Food Insecurity,Neighborhood Food Access,and Food Assistance in Philadelphia

An estimated 17.6 million American households were food insecure in 2012, meaning they were unable to obtain enough food for an active and healthy life. Programs to augment local access to healthy foods are increasingly widespread, with unclear effects on food security. At the same time, the US government has recently enacted major cuts to federal food assistance programs. In this study, we examined the association between food insecurity (skipping or reducing meal size because of budget), neighborhood food access (self-reported access to fruits and vegetables and quality of grocery stores), and receipt of food assistance using the 2008, 2010, and 2012 waves of the Southeastern Pennsylvania Household Health Survey. Of 11,599 respondents, 16.7 % reported food insecurity; 79.4 % of the food insecure found it easy or very easy to find fruits and vegetables, and 60.6 % reported excellent or good quality neighborhood grocery stores. In our regression models adjusting for individual- and neighborhood-level covariates, compared to those who reported very difficult access to fruits and vegetables, those who reported difficult, easy or very easy access were less likely to report food insecurity (OR 0.62: 95 % CI 0.43–0.90, 0.33: 95 % CI 0.23–0.47, and 0.28: 95 % CI 0.20–0.40). Compared to those who reported poor stores, those who reported fair, good, and excellent quality stores were also less likely to report food insecurity (OR 0.81: 95 % CI 0.60–1.08, 0.58: 95 % CI 0.43–0.78, and 0.43: 95 % CI 0.31–0.59). Compared to individuals not receiving food assistance, those receiving Supplemental Nutrition Assistance Program (SNAP) benefits were significantly more likely to be food insecure (OR 1.36: 95 % CI 1.11–1.67), while those receiving benefits from the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) (OR 1.17: 95 % CI 0.77–1.78) and those receiving both SNAP and WIC (OR 0.84: 95 % CI 0.61–1.17) did not have significantly different odds of food insecurity. In conclusion, better neighborhood food access is associated with lower risk of food insecurity. However, most food insecure individuals reported good access. Improving diet in communities with high rates of food insecurity likely requires not only improved access but also greater affordability.     

时尚饮食一族大聚会专家过来插插嘴

“我最爱吃炸薯条了,虽然身体渐渐发胖,但是还是不能抑制自己啊！” “我是爱喝茶的,怎么也离不开它,我还很讲究呢,非新茶不喝。” “呵呵,我爱喝咖啡,所以希望大家都喝咖啡。” “烧烤多棒啊,大家一起吧。” “我身体不好,要天天吃保健品,不吃不行呀。” “我们就是时尚饮食一族,我们有我们的饮食主义。” “这人谁呀?” “说是专家。” “听他说什么。”……     

Food reinforcement

The reinforcing value of food, measured by how hard someone is willing to work to obtain food, is influenced by food palatability, food deprivation and food variety, and may be a more powerful determinant of food intake than hedonics or liking. The reinforcing value of food is mediated in part by dopaminergic activity. Genotypes that influence dopamine transport and the density of dopamine D2 receptors interact with food reinforcement to influence eating behavior, and D2 receptor genotypes may influence food reinforcement and weight gain after smoking cessation. Inhibition of dopamine transport increases brain dopamine concentrations, which may influence weight gain after smoking cessation and can reduce energy intake in obese adults.     

Food allergy

Food allergies' following food incompatibilities, which are not caused immunologically. Mostly allergic symptoms are caused by cow's milk or chicken eggs. Allergic reactions are preceded by sensitizing events; certain characteristics of foodstuffs and conditions in the human body facilitate their development. Gastrointestinal symptoms very often are just accompanying signs. In differential diagnosis the so-called "pseudo-allergies' following food ingestion have to be separated. Most important diagnostic measures are clinical history, prick-/scratch test, RAST, gastrointestinal provocation and abstinence test. The therapeutic program consists of allergen abstinence, avoiding all allergy-arousing factors, oral desensitizing and pharmaceutical treatment.     

Food mutagens

Several lines of evidence indicate that diet and dietary behaviors can contribute to human cancer risk. One way that this occurs is through the ingestion of food mutagens. Sporadic cancers result from a gene-environment interactions where the environment includes endogenous and exogenous exposures. In this article, we define environment as dietary exposures in the context of gene-environment interactions. Food mutagens cause different types of DNA damage: nucleotide alterations and gross chromosomal aberrations. Most mutagens begin their action at the DNA level by forming carcinogen-DNA adducts, which result from the covalent binding of a carcinogen or part of a carcinogen to a nucleotide. However the effect of food mutagens in carcinogenesis can be modified by heritable traits, namely, low-penetrant genes that affect mutagen exposure of DNA through metabolic activation and detoxification or cellular responses to DNA damage through DNA repair mechanisms or cell death. There are some clearly identified (e.g., aflatoxin) and suspected (e.g., N-nitrosamines, polycyclic aromatic hydrocarbons or heterocyclic amines) food mutagens. The target organs for these agents are numerous, but there is target-organ specificity for each. Mutagenesis however is not the only pathway that links dietary exposures and cancers. There is growing evidence that epigenetic factors, including changes in the DNA methylation pattern, are causing cancer and can be modified by dietary components. Also DNA damage may be indirect by triggering oxidative DNA damage. When considering the human diet, it should be recognized that foods contain both mutagens and components that decrease cancer risk such as antioxidants. Thus nutritionally related cancers ultimately develop from an imbalance of carcinogenesis and anticarcinogenesis. The best way to assess nutritional risks is through biomarkers, but there is no single biomarker that has been sufficiently validated. Although panels of biomarkers would be the most appropriate, their use as a reflection of target-organ risk remains to be determined. Also even when new biomarkers are developed, their application in target organs is problematic because tissues are not readily available. For now most biomarkers are used in surrogate tissues (e.g., blood, urine, oral cavity cells) that presumably reflect biological effects in target organs. This article reviews the role of food mutagens in mutagenesis and carcinogenesis and how their effects are modified by heritable traits and discusses how to identify and evaluate the effects of food mutagens.