Disordered eating and eating competence in members of online irritable bowel syndrome support groups.

BACKGROUND: This study seeks to evaluate eating competence and disordered eating likelihood among members of online support groups for irritable bowel syndrome (IBS) and determine whether eating competence and disordered eating likelihood varies according to IBS symptom severity and subtype. METHODS: This cross-sectional study is based on an anonymous survey conducted from August to September 2021. Adults with IBS (N = 225) were recruited from online and social media IBS support forums. IBS symptom severity was assessed using the validated IBS Severity Scoring System (IBS-SSS), likelihood of disordered eating was assessed using the validated Eating Attitudes Test (EAT-26), and eating competence was assessed using the validated Satter Eating Competence Inventory (ecSI 2.0™). Multiple linear regression was used to predict EAT-26 total score from IBS-SSS score, age, and IBS subtype. ANOVAs were used to examine the relationships between IBS severity level, IBS subtype, and ecSI 2.0™ total score. KEY RESULTS: Eating competence among the sample was low at 17% while 27% was classified as likely or very likely disordered eating. IBS severity was positively associated with EAT-26 score (p = 0.011) and ecSI 2.0™ score was significantly lower in the severe IBS group compared to the moderate IBS group (p = 0.016). No relationship was detected between IBS subtype and EAT-26 or ecSI 2.0™ scores. CONCLUSIONS & INFERENCES: IBS severity was positively associated with disordered eating likelihood and negatively associated with eating competence. This sheds light on the importance of assessing eating competence and screening for disordered eating prior to selecting therapies for patients with IBS, particularly in females with severe symptoms.

Food security and food access during the COVID-19 pandemic: Impacts, adaptations, and looking ahead.

The coronavirus disease 2019 (COVID-19) pandemic continues to alter US household food consumption and food spending. Although terminology used to describe food insecurity has varied during the COVID-19 pandemic, many reliable estimates illustrate a dramatic increase in food insecurity from approximately 10% of US households before the pandemic to 25%-30% of households during the pandemic, with an even higher prevalence reported by more vulnerable and socially disadvantaged populations. To address the increase in food and economic insecurity, food and nutrition assistance policies and programs made innovative and temporary changes, and enrollment in these programs generally increased. However, some changes to food, nutrition, and income assistance programs are now expiring or contracting even as food insecurity prevalence is again on the rise and elevated food and nutrition assistance needs are expected to persist based on historical patterns. American Society for Parenteral and Enteral Nutrition (ASPEN) practitioners can play an important role in identifying clients at elevated risk of food insecurity-related acute and chronic conditions and connecting high-risk clients to resources. ASPEN practitioners can contribute to the evidence base linking food insecurity and nutrition outcomes. ASPEN practitioners can also advocate for addressing the root social and structural determinants of food insecurity and for the continuation of effective food and nutrition policy changes and innovations.

Associations of diet quality and blood serum lipoprotein levels in a population at high risk for diabetes: the Strong Heart Family Study.

BACKGROUND/OBJECTIVES: Previous studies consistently report that diet quality is inversely associated with risk of cardiovascular disease (CVD) and type 2 diabetes. However, few studies have assessed the association of diet quality with serum lipoproteins, an intermediate marker of cardio-metabolic health, or assessed whether type 2 diabetes modifies these associations. This study assessed associations of diet quality (evaluated using the Alternative Healthy Eating Index (AHEI)), and the interaction of diet quality with diabetes, on total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL-C), high-density lipoprotein (HDL-C), apolipoprotein A (apoA1), and apolipoprotein B (apoB) among American Indians (AIs). SUBJECTS/METHODS: Participants comprised AIs who participated in the Strong Heart Family Study (SHFS)-a study of CVD and its risk factors in 12 AI communities. Generalized estimated equations (GEEs) were used to examine the following associations: (1) the cross-sectional associations of diet quality (as determined by AHEI) with serum lipoproteins (n = 2200); and (2) the prospective associations of the AHEI measured at baseline with serum lipoproteins (n = 1899). RESULTS: In cross-sectional analyses, associations of AHEI with TC (p < 0.0001) LDL-C (p = 0.005), and ApoB (p = 0.002) differed according to diabetes status. In prospective analysis, AHEI was associated with more favorable levels of TC (p = 0.029) and LDL-C (p = 0.008) among participants with diabetes independent of other demographic, behavioral, and health factors; associations of diet quality with TC, LDL-C, and ApoB were much weaker among participants without diabetes. There was no association of diet quality with TG, HDL-C, or ApoA. CONCLUSIONS: The associations of diet quality with TC, LDL-C, and ApoB differ according to diabetes status.

