What does stunts your growth mean

Neerja Indian. Zira US English. Oliver British. Wendy British. Fred US English. Tessa South African. How to say stunted growth in sign language?

Numerology Chaldean Numerology The numerical value of stunted growth in Chaldean Numerology is: 4 Pythagorean Numerology The numerical value of stunted growth in Pythagorean Numerology is: 5. Select another language:. Please enter your email address: Subscribe.

Discuss these stunted growth definitions with the community: 1 Comment. Notify me of new comments via email. Kimano Lambert. Like Reply Report 2 3 years ago. Cancel Report. Create a new account. Log In. Powered by CITE. As is apparent, the density and richness of this network of fibres is far more elaborate in the non-stunted infant than in the stunted infant.

It is important to keep in mind that this is but a single albeit representative infant; thus, until these findings are replicated at the group level, such findings should be considered preliminary. These data were collected as part of an ambitious program of research taking place in Dhaka, Bangladesh Charles A.

Nelson, Ph. The goal of this work is to examine the effects of biological and psychosocial adversity on early brain development. Nadine Gaab, Ph. Stunting is a global problem. Although important progress has been made to reduce child stunting, stunting is declining too slowly and levels still remain unacceptably high.

In , UN agencies reported that million children under five — almost 22 percent of all children in the age range — were affected by the condition in , depriving many them of the opportunity to achieve their full potential before they even reach school age. Multiple forms of malnutrition are evident in many countries. HAZ is calculated by subtracting an age- and sex-appropriate median value from a standard population and dividing by the SD of the standard population 4.

The WHO growth standards are the recommended standard 5. Children who are stunted are a subset of those with linear growth retardation. Our objective is to show that many outcomes commonly presented as consequences of linear growth retardation and stunting are not causally linked. Second, we critically review the scientific evidence linking linear growth retardation and stunting to other outcomes.

Third, we recommend a fundamentally different evidence-based way of making use of linear growth retardation and stunting as measures of global development.

Linear growth retardation and stunting are associated with undesirable short-, medium-, and long-term outcomes in 5 domains: 1 delayed child development 6 , leading to lower school achievement and reduced earnings; 2 reduced physical strength and work capacity 7 , leading to reduced earnings; 3 physiologic changes, contributing to adult noncommunicable diseases and increased mortality 8 , 9 ; 4 increased risk of cephalopelvic disproportion, leading to dystocia, mortality, and morbidity 1 ; and 5 undesirable birth outcomes in the next generation 10 , i.

The scientific literature commonly presents these associations as being causal, i. A recent comprehensive literature review on the association between undernutrition in childhood and economic outcomes shows that this is a widely held view; over half of the 68 papers on linear growth or height made direct causal claims linking linear growth retardation or stunting to the 5 outcome domains Commonly accepted framework showing the importance of linear growth retardation A ; and proposed framework distinguishing between child linear growth as an indicator reflective of the past, as indicator predicting the future, and as an outcome in its own right B.

If linear growth retardation or stunting is a cause of these negative outcomes, then it logically follows that improving child linear growth will improve these outcomes. The causal claims imply that any intervention aimed at improving linear growth will subsequently and automatically lead to improved outcomes in these 5 domains.

We argue below that this causal evidence exists only for the last 2 domains. This causal view is strongly embedded in the nutrition community. An informal survey of agencies and donors active in nutrition shows that they have generally adopted the view that linear growth retardation and stunting is a cause of developmental delays, lower levels of schooling, reduced earnings, and chronic disease risk.

Eliminating linear growth retardation and stunting have become a primary development objective, based in part on believing that their elimination will lead to meaningful benefits in a large number of other domains. The causal thinking has also triggered research on, for example, aflatoxin and catch-up growth. The possible role of chronic exposure to aflatoxin a mycotoxin produced by the fungus Aspergillus sp.

The premise is that if aflatoxin exposure is a confirmed cause of linear growth retardation and stunting in children, then reducing aflatoxin exposure will ameliorate the negative consequences of poor growth 12— Since these consequences are limited see subsequent sections , this motivation for researching the link between aflatoxin and linear growth is questionable.

We add 2 nuances. First, effective aflatoxin control is important because aflatoxin is a group 1 carcinogen, and aflatoxin contamination of food crops impairs the ability of low- and middle-income countries to access export markets 16 , Second, aflatoxin and mycotoxin exposure may contribute to environmental enteric dysfunction, systemic inflammation, immunomodulation, and changes in the hepatic metabolism of micronutrients 14 , These short-term consequences if confirmed all warrant immediate preventive action.

