Wasting and stunting are often presented as two separate forms of malnutrition requiring different interventions for prevention and/or treatment. These two forms of malnutrition, however, are closely related and often occur together in the same populations and often in the same children. Wasting and stunting are both associated with increased mortality, especially when both are present in the same child. A better understanding of the pathophysiology of these two different forms of malnutrition is needed to design efficient programs. A greatly reduced muscle mass is characteristic of severe wasting, but there is indirect evidence that it also occurs in stunting. A reduced muscle mass increases the risk of death during infections and also in many other different pathological situations. Reduced muscle mass may represent a common mechanism linking wasting and stunting with increased mortality. This suggests that to decrease malnutrition-related mortality, interventions should aim at preventing both wasting and stunting, which often share common causes. Also, this suggests that treatment interventions should focus on children who are both wasted and stunted and therefore have the greatest deficits in muscle mass, instead of focusing on one or the other form of malnutrition. Interventions should also focus on young infants and children, who have a low muscle mass in relation to body weight to start with. Using mid-upper-arm circumference (MUAC) to select children in need of treatment may represent a simple way to target young wasted and stunted children efficiently in situations where these two conditions are present. Wasting is also associated with decreased fat mass. A decreased fat mass is frequent but inconsistent in stunting. Fat secretes multiple hormones, including leptin, which may have a stimulating effect on the immune system. Depressed immunity resulting from low fat stores may also contribute to the increased mortality observed in wasting. This may represent another common mechanism linking wasting and stunting with increased mortality in situations where stunting is associated with reduced fat mass. Leptin may also have an effect on bone growth. This may explain why wasted children with low fat stores have reduced linear growth when their weight-for-height remains low. It may also explain the frequent association of stunting with previous episodes of wasting. Stunting, however, can occur in the absence of wasting and even in overweight children. Thus, food supplementation should be used with caution in populations where stunting is not associated with wasting and low fat stores.

Wasting and stunting are common. They are implicated in the deaths of almost two million children each year and account for over 12% of disability-adjusted life years lost in young children. Wasting and stunting tend to be addressed as separate issues despite evidence of common causality and the fact that children may suffer simultaneously from both conditions (WaSt). Questions remain regarding the risks associated with WaSt, which children are most affected, and how best to reach them. A database of cross-sectional survey datasets containing data for almost 1.8 million children was compiled. This was analysed to determine the intersection between sets of wasted, stunted, and underweight children; the association between being wasted and being stunted; the severity of wasting and stunting in WaSt children; the prevalence of WaSt by age and sex, and to identify weight-for-age z-score and mid-upper arm circumference thresholds for detecting cases of WaSt. An additional analysis of the WHO Growth Standards sought the maximum possible weight-for-age z-score for WaSt children. All children who were simultaneously wasted and stunted were also underweight. The maximum possible weight-for-age z-score in these children was below − 2.35. Low WHZ and low HAZ have a joint effect on WAZ which varies with age and sex. WaSt and “multiple anthropometric deficits” (i.e. being simultaneously wasted, stunted, and underweight) are identical conditions. The conditions of being wasted and being stunted are positively associated with each other. WaSt cases have more severe wasting than wasted only cases. WaSt cases have more severe stunting than stunted only cases. WaSt is largely a disease of younger children and of males. Cases of WaSt can be detected with excellent sensitivity and good specificity using weight-for-age. The category “multiple anthropometric deficits” can be abandoned in favour of WaSt. Therapeutic feeding programs should cover WaSt cases given the high mortality risk associated with this condition. Work on treatment effectiveness, duration of treatment, and relapse after cure for WaSt cases should be undertaken. Routine reporting of the prevalence of WaSt should be encouraged. Further work on the aetiology, prevention, case-finding, and treatment of WaSt cases as well as the extent to which current interventions are reaching WaSt cases is required.

Complementing a recent systematic review and meta-analysis which showed that boys are more likely to be wasted, stunted, and underweight than girls, we conducted a narrative review to explore which early life mechanisms might underlie these sex differences. We addressed different themes, including maternal and newborn characteristics, immunology and endocrinology, evolutionary biology, care practices, and anthropometric indices to explore potential sources of sex differences in child undernutrition. Our review found that the evidence on why sex differences occur is limited but that a complex interaction of social, environmental, and genetic factors likely underlies these differences throughout the life cycle. Despite their bigger size at birth and during infancy, in conditions of food deprivation, boys experience more undernutrition from as early as the foetal period. Differences appear to be more pronounced in more severe presentations of undernutrition and in more socioeconomically deprived contexts. Boys are more vulnerable to infectious disease, and differing immune and endocrine systems appear to explain some of this disadvantage. Limited evidence also suggests that different sociological factors and care practices might exert influence and have the potential to exacerbate or reverse observed differences. Further research is needed to better understand sex differences in undernutrition and the implications of these for child outcomes and prevention and treatment programming.

The study describes the patterns of concurrent wasting and stunting (WaSt) among children age 6–59 months living in the 1980s in Niakhar, a rural area of Senegal under demographic surveillance. Wasting and stunting were defined by z scores lower than −2 in weight for height and height for age. Both conditions were found to be highly prevalent, wasting more so before age 30 months, stunting more so after age 30 months. As a result, concurrent WaSt peaked around age 18 months and its prevalence (6.2%) was primarily the product of the two conditions, with an interaction term of 1.57 ( p < 10 ⁻⁶ ). The interaction was due to the correlation between both conditions (more stunting if wasted, more wasting if stunted). Before age 30 months, boys were more likely to be concurrently wasted and stunted than girls (RR = 1.61), but the sex difference disappeared after 30 months of age. The excess susceptibility of younger boys could not be explained by muscle mass or fat mass measured by arm or muscle circumference, triceps, or subscapular skinfold. Concurrent WaSt was a strong risk factor for child mortality, and its effect was the product of the independent effect of each component, with no significant interaction.