Integrating public health students into interprofessional education.

Recognizing the public health professional are critical members of interprofessional teams, the Council on Education for Public Health (CEPH) recently added a required Masters of Public Health (MPH) student competency focused on interprofessional education (IPE). A student-centered approach to the design and evaluation of an emergency preparedness-focused curricular program to meet the interprofessional needs of MPH students was used to meet this expectation at the University of Washington. Curriculum design was informed by two 80-minute listening sessions with MPH students to better understand their current interprofessional educational experiences and needs, and how an emergency preparedness-focused two-hour Interprofessional Active Learning Series (iPALS) session could help them develop interprofessional competency. The resultant iPALS session was assessed with a short, paper-based questionnaire. We found MPH students have an interest in participating in IPE, and that all students who participated in the emergency preparedness-focused iPALS session reported significant increases in their interprofessional and disaster response abilities based on their pre- and post-session evaluations. Student-centered IPE curriculum focused on emergency preparedness can enhance the self-reported ability of students across the health sciences to perform on interprofessional teams while engaging in a topic that has relevance to MPH students.

Spot Urine Sodium-to-Potassium Ratio Is a Predictor of Stroke.

Background and Purpose- Dietary sodium reduction with concurrent increase in potassium intake is a current public health priority to reduce risk of cardiovascular events. This study explored associations between the spot urine sodium-to-potassium ratio and cardiovascular events in the MESA (Multi-Ethnic Study of Atherosclerosis) longitudinal cohort. Methods- The MESA is a prospective cohort study of 6814 adults from 4 ethnic groups (European-, Asian-, African- and Hispanic-American) with a mean age of 62 (±10.2) years and an average of 11.7 (±2.2) years of follow-up. Participants were free of clinical cardiovascular disease at baseline. Spot urine sodium and potassium excretion, as a marker of dietary intake, was collected at baseline. The impact of urinary sodium-to-potassium ratio on adjudicated cardiovascular events was assessed using Cox proportional hazards models. Results- Only 39% of MESA participants had a urinary sodium-to-potassium ratio ≤1, and these participants experienced only 74 of the 236 strokes. A sodium-to-potassium ratio >1 was associated with a hazard ratio of 1.47 (95% CI,1.07-2.00) for risk of stroke, adjusting for age, sex, race, cardiovascular risk factors, socio-demographic characteristics, body size, and kidney function. Conclusions- The spot urine sodium-to-potassium ratio (measurable in routine care) is associated with stroke. A urine sodium-to-potassium ratio of ≤1, may be related to a clinically relevant reduction in stroke risk and is a feasible target for health interventions.

The apolipoprotein-AI mimetic peptide L4F at a modest dose does not attenuate weight gain, inflammation, or atherosclerosis in LDLR-null mice.

