Prevalence of food insecurity among students attending four Historically Black Colleges and Universities.

Objective: This study examined the prevalence of food insecurity (FI) among students attending Historically Black Colleges and Universities (HBCUs) in the Southeastern United States. Participants: Students attending four HBCUs (N = 351) completed an anonymous Web-based survey. Methods: Food insecurity was assessed using the 2-item Hunger Vital Sign Tool. Summary statistics were used to quantify FI experiences. Logistic regression was conducted to determine if student demographic characteristics were significantly associated with FI outcomes. Results: Nearly 3 in 4 students (72.9%) reported some level of FI in the past year. Students representing all levels of postsecondary education reported FI. Meal plan participation did not prevent FI. Conclusions: Students attending HBCUs experience FI at levels that exceed estimates reported among students attending predominantly White institutions. More work is needed to understand the lived experience of food-insecure HBCU students as a means to ensure institution-level food policies support student academic success and wellbeing.

Food insecurity among university students in the United States amidst the COVID-19 pandemic.

OBJECTIVE: This study reports on food insecurity (FI) amidst the COVID-19 pandemic. PARTICIPANTS AND METHODS: College students in four regions of the US completed the two-item validated Hunger Vital Sign™ screening tool on Qualtrics. RESULTS: FI increased significantly after March 2020 among US students (worry about food running out: 25% to 35%; food did not last: 17% to 21%) with significant regional increase in the Midwest and South. An adjusted multivariable logistic regression model indicated students that ran out of food were significantly at greater odds of experiencing hardship with paying bills (AOR: 5.59, 95% CI =3.90-8.06). CONCLUSIONS: The findings identified an increase in the prevalence of FI among college students during the pandemic. Suggestions of how to address FI are discussed.

Homocysteinylated fibrinogen forms disulfide-linked complexes with albumin.

We have shown that homocysteinemic rabbits have altered fibrinogen that forms fibrin clots with increased resistance to fibrinolysis. Homocysteine thiolactone is a metabolite of homocysteine (Hcys) that can react with amines and introduce a new sulfhydryl group into proteins. Recent evidence suggests that Hcys thiolactone-lysine adducts form in vivo. We have shown that in vitro reaction of Hcys thiolactone with human fibrinogen (Hcys-fibrinogen) alters fibrinogen function in a manner similar to that in homocysteinemic rabbits. Several naturally-occurring mutations that introduce a new cysteine into fibrinogen are associated with clinical thrombosis due to increased resistance of clots to fibrinolysis. In those cases the new cysteine mediates disulfide formation between the mutant fibrinogen and albumin. We now report that Hcys-fibrinogen similarly forms disulfides with albumin in vitro, specifically through sites in its D-domain. However, fibrin clots formed from Hcys-fibrinogen-albumin show a similarly reduced ability to support plasminogen activation and a similar resistance to fibrinolysis as clots formed from Hcys-fibrinogen. Thus, fibrinogen-albumin conjugates may result from N-homocysteinylation of fibrinogen in vivo. However, there is no evidence that conjugation to albumin further impairs fibrinogen function above the defect induced by homocysteinylation of critical lysines. Similar to the utility of glycated hemoglobin as a marker for the deleterious effects of hyperglycemia, the level of fibrinogen-albumin complexes might possibly be a clinically useful marker for the level of homocysteine-associated damage in vivo.

Pro-thrombotic and pro-oxidant effects of diet-induced hyperhomocysteinemia.

Elevated plasma homocysteine levels are associated with the risk of atherosclerosis and arterial and venous thrombosis. We have previously demonstrated that rabbits rendered hyperhomocysteinemic by parenteral administration of homocysteine develop a dysfibrinogenemia that is associated with the formation of fibrin clots that are abnormally resistant to fibrinolysis. We suggested that this acquired dysfibrinogenemia contributes to the thrombotic tendency in hyperhomocysteinemia. However, it was possible that the homocysteine-associated dysfibrinogenemia was an artifact of the parenteral administration model. Therefore, the goals of the current study were to develop a diet-induced model of homocysteinemia in rabbits and determine whether a dysfibrinogenemia and evidence of oxidative stress develop in this model as they do when homocysteine is injected. We found that rabbits fed a diet severely deficient in folate and mildly deficient in choline develop mild hyperhomocysteinemia: 14.8+/-4.0 microM in deficient rabbits compared to 9.0+/-1.7 microM in controls. The deficient rabbits also develop evidence of oxidant stress: increased lipid peroxidation in liver, impaired mitochondrial enzyme activities in liver and elevated caspase-3 levels in plasma. Most importantly, the deficient rabbits also develop a dysfibrinogenemia characterized by increased resistance to fibrinolysis. We believe that this dietary model of homocysteinemia is clinically relevant and reproduces many features associated with hyperhomocysteinemia in previous work using in vitro and in vivo models. Our findings suggest that an acquired dysfibrinogenemia could play a role in the increased risk of atherothrombotic disease in mildly hyperhomocysteinemic human subjects.

Muscadine grape products intake, diet and blood constituents of non-diabetic and type 2 diabetic subjects.