Furthermore, they all potentially limit young children's ability to fully develop into healthy and productive adults 19— Research should focus on these potential consequences of mycotoxin exposure, rather than on its contribution to linear growth retardation and stunting. Catch-up growth refers to accelerated growth that reduces a child's accumulated height deficit Much recent work has reported catch-up growth in the absence of any nutrition intervention 23— Some studies reported an association between catch-up growth and child development, concluding that promoting growth during infancy and early childhood might contribute to better child development 25— These reports have received media attention These conclusions are misleading for 2 reasons.

First, much of the catch-up growth work has assumed that linear growth retardation and stunting negatively affect child cognitive development, and recovery from linear growth retardation or stunting is presented as if it will lead to improved cognitive outcomes 23— We show below that there is no evidence that linear growth and cognitive development are causally linked.

Second, the recent studies use height-for-age z scores HAZ , a measure that is statistically inappropriate to assess catch-up growth In conclusion, none of these studies provided evidence of catch-up growth or determined that catch-up growth has long-term positive consequences on child development.

Rather, they confirm that better linear growth is associated with better cognitive development, which is in line with existing knowledge 6.

We add 2 caveats. First, the motivation for a much-cited study on catch-up growth is maternal short stature as a cause of poor birth outcomes 30 , but the analyses used the statistically inappropriate HAZ Second, recovery from child linear growth retardation or stunting may or may not be possible, but the reviewed studies do not provide evidence that it is.

Linear growth retardation is associated with reduced cognition and motor development in middle- and low-income countries 6 ; the association between stunted growth and socioemotional development has received less attention 6. Linear growth retardation and poor development are associated through a set of shared determinants suboptimal nutrition, inadequate care, and repeated infections. Based on current understanding, however, linear growth retardation is not part of the mechanistic path leading to delayed cognitive, motor, or socioemotional development Two mechanisms have been raised as potentially causal.

The first one is the hypothesized direct effect of smaller body size on reduced motor activity, which would limit the child's ability to explore and access stimulation 6 , 32 and reduce opportunities for language, socioemotional, and cognitive development Motor development, however, appears to be a consequence of factors including balance, myelination, muscle strength, and endurance, but not of body length This mechanism is not likely to be important in societies in which the majority of children suffer from some degree of linear growth retardation.

In conclusion, there is no evidence that linear growth retardation or stunting causes delays in child development, and based on our current understanding of mechanisms, it is not likely that they are causally related.

In both developed economies and low-income settings, earnings are associated with height 7. Taller individuals have more schooling and better skills, which could explain the association, but the height-earnings association remains after controlling for cognitive and socioemotional capacity 7.

There are several reasons to question the causality of this association. First, we could not find evidence for a credible biological or other mechanism that would explain the effect of stature on earnings at the population level. Second, the height-earnings association in developed economies indicates that relative height rather than height in absolute terms is of importance.

The association will therefore not disappear when linear growth retardation is eliminated since that would not remove the distribution of heights at the population level.

Third, with the use of longitudinal data from the Oriente study in Guatemala, Behrman et al. We are not aware of other studies that used this method. In this population largely active in the agricultural sector, only intellectual and not physical human capital increased annual income We conclude that a causal link between linear growth retardation or stunting and lower earnings is not supported by current evidence.

Environmental influences during early development, such as poor nutrition, increase chronic disease risk later in life Much early work on the developmental origins of disease focused on birth weight and infant size as measures of exposure 36 , 37 , which may have contributed to the belief that linear growth retardation and stunting are a cause of adult chronic disease risk 8 , 9.

Three interrelated categories of mechanisms underlying the effect of early environmental influences on chronic disease have been identified: changes in the structure and function of critical organs such as the brain, the pancreas, and the kidney; changes in gene expression; and changes in cellular senescence Based on current knowledge, however, linear growth retardation and stunting are not part of the mechanistic path.

Additionally, recent evidence from carefully conducted epidemiologic studies does not show an association between linear growth retardation or stunting and a number of chronic disease risk factors. Analyses of pooled data from 5 birth cohort studies in low- and middle-income countries India, the Philippines, South Africa, Guatemala, and Brazil showed that neither lower birthweight birth length was not included nor lower linear growth rates in the first 2 y of life were associated with increases in adult cardiovascular risk or plasma glucose concentration A long-term follow-up of a South African cohort showed that children not stunted at 24 mo had a higher BMI-for-age z score BMIZ at 18 y than those who were stunted at 24 mo Likewise, stunting at 12 mo of age in Peru was associated with a decreased risk of having a high BMIZ We conclude that the evidence does not support a causal link between linear growth retardation or stunting and chronic disease.