OBJECTIVE: High density lipoprotein (HDL) cholesterol levels are inversely related to cardiovascular disease risk and associated with a reduced risk of type 2 diabetes. Apolipoprotein A-I (apoA-I; major HDL protein) mimetics have been reported to reduce atherosclerosis and decrease adiposity. This study investigated the effect of L4F mimetic peptide and apoA-I overexpression on weight gain, insulin resistance, and atherosclerosis in an LDL receptor deficient (Ldlr-/-) model fed a high fat high sucrose with cholesterol (HFHSC) diet. METHODS: Studies in differentiated 3T3-L1 adipocytes tested whether L4F could inhibit palmitate-induced adipocyte inflammation. In vivo studies used male Ldlr-/- mice fed a HFHSC diet for 12 weeks and were injected daily with L4F (100 µg/mouse) subcutaneously during the last 8 weeks. Wild-type and apoA-I overexpressing Ldlr-/- mice were fed HFHSC diet for 16 weeks. RESULTS: Neither L4F administration nor apoA-I overexpression affected weight gain, total plasma cholesterol or triglycerides in our studies. While pre-treatment of 3T3-L1 adipocytes with either L4F or HDL abolished palmitate-induced cytokine expression in vitro, L4F treatment did not affect circulating or adipose tissue inflammatory markers in vivo. Neither L4F administration nor apoA-I overexpression affected glucose tolerance. ApoA-I overexpression significantly reduced atherosclerotic lesion size, yet L4F treatment did not affect atherosclerosis. CONCLUSION: Our results suggest that neither L4F (100 µg/day/mouse) nor apoA-I overexpression affects adiposity or insulin resistance in this model. We also were unable to confirm a reduction in atherosclerosis with L4F in our particular model. Further studies on the effect of apoA-I mimetics on atherosclerosis and insulin resistance in a variety of dietary contexts are warranted.

Macrophage metalloelastase (MMP12) regulates adipose tissue expansion, insulin sensitivity, and expression of inducible nitric oxide synthase.

Macrophage metalloelastase, a matrix metallopeptidase (MMP12) predominantly expressed by mature tissue macrophages, is implicated in pathological processes. However, physiological functions for MMP12 have not been described. Because mRNA levels for the enzyme increase markedly in adipose tissue of obese mice, we investigated the role of MMP12 in adipose tissue expansion and insulin resistance. In humans, MMP12 expression correlated positively and significantly with insulin resistance, TNF-α expression, and the number of CD14(+)CD206(+) macrophages in adipose tissue. MMP12 was the most abundant matrix metallopeptidase detected by proteomic analysis of conditioned medium of M2 macrophages and dendritic cells. In contrast, it was detected only at low levels in bone marrow derived macrophages and M1 macrophages. When mice received a high-fat diet, adipose tissue mass increased and CD11b(+)F4/80(+)CD11c(-) macrophages accumulated to a greater extent in MMP12-deficient (Mmp12(-/-)) mice than in wild-type mice (Mmp12(+/+)). Despite being markedly more obese, fat-fed Mmp12(-/-) mice were more insulin sensitive than fat-fed Mmp12(+/+) mice. Expression of inducible nitric oxide synthase (Nos2) by Mmp12(-/-) macrophages was significantly impaired both in vivo and in vitro, suggesting that MMP12 might mediate nitric oxide production during inflammation. We propose that MMP12 acts as a double-edged sword by promoting insulin resistance while combatting adipose tissue expansion.

T cell activation inhibitors reduce CD8+ T cell and pro-inflammatory macrophage accumulation in adipose tissue of obese mice.

Adipose tissue inflammation and specifically, pro-inflammatory macrophages are believed to contribute to insulin resistance (IR) in obesity in humans and animal models. Recent studies have invoked T cells in the recruitment of pro-inflammatory macrophages and the development of IR. To test the role of the T cell response in adipose tissue of mice fed an obesogenic diet, we used two agents (CTLA-4 Ig and anti-CD40L antibody) that block co-stimulation, which is essential for full T cell activation. C57BL/6 mice were fed an obesogenic diet for 16 weeks, and concomitantly either treated with CTLA-4 Ig, anti-CD40L antibody or an IgG control (300 µg/week). The treatments altered the immune cell composition of adipose tissue in obese mice. Treated mice demonstrated a marked reduction in pro-inflammatory adipose tissue macrophages and activated CD8+ T cells. Mice treated with anti-CD40L exhibited reduced weight gain, which was accompanied by a trend toward improved IR. CTLA-4 Ig treatment, however, was not associated with improved IR. These data suggest that the presence of pro-inflammatory T cells and macrophages can be altered with co-stimulatory inhibitors, but may not be a significant contributor to the whole body IR phenotype.

