the water and sanitation facilities and practices at the community level. It is important to reiterate that chronic undernutrition through deficiencies of certain nutrients, for example vitamin A and zinc, compromise the immune system, leaving a child more susceptible to infectious diseases including diarrhea, malaria, and measles among other communicable diseases. Pathogens in the environment affect children and can lead to children becoming stunted. In an ecological analysis, a 10% increase in occurrence of open defecation was found to increase stunting by 0.7% points (47). There is a downward spiral of disease and malnutrition that is important to acknowledge as both cause and consequence of chronic malnutrition.

Another contributor to stunting related to quality of food and the disease environment are toxins. This includes both naturally occurring toxins, such as Aflatoxin, and man-made toxins, such as pesticides. For a large portion of toxins, the long-term health impacts on humans are unknown, particularly the impacts on children.

Aflatoxin, a secondary metabolite of Aspergillus flavus and Aspergillus Parasiticus fungi, is most often found in food crops in tropical and subtropical regions. The most common food crops include maize, groundnuts, oilseeds, and tree nuts. Aflatoxin is produced most frequently during the wet season. Aflatoxin toxicity can be fatal to humans if consumed in high doses. Non-fatal exposure has also been associated with growth impairment in children through immune system suppression, impairment of protein synthesis, and changes in the hepatic metabolism of micronutrients. Exposure to Aflatoxin in children has been identified to occur through passage from the mother, either in utero or from breast milk, and through the child’s consumption of complementary foods containing maize and groundnuts (48). More research is needed on the exact mechanisms related to growth impairment from Aflatoxins.

The exposure of both pregnant women and young children to pesticides can have an impact on the growth and development of children. There has been anthropological research showing neurological deficits in children exposed to pesticides (49). This finding points to the need for further clinical research to understand the biological impacts and pathways that pesticides have on children, both in terms of neurological development and the impact on child nutrition. A study on Ecuadorian children discusses the potential compounding effect of pesticides and chronic malnutrition on neurological development (50). The interaction between exposure to toxins and malnutrition on child development is an area in need of further research.

Evidence shows that growth faltering can begin in utero and continue until approximately 24 months (51). This knowledge has led to what is commonly referred to as the window of opportunity or the first 1,000 days of growth and development. This time period is when a significant amount of critical growth and development takes place. The timing of stunting is not necessarily dictated by the causes but rather by which cause happens at specific growth stages during childhood. Intrauterine growth restriction is a form of chronic undernutrition, which leads to infants being born small or stunted at birth. Intrauterine growth restriction is caused when the mother has not met the nutritional requirements of pregnancy. Maternal body composition (stature and BMI) and mother’s age at childbirth are predictors for stunting (15). In addition, growth failure prior to 12 months of age is most closely associated with low stature of the mother (52).

There is a difference between becoming stunted and already being stunted. In addition to the criteria of falling at or below 2 SD on the height-for-age growth standard, the distinction is particularly important to consider in regards to ability to catch up height later in life. In a study by Mendez and Adair, it was found that children who became stunted earlier in utero or in early infancy were more likely to be severely stunted (−3 SD below the mean) (53). Furthermore, the earlier a child becomes stunted, the greater the long-term consequences (9). The timing of becoming stunted earlier in life creates greater potential for detrimental short- and long-term consequences. Stunting beyond the age of 2 years has been shown in children already stunted, suggesting that children who have become stunted in the first 2 years may be chronically at a disadvantage to regain height later in childhood (54).

The consequences of stunting can be both short- and long-term. In the short-term, stunting can result in increased risk of mortality. Mortality is complex to measure, since a child may not die from being stunted as a primary cause. Rather, stunting can be an underlying factor contributing to a child’s vulnerability and susceptibility to morbidities. In 2010, child and maternal undernutrition (including both acute and chronic malnutrition) were responsible for 1.4 million deaths or 6.7% of all DALYs (disability adjusted life years) according to the Global Burden of Disease Study (55). Within the 1.4 million, 0.9 million deaths were due to stunting of children under 5 years. A study of multiple cohorts shows a compounding effect of multiple anthropometric failures (height-for-age, weight-for-age, and weight-for-height) on selective mortality (56).

Morbidity or burden of disease can be caused by both the suppression of the immune system and subsequent long-term chronic health problems. Vitamin A, zinc, and iron are all related to compromised immune function, increased occurrence of infections, and increased risk of stunting (57, 58). Stunting and lowered immune function can lead to higher risk of infectious diseases. This includes susceptibility to diarrhea, as an immediate cause of chronic undernutrition, and other infectious diseases, and can lead to a cyclic effect of infection and malnutrition.

Long-term effects of stunting impact the health, education, and productivity of children as they become adults. One long-term consequence of chronic undernutrition is a decrease in cognitive ability. There has been much research on this association both with educational attainment and wages gained in adulthood. In a study of Peruvian children, chronic malnutrition, as measured by stunting in infancy, leads to poor cognitive development later in childhood (59). Additionally, the Young Lives Study showed that grade achievement and test scores were affected by stunting, but children who were able to catch up in height between 1 and 8 years were also able to catch up cognitively (60). There are several studies that demonstrate the importance of the timing of catch up associated with educational attainment (61, 62). As discussed earlier, interventions in earlier stages of growth and development had larger impacts on long-term wellbeing.

