Many opportunities exist to reduce enteric methane (CH4) and other greenhouse gas (GHG) emissions per unit of product from ruminant livestock. Research over the past century in genetics, animal health, microbiology, nutrition, and physiology has led to improvements in dairy production where intensively managed farms have GHG emissions as low as 1 kg of CO2 equivalents (CO2e)/kg of energy-corrected milk (ECM), compared with >7 kg of CO2 e/kg of ECM in extensive systems. The objectives of this review are to evaluate options that have been demonstrated to mitigate enteric CH4 emissions per unit of ECM (CH4/ECM) from dairy cattle on a quantitative basis and in a sustained manner and to integrate approaches in genetics, feeding and nutrition, physiology, and health to emphasize why herd productivity, not individual animal productivity, is important to environmental sustainability. A nutrition model based on carbohydrate digestion was used to evaluate the effect of feeding and nutrition strategies on CH4/ECM, and a meta-analysis was conducted to quantify the effects of lipid supplementation on CH4/ECM. A second model combining herd structure dynamics and production level was used to estimate the effect of genetic and management strategies that increase milk yield and reduce culling on CH4/ECM. Some of these approaches discussed require further research, but many could be implemented now. Past efforts in CH4 mitigation have largely focused on identifying and evaluating CH4 mitigation approaches based on nutrition, feeding, and modifications of rumen function. Nutrition and feeding approaches may be able to reduce CH4/ECM by 2.5 to 15%, whereas rumen modifiers have had very little success in terms of sustained CH4 reductions without compromising milk production. More significant reductions of 15 to 30% CH4/ECM can be achieved by combinations of genetic and management approaches, including improvements in heat abatement, disease and fertility management, performance-enhancing technologies, and facility design to increase feed efficiency and life-time productivity of individual animals and herds. Many of the approaches discussed are only partially additive, and all approaches to reducing enteric CH4 emissions should consider the economic impacts on farm profitability and the relationships between enteric CH4 and other GHG.

Retinal neovascularization is the major cause of untreatable blindness. The role of growth hormone (GH) in ischemia-associated retinal neovascularization was studied in transgenic mice expressing a GH antagonist gene and in normal mice given an inhibitor of GH secretion (MK678). Retinal neovascularization was inhibited in these mice in inverse proportion to serum levels of GH and a downstream effector, insulin-like growth factor-I (IGF-I). Inhibition was reversed with exogenous IGF-I administration. GH inhibition did not diminish hypoxia-stimulated retinal vascular endothelial growth factor (VEGF) or VEGF receptor expression. These data suggest that systemic inhibition of GH or IGF-I, or both, may have therapeutic potential in preventing some forms of retinopathy.