Apolipoprotein AI and high-density lipoprotein have anti-inflammatory effects on adipocytes via cholesterol transporters: ATP-binding cassette A-1, ATP-binding cassette G-1, and scavenger receptor B-1.

RATIONALE: Macrophage accumulation in adipose tissue associates with insulin resistance and increased cardiovascular disease risk. We previously have shown that generation of reactive oxygen species and monocyte chemotactic factors after exposure of adipocytes to saturated fatty acids, such as palmitate, occurs via translocation of NADPH oxidase 4 into lipid rafts (LRs). The anti-inflammatory effects of apolipoprotein AI (apoAI) and high-density lipoprotein (HDL) on macrophages and endothelial cells seem to occur via cholesterol depletion of LRs. However, little is known concerning anti-inflammatory effects of HDL and apoAI on adipocytes. OBJECTIVE: To determine whether apoAI and HDL inhibit inflammation in adipocytes and adipose tissue, and whether this is dependent on LRs. METHODS AND RESULTS: In 3T3L-1 adipocytes, apoAI, HDL, and methyl-ß-cyclodextrin inhibited chemotactic factor expression. ApoAI and HDL also disrupted LRs, reduced plasma membrane cholesterol content, inhibited NADPH oxidase 4 translocation into LRs, and reduced palmitate-induced reactive oxygen species generation and monocyte chemotactic factor expression. Silencing ATP-binding cassette A-1 abrogated the effect of apoAI, but not HDL, whereas silencing ATP-binding cassette G-1 or scavenger receptor B-1 abrogated the effect of HDL but not apoAI. In vivo, apoAI transgenic mice fed a high-fat, high-sucrose, cholesterol-containing diet showed reduced chemotactic factor and proinflammatory cytokine expression and reduced macrophage accumulation in adipose tissue. CONCLUSIONS: ApoAI and HDL have anti-inflammatory effects in adipocytes and adipose tissue similar to their effects in other cell types. These effects are consistent with disruption and removal of cholesterol from LRs, which are regulated by cholesterol transporters, such as ATP-binding cassette A-1, ATP-binding cassette G-1, and scavenger receptor B-1.

Novel insights into the role of S100A8/A9 in skin biology.

S100A8 and S100A9 belong to the damage-associated molecular pattern molecules. They are upregulated in a number of inflammatory skin disorders. Owing to their abundance in myeloid cells, the main function of S100A8/A9 has been attributed to their role in inflammatory cells. However, it is becoming increasingly clear that they also exert important roles in epithelial cells. In this review, we discuss the context-dependent function of S100A8/A9 in epithelial cells and their impact on wound healing, psoriasis and other skin diseases.

Unique proteomic signatures distinguish macrophages and dendritic cells.

Monocytes differentiate into heterogeneous populations of tissue macrophages and dendritic cells (DCs) that regulate inflammation and immunity. Identifying specific populations of myeloid cells in vivo is problematic, however, because only a limited number of proteins have been used to assign cellular phenotype. Using mass spectrometry and bone marrow-derived cells, we provided a global view of the proteomes of M-CSF-derived macrophages, classically and alternatively activated macrophages, and GM-CSF-derived DCs. Remarkably, the expression levels of half the plasma membrane proteins differed significantly in the various populations of cells derived in vitro. Moreover, the membrane proteomes of macrophages and DCs were more distinct than those of classically and alternatively activated macrophages. Hierarchical cluster and dual statistical analyses demonstrated that each cell type exhibited a robust proteomic signature that was unique. To interrogate the phenotype of myeloid cells in vivo, we subjected elicited peritoneal macrophages harvested from wild-type and GM-CSF-deficient mice to mass spectrometric and functional analysis. Unexpectedly, we found that peritoneal macrophages exhibited many features of the DCs generated in vitro. These findings demonstrate that global analysis of the membrane proteome can help define immune cell phenotypes in vivo.

