Impact of CGIAR maize germplasm in Sub-Saharan Africa.

This study reports on the adoption and impacts of CGIAR-related maize varieties in 18 major maize-producing countries in sub-Saharan Africa (SSA) during 1995-2015. Of the 1345 maize varieties released during this timeframe, approximately 60% had a known CGIAR parentage. About 34% (9.5 million ha) of the total maize area in 2015 was cultivated with 'new' CGIAR-related maize varieties released between 1995 and 2015. In the same year, an additional 13% of the maize area was cultivated with 'old' CGIAR-related maize varieties released before 1995. The aggregate annual economic benefit of using new CGIAR-related maize germplasm for yield increase in SSA was estimated at US$1.1-1.6 billion in 2015, which we attributed equally to co-investments by CGIAR funders, public-sector national research and extension programs, and private sector partners. Given that the annual global investment in CGIAR maize breeding at its maximum was US$30 million, the benefit-cost ratios for the CGIAR investment and CGIAR-attributable portion of economic benefits varied from 12:1-17:1, under the assumption of a 5-year lag in the research investment to yield returns. The study also discusses the methodological challenges involved in large-scale impact assessments. Post-2015 CGIAR tropical maize breeding efforts have had a strong emphasis on stress tolerance.

Nutrition, infection and stunting: the roles of deficiencies of individual nutrients and foods, and of inflammation, as determinants of reduced linear growth of children.

The regulation of linear growth by nutritional and inflammatory influences is examined in terms of growth-plate endochondral ossification, in order to better understand stunted growth in children. Linear growth is controlled by complex genetic, physiological, and nutrient-sensitive endocrine/paracrine/autocrine mediated molecular signalling mechanisms, possibly including sleep adequacy through its influence on growth hormone secretion. Inflammation, which accompanies most infections and environmental enteric dysfunction, inhibits endochondral ossification through the action of mediators including proinflammatory cytokines, the activin A-follistatin system, glucocorticoids and fibroblast growth factor 21 (FGF21). In animal models linear growth is particularly sensitive to dietary protein as well as Zn intake, which act through insulin, insulin-like growth factor-1 (IGF-1) and its binding proteins, triiodothyronine, amino acids and Zn2+ to stimulate growth-plate protein and proteoglycan synthesis and cell cycle progression, actions which are blocked by corticosteroids and inflammatory cytokines. Observational human studies indicate stunting to be associated with nutritionally poor, mainly plant-based diets. Intervention studies provide some support for deficiencies of energy, protein, Zn and iodine and for multiple micronutrient deficiencies, at least during pregnancy. Of the animal-source foods, only milk has been specifically and repeatedly shown to exert an important influence on linear growth in both undernourished and well-nourished children. However, inflammation, caused by infections, environmental enteric dysfunction, which may be widespread in the absence of clean water, adequate sanitation and hygiene (WASH), and endogenous inflammation associated with excess adiposity, in each case contributes to stunting, and may explain why nutritional interventions are often unsuccessful. Current interventions to reduce stunting are targeting WASH as well as nutrition.