Food insecurity is a hot topic right now given the turbulent food prices that have marked the last three years. Food insecurity occurs whenever a household or individual lacks predictable access to foods in sufficient quantity and quality to maintain an active and healthy lifestyle. The concept rests on three pillars: availability, access, and utilization. Availability refers to the overall abundance of food but as Sen and others have pointed out, availability does not ensure access. The world produces more than enough food, but an unknown (but probably quite large) number of people cannot reliably access this food. Accessing food is critical and it is for this reason much research has focused on measuring the access component of food insecure. As more studies are conducted examining the relationship between new food insecurity measurement tools and children’s nutritional status, I have found it to be quite striking how little of the variation in children’s nutritional status is accounted for by household food insecurity. This got me thinking last night about the third component of food insecurity.
This third component is utilization of food. This pillar represents how well individuals utilize the food that they can access. When this pillar is discussed or assessed in the food insecurity literature it has often been in reference to dietary quality and dietary choices: What foods do people actually consume? Rarely have researchers explicitly linked one’s ability to absorb the nutrients they are consuming but if one were only absorbing a fraction of their dietary intake then this would indicate reduced utilization, and thus food insecurity. In other words, if there is sufficient availability of food and one can access it but only utilize a portion then one would, by definition, be food insecure, right?
How might we assess this level of utilization? In a series of papers Lunn, a biological anthropologist, and colleagues argued that the mucosal lining of the gastrointestinal tract represents a major interface between the body and the environment. A series of historical studies with severely malnutrition and hospitalized children have shown that among these children, the interface, the intestinal villi of the mucosal lining, was frequently severely atrophied – a condition known as tropical enteropathy (see figure above). Such atrophied villi were thought, initially, to be an outcome of severe malnutrition but subsequent thinking has reversed this order and suggested that degradation of the mucosal lining preceded severe malnutrition. In a fascinating cross-cultural study, Menzies and colleagues compared estimates of mucosal damage among adult visitors and residents in tropical and temperate countries. Residents and visitors to tropical areas showed “higher intestinal permeability and lower absorptive capacity” and all of the evidence indicated that compromised gut function was due to environmental factors. Even among affluent travelers, traveling in the tropics was associated with sub-clinical intestinal damage. Menzies et al’s work and others strongly suggested a link with poverty and unhygienic conditions. Lunn and others followed up on this work and outlined two pathways through which degradation of the mucosal lining could lead to malnutrition. First, lactase, the enzyme that is responsible for breaking down lactose, is found in the brush border of the intestinal lining. If the intestinal villi were damaged then lactase production might be curtailed and lactose unable to be absorbed. This would be a particularly important pathway for infants who were deriving a substantial portion of their energetic intakes from milk. Second, the damage to the intestinal villi may allow translocation of molecules into the body, which would trigger the immune system, which itself requires energy (which would in turn not be devoted to growth, a classic life history tradeoff, see McDade et al)). This would predict a link between mucosal damage and immunostimulation, which has been confirmed.
Consistent with these predicted pathways, Lunn and colleagues assessed the mucosal damage among Gambia infants and children and showed that by 6 months of age, 50% of the children showed evidence of damaged mucosa and this rose to 96% among infants aged 10 months. The degree of damage was directly related to the degree of stunting and in the statistical models mucosal damage explained ~40% of the variation in length growth and weight gain over a 9 month period. Subsequent work by Lunn and colleagues suggest that both pathways were important. Work from Nepal and the UK by Panter-Brick and colleagues also showed a high prevalence of mucosal damage and this was higher among children living in squatter settlements when compared with middle-income children.
All of this suggest that unhygienic environments, perhaps more so than access to food, contribute to childhood growth. At least among children, there is other evidence that dietary quality and quantity (and disease), standard measures of food insecurity, are not necessarily responsible for the high prevalence of stunting and underweight observed in many low-income, high mortality countries. Part of this evidence comes from nutritional supplementation trials that tend to show limited positive impacts on nutritional outcomes. And part of this evidence comes from data showing that secular improvements in diarrheal prevalence are not associated with parallel improvements in nutritional stunting, or within-children that diarrhea episodes appear to have limit if any detectable impact on children’s growth outcomes several months after the episode. Finally, and intriguingly, data from at least two studies that actually measured the amount of food that children did not eat (but were offered) reveal that stunted children ate only ~70% of what they were offered. In a study from Huascar, Peru in the 1990s stunted infants tended to consume more each day than the non-stunted but both groups only consumed 65-70% of what they were offered. Similarly a study of 2-5 year olds in Mexico also showed that despite being stunted, which would classify them as hungry by some measures, these children consumed only 1528 of the 2029 kcals that were available to them. Of course, if stunting was directly equated with hunger or lack of food then food waste would not be expected. All of this suggests that utilization is potentially more important than once thought (or, at least more than I thought) – or rather that access and availability aren’t the whole story.
If food utilization is compromised by damaged mucosa in children living in unhygienic settings then this may help explain why the relationship between measures of food insecurity and the prevalence of undernutrition varies widely between sites and is often only weakly related. It also suggests that questionnaire based methods of food insecurity (or even observations of food intake) will routinely underestimate the utilization component of food insecurity and this will be biased such that less hygienic environments will typically show a greater mismatch between subjective measures or experience based measures of food insecurity and measures of undernutrition. This complicates the utilization components of food insecurity too, and suggests that we need to look not only at the food choices that people make but also at to what extent those foods are actually absorbed into the body. Finally, thinking across the pillars suggests that different components of food insecurity may differentially impact on health and wellbeing outcomes and these might interact with one another. Does this mean that access scales are missing a (big) piece of the picture or that they will be most effective when additional measures of hygiene exist?
– Craig Hadley
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