Reducing Malnutrition: Time to Consider Potential Links Between Stunting and Mycotoxin Exposure?

Etzel, Ruth A.

doi:10.1542/peds.2014-0827

Cited by 34 publications

(26 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Mycotoxins are fungal metabolites that frequently contaminate staple foods such as maize and ground nuts in developing countries; infants tend to be particularly vulnerable to exposure in the food chain. 205 Levels of aflatoxin were related to stunting in a cross-sectional study of children aged 9 months to 5 years in Benin and Togo 206 and in Tanzania, exposure to fumonisin was inversely associated with linear growth in infancy. 207 Mycotoxins might mediate stunting through multiple pathways, including enteropathy, although further studies are needed to clarify causation.…”

Section: The Pathogenesis Of Stuntingmentioning

confidence: 99%

The stunting syndrome in developing countries

Prendergast

Humphrey

2014

Paediatrics and International Child Health

818

653

View full text Add to dashboard Cite

Linear growth failure is the most common form of undernutrition globally. With an estimated 165 million children below 5 years of age affected, stunting has been identified as a major public health priority, and there are ambitious targets to reduce the prevalence of stunting by 40% between 2010 and 2025. We view this condition as a ‘stunting syndrome’ in which multiple pathological changes marked by linear growth retardation in early life are associated with increased morbidity and mortality, reduced physical, neurodevelopmental and economic capacity and an elevated risk of metabolic disease into adulthood. Stunting is a cyclical process because women who were themselves stunted in childhood tend to have stunted offspring, creating an intergenerational cycle of poverty and reduced human capital that is difficult to break. In this review, the mechanisms underlying linear growth failure at different ages are described, the short-, medium- and long-term consequences of stunting are discussed, and the evidence for windows of opportunity during the life cycle to target interventions at the stunting syndrome are evaluated.

show abstract

Section: The Pathogenesis Of Stuntingmentioning

confidence: 99%

The stunting syndrome in developing countries

Prendergast

Humphrey

2014

Paediatrics and International Child Health

818

653

View full text Add to dashboard Cite

show abstract

“…Recently, documented high prevalence of exposure during pregnancy has directed focus on aflatoxins as a potential harmful exposure during the first 1,000 days23,26—the developmentally sensitive period from conception to 2 years of age. There are no published randomized controlled trials evaluating the effect of aflatoxin exposure during pregnancy.…”

Section: Introductionmentioning

confidence: 99%

Aflatoxin Exposure During Pregnancy, Maternal Anemia, and Adverse Birth Outcomes

Smith

Prendergast

Turner

et al. 2017

The American Society of Tropical Medicine and Hygiene

View full text Add to dashboard Cite

Pregnant women and their developing fetuses are vulnerable to multiple environmental insults, including exposure to aflatoxin, a mycotoxin that may contaminate as much as 25% of the world food supply. We reviewed and integrated findings from studies of aflatoxin exposure during pregnancy and evaluated potential links to adverse pregnancy outcomes. We identified 27 studies (10 human cross-sectional studies and 17 animal studies) assessing the relationship between aflatoxin exposure and adverse birth outcomes or anemia. Findings suggest that aflatoxin exposure during pregnancy may impair fetal growth. Only one human study investigated aflatoxin exposure and prematurity, and no studies investigated its relationship with pregnancy loss, but animal studies suggest aflatoxin exposure may increase risk for prematurity and pregnancy loss. The fetus could be affected by maternal aflatoxin exposure through direct toxicity as well as indirect toxicity, via maternal systemic inflammation, impaired placental growth, or elevation of placental cytokines. The cytotoxic and systemic effects of aflatoxin could plausibly mediate maternal anemia, intrauterine growth restriction, fetal loss, and preterm birth. Given the widespread exposure to this toxin in developing countries, longitudinal studies in pregnant women are needed to provide stronger evidence for the role of aflatoxin in adverse pregnancy outcomes, and to explore biological mechanisms. Potential pathways for intervention to reduce aflatoxin exposure are urgently needed, and this might reduce the global burden of stillbirth, preterm birth, and low birthweight.

show abstract

“…Many observations link chronic aflatoxin ingestion with childhood stunting. 3 - 5 Aflatoxins are toxic growth products (mycotoxins) produced by Aspergillus species 6 , 7 , of which aflatoxin B1 (AFB1) is one of the most potent. Exposure typically occurs via ingestion of contaminated foods, with toxicity likely related to frequency and magnitude of exposure.…”

Section: Introductionmentioning

confidence: 99%

Dietary aflatoxin-induced stunting in a novel rat model: evidence for toxin-induced liver injury and hepatic growth hormone resistance

et al. 2015

View full text Add to dashboard Cite

Background Despite a strong statistical correlation between dietary aflatoxin B1 (AFB1)-exposure and childhood stunting, the causal mechanism remains speculative. This issue is important because of emerging interest in reduction of human aflatoxin exposure to diminish the prevalence and complications of stunting. Pediatric liver diseases cause growth impairment, and AFB1 is hepatotoxic. Thus, liver injury might mediate AFB1-associated growth impairment. We have developed a rat model of dietary AFB1-induced stunting to investigate these questions. Methods Newly-weaned rats were given AFB1-supplemented- or control-diets from age 3-9 weeks, and then euthanized for serum- and tissue-collection. Food intake and weight were serially assessed, with tibial-length determined at the experimental endpoint. Serum AFB1-adducts, hepatic gene and protein expression, and liver injury markers were quantified using established methodologies. Results AFB1-albumin adducts correlated with dietary toxin contamination, but such contamination did not affect food consumption. AFB1-exposed animals exhibited dose-dependent wasting and stunting, liver pathology, and suppression of hepatic targets of growth hormone (GH) signaling, but did not display increased mortality. Conclusion These data establish toxin-dependent liver injury and hepatic GH-resistance as candidate mechanisms by which AFB1-exposure causes growth impairment in this mammalian model. Interrogation of modifiers of stunting using this model could guide interventions in at-risk and affected children.

show abstract

Reducing Malnutrition: Time to Consider Potential Links Between Stunting and Mycotoxin Exposure?

Cited by 34 publications

References 23 publications

The stunting syndrome in developing countries

The stunting syndrome in developing countries

Aflatoxin Exposure During Pregnancy, Maternal Anemia, and Adverse Birth Outcomes

Dietary aflatoxin-induced stunting in a novel rat model: evidence for toxin-induced liver injury and hepatic growth hormone resistance

Contact Info

Product

Resources

About