Equity, food security and health equity in the Asia Pacific region.

What, and how much, people eat is a response to their socio-political, socio-economic, socio-environmental and socio-cultural environments. Good nutrition is central to good health. Globally, health has improved for many but not for everyone equally. That food and nutrition-related health is unequally distributed is a marker of societal failure. For some individuals, communities and even nations, it is a matter of not having enough food, of being unable to afford food and there being little nutritious food readily available. For others there is an over abundance of food but its nutritional quality is compromised, access to healthy food is poor and cost of food is high relative to other commodities. Human development and poverty reduction in the Asia Pacific region cannot be achieved without improving nutrition in an equitable way. There is no biological reason for the scale of difference in health, including diet-related health that is observed in the Asia Pacific region. That it exists is unethical and inequitable. Asymmetric economic growth, unequal improvements in daily living conditions, unequal distribution of technical developments and suppression of human rights have seen health inequities perpetuate and worsen, particularly over the last three decades. Addressing diet-related health inequities requires attention to the underlying structural drivers and inequities in conditions of daily living that disempower individuals, social groups and even nations from the pursuit of good nutrition and health. These are matters of economic and social policy at the global, regional and national level.

Role of gut microbiota in Crohn's disease.

Crohn's disease (CD), a form of inflammatory bowel disease (IBD), provides a complex model of host-microbe interactions underpinning disease pathogenesis. Although there is not widespread agreement on the etiology of CD, there is evidence that microorganisms lead to the often severe inflammatory response characteristic of the disease. Despite several microbial candidates, no specific microbe has been considered pathogenic. Instead, the concept of the 'pathogenic community' has emerged from the evidence, whereby the stability of the microbial ecosystem of the healthy human gut is disrupted in response to host genetics and destabilized immunity, perhaps through changing public health practices leading to altered microbial exposures over time. We discuss the complex microbial ecosystem of the mammalian gut, the underlying genetic factors that predispose to CD, and how these gene variants may alter host-microbe interactions and propagate inflammation. Over the next 5 years, the increased understanding of genes involved in CD and the way in which individuals with variants of these genes respond differently to nutrients and drugs will enable the rational development of personalized therapies, using pharmacogenomic and nutrigenomic approaches.