Diabetes promotes an inflammatory macrophage phenotype and atherosclerosis through acyl-CoA synthetase 1.

The mechanisms that promote an inflammatory environment and accelerated atherosclerosis in diabetes are poorly understood. We show that macrophages isolated from two different mouse models of type 1 diabetes exhibit an inflammatory phenotype. This inflammatory phenotype associates with increased expression of long-chain acyl-CoA synthetase 1 (ACSL1), an enzyme that catalyzes the thioesterification of fatty acids. Monocytes from humans and mice with type 1 diabetes also exhibit increased ACSL1. Furthermore, myeloid-selective deletion of ACSL1 protects monocytes and macrophages from the inflammatory effects of diabetes. Strikingly, myeloid-selective deletion of ACSL1 also prevents accelerated atherosclerosis in diabetic mice without affecting lesions in nondiabetic mice. Our observations indicate that ACSL1 plays a critical role by promoting the inflammatory phenotype of macrophages associated with type 1 diabetes; they also raise the possibilities that diabetic atherosclerosis has an etiology that is, at least in part, distinct from the etiology of nondiabetic vascular disease and that this difference is because of increased monocyte and macrophage ACSL1 expression.

S100A8 and S100A9 in cardiovascular biology and disease.

There is recent and widespread interest in the damage-associated molecular pattern molecules S100A8 and S100A9 in cardiovascular science. These proteins have a number of interesting features and functions. For example, S100A8 and S100A9 (S100A8/A9) have both intracellular and extracellular actions, they are abundantly expressed in inflammatory and autoimmune states, primarily by myeloid cells but also by other vascular cells, and they modulate inflammatory processes, in part through Toll-like receptor 4 and the receptor for advanced glycation end products. S100A8/A9 also have anti-inflammatory and immune regulatory actions. Furthermore, increased plasma levels of S100A8/A9 predict cardiovascular events in humans, and deletion of these proteins partly protects Apoe(-)(/)(-) mice from atherosclerosis. Understanding the roles of S100A8 and S100A9 in vascular cell types and the mechanisms whereby these proteins mediate their biological effects may offer new therapeutic strategies to prevent, treat, and predict cardiovascular diseases.

S100A9 differentially modifies phenotypic states of neutrophils, macrophages, and dendritic cells: implications for atherosclerosis and adipose tissue inflammation.

BACKGROUND: S100A9 is constitutively expressed in neutrophils, dendritic cells, and monocytes; is associated with acute and chronic inflammatory conditions; and is implicated in obesity and cardiovascular disease in humans. Most of the constitutively secreted S100A9 is derived from myeloid cells. A recent report demonstrated that mice deficient in S100A9 exhibit reduced atherosclerosis compared with controls and suggested that this effect was due in large part to loss of S100A9 in bone marrow-derived cells. METHODS AND RESULTS: To directly investigate the role of bone marrow-derived S100A9 in atherosclerosis and insulin resistance in mice, low-density lipoprotein receptor-deficient, S100A9-deficient bone marrow chimeras were generated. Neither atherosclerosis nor insulin resistance was reduced in S100A9-deficient chimeras fed a diet rich in fat and carbohydrates. To investigate the reason for this lack of effect, myeloid cells were isolated from the peritoneal cavity or bone marrow. S100A9-deficient neutrophils exhibited a reduced secretion of cytokines in response to toll-like receptor-4 stimulation. In striking contrast, S100A9-deficient dendritic cells showed an exacerbated release of cytokines after toll-like receptor stimulation. Macrophages rapidly lost S100A9 expression during maturation; hence, S100A9 deficiency did not affect the inflammatory status of macrophages. CONCLUSIONS: S100A9 differentially modifies phenotypic states of neutrophils, macrophages, and dendritic cells. The effect of S100A9 deficiency on atherosclerosis and other inflammatory diseases is therefore predicted to depend on the relative contribution of these cell types at different stages of disease progression. Furthermore, S100A9 expression in nonmyeloid cells is likely to contribute to atherosclerosis.

