In 2020, approximately 55% of households facing food insecurity participated in one or more of the three largest federal nutrition assistance programs. Food insecurity rates have been relatively unchanged since 2019 but federal nutrition assistance programs have continued to see a decline in participation. Many families meet the income guidelines to participate in both the Supplemental Nutrition Assistance Program (SNAP) and the Special Supplemental Nutrition Assistance Program for Women, Infants and Children (WIC) programs, yet almost half of those participants are not utilizing WIC. The WIC program is an essential safety net for low-income families to combat food insecurity and improve diet quality. The purpose of this study was to examine differences in household characteristics among families participating in SNAP only and households participating in both SNAP and WIC. Additionally, we examined potential barriers and facilitators to participating in WIC among WIC-eligible SNAP participants. Hispanics made up 40% of SNAP Only households and about 65% of SNAP and WIC. Households with a larger number of beneficiaries and those with an infant in the household were more likely to participate in both SNAP and WIC. The main barriers identified by respondents previously enrolled in WIC were a lack of knowledge regarding WIC eligibility and issues with appointments. The two most common misconceptions regarding WIC eligibility were being unaware that simultaneous enrollment in both programs was allowable, and being unaware that household members were still eligible for WIC services. For the facilitators toward WIC enrollment, more than half of respondents knew to enroll in WIC when they needed nutrition or breastfeeding assistance. Results from this study suggest the need for targeted outreach campaigns that highlight the possibility and benefits of dual participation in SNAP and WIC. Understanding how SNAP can increase enrollment in WIC demonstrates to policymakers the benefits of streamlining the certification process.

The incidence of childhood obesity has become increasingly prevalent in the United States in recent years. The development of obesity at any age, but especially in adolescence, can have lasting negative effects in the form of cardiometabolic disease, increased incurred healthcare costs, and potential negative effects on quality of life. In recent years, a rising trend of obesity, in both adults and adolescents, has been observed in lower income and ethnic groups. Increased adiposity can be influenced by modifiable factors -(physical activity, caloric intake, or sleep) or by non-modifiable factors (ethnicity, genetic predispositions, and socioeconomic status). The influence of these factors can be observed in individuals of all ages, including infants. A common indicator of the development of childhood obesity is rapid weight gain (RWG) within an infant’s first year of life. The composition of the gut microbiome can act as a predictor for RWG and the development of childhood obesity. Infants are exposed to an immense microbial load when they are born and their gut microbiome is continually diversified through their method of feeding and the subsequent introduction to solid foods. While currently understudied, it is understood that cultural and socioeconomic factors influence the development of the gut microbiome, which is further explored in this analysis. The DNA from 51 fecal samples from infants ranging from 3 weeks to 12 months in age was extracted and sequenced using next-generation sequencing, and the resulting sequences were analyzed using QIIME 2. Results from alpha-diversity and beta-diversity metrics showed significant differences in the gut microbiome of infants when comparing groups based on baby race/ethnicity, household income, and mom’s education. These findings suggest the importance of sociodemographic characteristics in shaping the gut microbiome and suggest the importance of future studies including diverse populations in gut microbiome work.

Obesity increases the risk for colorectal cancer. In mice, a pro-obesity high-fat-diet (HFD) leads to an intestinal phenotype characterized by enhanced proliferation, numbers, function and tumor-initiating capacity of stem cells, the cell-of-origin for many intestinal cancers. This phenotype is driven by a lipid metabolism program facilitated by an intrinsic Peroxisome Proliferator-Activated Receptor/Fatty Acid Oxidation (PPAR/FAO) axis that senses and utilizes cellular lipids. However, the microbiome is a known regulator of lipid metabolism in the gut, but little is understood about how the gut commensals affect access to the lipids and alter stem cell function. Here, we use the long term HFD-fed mouse model to analyze the phenotypic changes in the intestinal stem cells (ISCs) after depletion of the gut microbiota. We find that the loss of the gut microbiome after four weeks of antibiotic treatment imposes significant changes in ISC function leading to reduced HFD ISC regenerative potential. These results indicate that the gut microbiome plays a crucial role in the lipid metabolic process which regulates and maintains the HFD ISC phenotype, and further suggests that the gut microbiome may augment the diet-induced tumor initiating capacity by altering the stem cell function.