OBJECTIVE: Red wines and grape juices contain polyphenolics with antioxidant and antiplatelet properties that may be protective against oxidative stress leading to hypertension, insulin resistance, and type 2 diabetes (T2D). This study evaluated the effects of supplementing meals of subjects with 150 mL of muscadine grape juice (MJ), muscadine grape wine (MW), and dealcoholized muscadine grape wine (Dz-W) on glycemic indices, blood constituents, lipid profile, anthropometric, and nutrient intakes of healthy and T2D subjects over a 28-d period. METHODS: Subjects with T2D were assigned to take MJ, MW, or Dz-W. Non-diabetics consumed MJ and controls were given no test drinks. Several metabolic indicators associated with diabetic conditions were measured at baseline and repeated after 28 d. RESULTS: Diabetics given MW and Dz-W showed lower levels of blood glucose, insulin, and glycated hemoglobin, indicating better glycemic control. Elevated dietary vitamin C and E levels were observed in diabetics given Dz-W, indicating improved antioxidant status. Decreased red blood cell membrane saturated fatty acids and increased mono- and polyunsaturated fatty acids for subjects with T2D given MW suggested improved membrane fluidity. Lower sodium and chloride values for subjects T2D given MW suggested lower risk for developing hypertension. Improved hepatic conditions were noted by decreases in alanine aminotransferase and aspartate aminotransferase among subjects with T2D given MW, indicating better insulin sensitivity and decreased tendency toward impaired liver function. CONCLUSION: Daily intake of 150 mL of MW or Dz-W with meals improved several metabolic responses among diabetics compared with diabetics given MJ.

Modification of fibrinogen by homocysteine thiolactone increases resistance to fibrinolysis: a potential mechanism of the thrombotic tendency in hyperhomocysteinemia.

We have previously shown functional differences in fibrinogen from hyperhomocysteinemic rabbits compared to that in control rabbits. This acquired dysfibrinogenemia is characterized by fibrin clots that are composed of abnormally thin, tightly packed fibers with increased resistance to fibrinolysis. Homocysteine thiolactone is a metabolite of homocysteine (Hcys) that can react with primary amines. Recent evidence suggests that Hcys thiolactone-lysine adducts form in vivo. We now demonstrate that the reaction of Hcys thiolactone with purified fibrinogen in vitro produces fibrinogen (Hcys fibrinogen) with functional properties that are strikingly similar to those we have observed in homocysteinemic rabbits. Fibrinogen purified from homocysteinemic rabbits and Hcys fibrinogen are similar in that (1) they both form clots composed of thinner, more tightly packed fibers than their respective control rabbit and human fibrinogens; (2) the clot structure could be made to be more like the control fibrinogens by increased calcium; and (3) they both form clots that are more resistant to fibrinolysis than those formed by the control fibrinogens. Further characterization of human fibrinogens showed that Hcys fibrin had similar plasminogen binding to that of the control and an increased capacity for binding tPA. However, tPA activation of plasminogen on Hcys fibrin was slower than that of the control. Mass spectrometric analysis of Hcys fibrinogen revealed twelve lysines that were homocysteinylated. Several of these are close to tPA and plasminogen binding sites. Lysines are major binding sites for fibrinolytic enzymes and are also sites of plasmin cleavage. Thus, modification of lysines in fibrinogen could plausibly lead to impaired fibrinolysis. We hypothesize that the modification of lysine by Hcys thiolactone might occur in vivo, lead to abnormal resistance of clots to lysis, and thereby contribute to the prothrombotic state associated with homocysteinemia.

Differences in the metabolic response to exogenous homocysteine in juvenile and adult rabbits.

Homocysteine has recently received a lot of attention as an independent risk factor for atherosclerotic and thrombotic cardiovascular disease. Plasma homocysteine levels tend to rise with age, but are also greatly influenced by nutritional factors. Early reports suggested that there were differences in the metabolism of homocysteine in adult and immature animals. The current work tests the hypothesis that adult and juvenile animals respond differently to chronic administration of homocysteine. We have previously found that adult rabbits given homocysteine parenterally twice daily for seven weeks developed progressive folate deficiency and concurrently developed an impairment of homocysteine metabolism. We now report that juvenile rabbits do not develop folate deficiency with chronic homocysteine loading and do not have progressively higher trough levels of homocysteine, as do the adults. In addition, juvenile rabbits that have been chronically pre-treated with homocysteine exhibit a lower peak homocysteine level after a single dose than do juvenile rabbits that have never received homocysteine. This adaptation did not occur in the adult rabbits. In addition, adult homocysteine-treated rabbits had evidence of oxidative stress as evidenced by higher levels of malondialdehyde in liver tissue than adult controls. The homocysteine-treated juvenile rabbits had the same levels of malondialdehyde as the juvenile control rabbits. We conclude that the plasma elimination kinetics are altered in juvenile rabbits in response to homocysteine pre-treatment. The difference in metabolism of homocysteine may protect the juvenile rabbits from the damaging effects of homocysteine. Future studies are planned to elucidate the mechanism of this adaptive response.