Lipids versus glucose in inflammation and the pathogenesis of macrovascular disease in diabetes.

Type 1 and type 2 diabetes both accelerate cardiovascular disease, yet the triggers are likely different for the two types of diabetes. Results from large-scale clinical trials suggest that intense blood glucose control can reduce cardiovascular events many years later in patients with type 1 diabetes. In type 2 diabetes, mechanisms related to insulin resistance and obesity may be more prominent in promoting atherosclerosis. In this article, we discuss the potential effects of hyperglycemia and diabetes-induced lipid abnormalities on atherosclerosis, particularly focusing on advanced stages of atherosclerosis and evidence from mouse models. In addition, we discuss new research findings in monocyte/macrophage biology that may present intriguing new areas of research related to diabetes and atherosclerosis.

Neither antioxidants nor genistein inhibit the progression of established atherosclerotic lesions in older apoE deficient mice.

Supplements and diets enriched in antioxidants and soy isoflavones are purported to reduce cardiovascular disease risk. Many experimental studies have demonstrated inhibitory effects of antioxidants and soy isoflavones on the development of fatty streaks in animal models. However, it is still unknown whether antioxidants and isoflavones have comparable inhibitory effects on the progression of advanced stages of atherosclerosis. This is an important question because clinical trials in humans have not supported a cardio-protective role for antioxidants or isoflavones. Thus, we examined the effects of antioxidants and genistein on the progression and composition of established, advanced atherosclerotic lesions in the innominate arteries (IA) of older apolipoprotein E-deficient (apoE(-/-)) mice. Thirty-week-old male apoE(-/-) mice were fed chow with or without genistein (0.27%, w/w) for 6, 12 and 24 weeks. Twenty-week-old male apoE(-/-) mice were fed chow with or without a cocktail of antioxidants (vitamin E 0.2%, w/w; vitamin C 0.05%, w/w; and beta carotene 0.5%, w/w) for 10, 16, and 22 weeks. There were no significant differences in total plasma cholesterol, body weight, average lesion or medial area, or changes in lesion composition with either treatment in comparison to control mice.

Progression and disruption of advanced atherosclerotic plaques in murine models.

The innominate artery is a predilection site for atherosclerotic lesion formation in hyperlipidemic mice. The lesions at this site in chow-fed apo E-/- mice progress from fatty streaks through stages that include atheroma with large necrotic areas, fibro-fatty nodules containing chondrocyte-like cells and highly calcified, acellular plaques. The advanced lesions in the innominate arteries of the apo E-/- mice exhibit a reproducible frequency of intra-plaque hemorrhage that occurs primarily as a result of fissures through lateral fatty streaks that form adjacent to or on top of the established plaques. However, this plaque disruption is not equivalent to plaque rupture in human lesions where there is rupture of well formed fibrous caps. The plaque disruption in the lesions of the chow-fed apo E-/- mice also do not lead to formation of occlusive thrombi, the predominant marker of plaque rupture in humans. Thus, although the lesions in the innominate arteries of hyperlipidemic mice progress to very advanced stages of the disease, they are not, in our opinion a model in which to study the mechanisms of plaque rupture in humans. The advanced lesions in the innominate arteries of the apo E-/- mice may however be adequate models for studying vascular fibrosis and calcification.