Linear growth retardation at childhood reduces adult height. Shorter stature in women at adulthood, in turn, is associated with a higher risk of dystocia or difficult labor 1. Mechanical dystocia, or cephalopelvic disproportion, is a major cause of maternal and neonatal mortality and morbidity; the sequelae have important social, economic, and marital consequences The association between maternal height and difficult labor is mediated by the size of the pelvic inlet; shorter women have a smaller pelvic inlet and are thus more likely to suffer from a mismatch between the size of fetal head and the dimensions of the birth canal 42 , Since both stature and pelvic size are linked to skeletal size, we can assume that the association between linear growth retardation at childhood and obstructed labor at adulthood is causal.

Which proportion of the mortality and disability burden could be averted by eliminating maternal short stature is not known. In conclusion, short stature and obstructed labor are causally linked, their mortality and morbidity burden is relatively small and declining, and the fraction of the mortality and morbidity burden attributable to linear growth retardation earlier in life is not known.

A short mother which could be due to linear growth retardation during her childhood is more likely to have SGA children. This association is considered causal and due in part to maternal physical constraints associated with short stature SGA children are at increased risk of neonatal and infant mortality and morbidity during the neonatal period and beyond Reducing SGA from its current prevalence of Combining both estimates, eliminating SGA births that are due to maternal short stature would reduce neonatal deaths by an estimated 3.

Which proportion of the SGA-associated morbidity could be averted when eliminating maternal short stature is unknown. In conclusion, linear growth retardation at childhood is causally linked to an increased risk of giving birth to SGA children. Eliminating maternal short stature would have a modest effect on neonatal mortality and an unknown effect on child morbidity.

Linear growth retardation and stunting are associated with—but based on available evidence do not cause—delayed child development, reduced earnings at adulthood, and chronic diseases. Linear growth retardation is a cause of difficult birth and poor birth outcomes. From these findings, we identify 2 distinct uses of linear growth retardation and stunting. Second, the causal links with difficult birth and poor birth outcomes makes linear growth retardation and stunting outcomes of intrinsic value Figure 1B.

This marker compared with outcome distinction in relation to linear growth retardation and stunting has been made previously 49 , Healthy linear growth requires children to consume adequate diets, to receive proper care, and to be healthy.

A change in the severity of linear growth retardation or stunting is indicative of changes in these immediate and underlying determinants. Linear growth retardation and stunting are markers of the inadequacy of the environment to which children have been exposed. Since linear growth retardation and poor cognition share many of the same determinants including suboptimal nutrition, inadequate care, and repeated infections , improvements in these determinants can be expected to improve both growth and cognition.

Improved linear growth does not lead to improved cognition per se, but it can predict better cognition. Linear growth retardation and stunting in groups of children predict future poor school achievement and progress, lower cognition, reduced earnings, and a higher probability of living in poverty 51 , Linear growth retardation and stunting often are used implicitly as markers of both the past and future.

When a high stunting prevalence is reported for a region, 2 messages are implied. First, children grow up in a deficient growth environment.

Second, as a consequence of growing up in this environment, they are unlikely to realize their full developmental and economic potential in the future. Linear growth retardation is causally linked to difficult child birth and poor birth outcomes.

Linear growth retardation is therefore an outcome of intrinsic value, since a reduction in linear growth retardation or stunting is expected to directly improve these outcomes. Linear growth here is part of the mechanistic path and not just a marker of other outcomes Figure 1B. A more careful distinction between linear growth retardation or stunting as a marker compared with an outcome has a number of practical implications. Interventions may positively and meaningfully affect important nutrition outcomes without providing the dose or inputs necessary to improve linear growth.

That is, for many nutrition outcomes e. For example, a combination of interpersonal counseling, a national mass media campaign, and community mobilization in Vietnam and Bangladesh successfully improved complementary feeding practices, but not linear growth 53 , Impacts on linear growth retardation or stunting possibly required larger improvements in feeding practices or improvements in other determinants such as health.

Furthermore, equating lack of impact on linear growth to program failure discounts the importance of other outcomes and interventions to improve them.

Finally, several nutrition interventions are highly effective at improving children's well-being but have no effect on linear growth.