Few school-age youth consume the recommended amounts of fruits and vegetables, and increasing fruit and vegetable intake in children and adolescents is an important public health goal to maintain long-term good health and to decrease risk of chronic disease and obesity. School salad bars are an important tool to promote fruit and vegetable consumption among schoolchildren. Studies show that introduction of school salad bars increases the amount and variety of fruits and vegetables consumed by children in schools. However, many schools cannot afford the capital investment in the salad bar equipment. In 2010, the National Fruit & Vegetable Alliance (NFVA), United Fresh Produce Association Foundation, the Food Family Farming Foundation, and Whole Foods Market launched Let’s Move Salad Bars to Schools (LMSB2S) in support of First Lady Michelle Obama’s Let’s Move! initiative. The goal of LMSB2S is to place 6000 salad bars in schools over 3 years. As of June, 2012, over 1400 new salad bar units have been delivered to schools across the United States, increasing access to fruits and vegetables for over 700,000 students. Any K through 12 school district participating in the National School Lunch Program is eligible to submit an application at www.saladbars2schools. org/. Requests for salad bar units ($2625 each unit) are fulfilled through grassroots fund raising in the school community and through funds raised by the LMSB2S partners from corporate and foundation sources. LMSB2S is a model for coalition-building across many government, nonprofit, and industry partners to address a major public health challenge.

No abstract

majority of drugs are broken down by a surprisingly small number of metabolic pathways via microsomal enzymes localized mainly in the liver and small intestine. But differentiating between the contribution of genetic and environmental factors to drug response was a painstaking task: "The field was slow in taking off," says Motulsky, "because of the difficulty of identifying 'clean' single-gene determined drug reactions." In effect, drug metabolism was sufficiently redundant-and the impact of epigenetic factors sufficiently large-to mask the effect of many single enzyme variants and their recognition by classic studies of Mendelian (monogenic) inheritance.In an age when people in developed societies expect individual treatment in all spheres of life, the provision of drugs often appears clumsy. Medicine today is geared around taking statistical information about the general population and then applying it to the individual: Physicians are forced to make empirical decisions about types of treatment and drug dosage based on information that has been gathered on the basis of population averages, rather than individual profiles. Drug developers have advanced chemical and biological production methods that can provide an exquisite variety of compounds, but they devote little effort to differentiating groups of patients who respond in different ways to their products. Little surprise then, that "consumers" flock to "alternative therapies" that, if nothing else, claim to deliver attention to individual needs and desires.With recent advances in molecular genetics, drug makers now have at their fingertips methods for unraveling human diversity and the complex mechanisms that lie behind variations in drug response. A new field of "pharmacogenomics" is emerging that will impact the way in which drugs are discovered, developed, and prescribed. In this first article, I focus on the molecular mechanisms underpinning drug metabolism and efficacy and the genetic approaches being used to uncover them. In the next article (p. 6), I discuss some of the ways in which drug makers may apply these methods to reduce clinical development times and costs, reveal new indications for existing drugs, and ultimately pave the way for a new generation of personalized medicines. Slow beginnings in pharmacogeneticsPharmacogenomics has its roots in pharmacogenetics, a field dating back to the 1950s that studies the linkage of genetic differences (polymorphisms) in drug metabolism with the safety and efficacy of a therapeutic. Two seminal papers in 1957-one by Arno Motulsky 1 at the University of Washington, Seattle, the other by Werner Kalow 2 and colleagues at the University of Toronto-first suggested that adverse drug responses could be caused by otherwise innocuous genetic differences in enzyme activity between individuals. Following on from these studies, investigators learned that the vast One way around the problem of distinguishing the hereditary and environmental components of variability in drug response was to study identical and dizygoti...

No abstract

No abstract