Chronic malnutrition in early childhood not only affects educational attainment but also cognitive ability as an adult and therefore economic earnings in the long-term (63). In rural Zimbabwe, the impact of stunting in pre-school aged children is correlated with lower human capital potential in adulthood (64). Additionally, there has been shown to be an association between linear growth failure at 2 years of age and work status (either working, unemployed, or informal work), whereas stunting at 2 years of age was more closely associated with unemployment or informal work (65). One challenge in measuring employment opportunities and economic capital later in life is due to gender imbalance. While many people work in the informal sector in developing countries, women account for most of this sector, and in some cultural contexts, girls are more likely to suffer from stunting than boys.

Another long-term effect of stunting on morbidity is an increase in the risk of non-communicable diseases such as cardiovascular disease and diabetes related to being overweight or obese. In biological terms, stunting leads to impaired fat oxidation and glucose intolerance (58). Several studies have drawn the association between stunting in early childhood and obesity later in life (66, 67). In some populations, young children have been found to be both stunted and overweight. This relationship, found in rural Mexico, was closely associated with younger mothers, lower socioeconomic status, lower education level of mothers, maternal stature, and household size (68). Furthermore, rapid weight gain and linear growth in children in low and middle-income countries is associated with increased survival and improved cognitive development but may also lead to increased risk of obesity and related adult cardio-metabolic diseases (69). The “thrifty gene” or Barker hypothesis explains that catch up growth later in childhood after experiencing growth failure can increase the risk of adult obesity, which can lead to type-2 diabetes and cardiovascular disease (70). Additionally, research has shown that stunting in early childhood may increase the risk of elevated systolic blood pressure in later life (71). It is important to note that the concept of catch up from being stunted can create some protection from adult chronic disease risk factors. However, the “catch up dilemma” is that increased linear growth can lead to improved health outcomes but too rapid linear growth may be associated with an increased risk for the chronic diseases mentioned (69). This increase in obesity and potential for non-communicable diseases is most often seen in countries facing an epidemiological transition due to globalization, economic growth, and drastic changes in the food environment. Globally, there has been a 54% increase in overweight children under 5 years between 1990 and 2011 (5).

Beyond the long-term effects of stunting, there are effects that transcend generations. Stunted children become stunted adolescents, who then become stunted adults who give birth to stunted infants. More specifically, as mentioned, intrauterine growth restriction can cause the child in utero to be small-for-gestational age, which manifests as a low-birth-weight infant at birth. This is most easily seen in the nutritional relationship between mother and child throughout both pregnancy and infancy. If a mother enters her pregnancy with poor nutrition status, she is more likely to give birth to a low-birth-weight or stunted infant (5). Beyond the mother-to-child transmission of nutrition status, there is a cyclical and transgenerational link between agricultural productivity and nutrition status that is important to note (72). The long-term impacts of stunting have a strong impact on agricultural productivity in adulthood, which can further create deficits for future generations. This cycle can be thought of as a nutritional poverty trap. Analysis has shown that the transgenerational effect can be seen through trends in adult height, which can be predicted by height at 2 years (73). Similarly, there have been other papers on the transgenerational consequences of stunting (74, 75).

As discussed, the consequences of stunting can be both detrimental to the individual and community and can have both short-term and long-term impacts throughout the lifecycle. The definition of catch up is a reduction of the stunted child’s height deficit, which occurs in early childhood and involves an increased velocity of linear growth (76). An important question is whether or not there is an opportunity for children to “catch up” in height. An analysis of children from low- and middle-income countries found that 70% of the growth deficit found at the age of 5 years can be attributed to stunting occurring in the first 1,000 days of life (54). Prentice et al. contradict the common belief that there is only one critical window for growth between the ages of conception and 24 months, stating that there are two rapid periods of growth for children, one in early childhood and one during puberty (77). The core argument is that there is a maturational delay in stunted children, which allows growth catch up potential in later childhood by prolonging the pubertal growth phase. Furthermore, there have been documented delays in menarche, which can lead to this opportunity for catch-up growth, particularly in adolescent girls (78).

Timing is critical in terms of achieving catch-up growth. By the age of 3 years, the nutrient requirements drop, making it easier to meet a child’s dietary requirements and making the child less susceptible to chronic undernutrition (9). A study by Outes and Porter in Ethiopia shows that catch up is possible, especially for children from wealthier households, but the window for catch up ended by the age of 5 years (79). Similarly, a study demonstrated that children who displayed catch-up growth had similar cognitive ability later in childhood when compared to children who had never been stunted (80). There are also studies, which have shown that early growth improvements prior to 2 years can have a positive association with school outcomes and cognitive ability (60). Further research is needed to determine the timing and ability of stunted children to catch up both physically and mentally to their non-stunted peers.