Behavioural strategies to reduce obesity among lower socio-economic adults living in high-income countries: a Grades of Recommendation, Assessment, Development and Evaluation-assessed systematic review and meta-analysis of randomised controlled trials.

Adult obesity disproportionately affects lower socio-economic groups in high-income countries and perpetuates health inequalities, imposing health and socio-economic burden. This review evaluates the effectiveness of behavioural strategies in reducing weight and cardiovascular disease (CVD) risks among low-income groups based in high-income countries. We searched major databases for randomised controlled trials published between 1 November 2011 and 1 May 2023. Meta-analyses and subgroup analyses were undertaken to analyse the pooled and individual effects of behavioural strategies. Cochrane Risk of bias (RoB 2·0) tool and Grades of Recommendation, Assessment, Development and Evaluation (GRADE) criteria were used to assess the quality and certainty of evidence. Fourteen trials (3618 adults, aged 40·2 ± 9·7 years with BMI 33·6 ± 2·8 kg/m2) and nine unique interventions were identified. Three trials with high RoB were omitted. Meta-analysis favoured interventions, demonstrating significant reductions in body weight (MD: -1·56 kg, (95 % CI -2·09, -1·03)) and HbA1c (MD: -0·05 %, (95 % CI - 0·10, -0·001)) at intervention end. Sub-group analysis showed no differences in waist circumference, blood pressure or serum lipids. Financial incentives and interactive feedback produced greatest amounts of weight losses ≥ 2 kg (GRADE: moderate). Behavioural strategies are effective weight loss interventions among lower socio-economic groups living in high-income nations. However, the impact on CVD risk remains unclear.

Macronutrient and micronutrient requirements and therapeutic effects in critically ill patients with SARS-CoV-2: A narrative review.

BACKGROUND: COVID-19 can lead to critical illness and induce hypermetabolism, protein catabolism, and inflammation. These pathological processes may alter energy and protein requirements, and certain micronutrients may attenuate the associated detriments. This narrative review summarizes the macronutrient and micronutrient requirements and therapeutic effects in critically ill patients with SARS-CoV-2. METHODS: We searched four databases for randomized controlled trials (RCTs) and studies that measured macronutrient and micronutrient requirements, published from February 2020 to September 2022. RESULTS: Ten articles reported on energy and protein requirements, and five articles reported the therapeutic effects of ω-3 (n = 1), group B vitamins (n = 1), and vitamin C (n = 3). Patients' resting energy expenditure gradually increased with time, measuring approximately 20 kcal/kg body weight (BW), 25 kcal/kg BW, and 30 kcal/kg BW for the first, second, and third week onwards, respectively. Patients remained in negative nitrogen balances in the first week, and a protein intake of ≥1.5 g/kg BW may be necessary to achieve nitrogen equilibrium. Preliminary evidence suggests that ω-3 fatty acids may protect against renal and respiratory impairments. The therapeutic effects of group B vitamins and vitamin C cannot be ascertained, although intravenous vitamin C appears promising in reducing mortality and inflammation. CONCLUSION: There are no RCTs to guide the optimal dose of energy and protein in critically ill patients with SARS-CoV-2. Additional larger-scale, well-designed RCTs are needed to elucidate the therapeutic effects of ω-3, group B vitamins, and vitamin C.

An analysis of nonnutritive calories from propofol, dextrose, and citrate among patients who are critically ill that are receiving continuous renal replacement therapy.

BACKGROUND: Propofol, dextrose, and citrate infusions are necessary treatment modalities in the intensive care units (ICUs). They are, however, a potential source of nonnutritive calories (NNCs), which may cause overfeeding and adverse complications. The literature surrounding the role of NNCs is limited. We aimed to examine the energy contribution of NNCs. Our secondary aim is to assess the nutrition impact of NNCs, especially among patients receiving continuous renal replacement therapy (CRRT). MATERIALS/METHODS: We enrolled 177 mechanically ventilated patients admitted to medical-surgical ICUs from August to December 2019. Patients were monitored over the first 7 days of admission. Infusion rates of enteral nutrition/parenteral nutrition and NNCs, as well as clinical characteristics, were examined. Patients receiving CRRT were compared with those without. RESULTS: In total, 24% of patients additional energy from citrate. Patients received a maximum of 331 kcal from citrate, 492 kcal from propofol, and 992 kcal from dextrose per ICU day. CRRT group achieved higher total energy on the first 2 days (day 1: 55.1% vs 46.4%, P = 0.008; day 2: 73.2% vs 55.4%, P = 0.025). They also received higher mean NNCs on all days, except for day 1 (P = 0.068). CONCLUSION: NNCs, especially citrate, are significant sources of energy. Patients receiving CRRT were more likely to be malnourished. There should be close monitoring and adaption of energy prescription accordingly to prevent overfeeding.

Culinary Education Programs for Children in Low-Income Households: A Scoping Review.

Child obesity in the United States is at an all-time high, particularly among underserved populations. Home-cooked meals are associated with lower rates of obesity. Helping children develop culinary skills has been associated with improved nutrition. The purpose of this study is to report results from a scoping review of culinary education interventions with children from low-income families. Three databases and hand searches of relevant articles were examined. Retained articles met inclusionary criteria. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed, as appropriate. A data extraction template was developed. Data were independently extracted and verified. Only nine out of 370 articles met the inclusionary criteria and were included in the review. Most interventions were school-based, used a quasi-experimental design, and recruited minority children. Children-only was the primary intervention focus. Primary outcomes were mostly psychosocial from child self-report. Most interventions focused on children only and were guided by Social Cognitive Theory. Most reported stakeholder involvement; however, type and degree varied. All had an in-person component; only one used technology. Few reported training program leaders. Culinary education programs for children from low-income families could benefit from a broader theoretical grounding, program leader training, and greater parental involvement.

Cytotoxic and proinflammatory CD8+ T lymphocytes promote development of vulnerable atherosclerotic plaques in apoE-deficient mice.

BACKGROUND: Heart attacks and strokes, leading causes of deaths globally, arise from thrombotic occlusion of ruptured vulnerable atherosclerotic plaques characterized by abundant apoptosis, large necrotic cores derived from inefficient apoptotic cell clearance, thin fibrous caps, and focal inflammation. The genesis of apoptosis and necrotic cores in these vulnerable atherosclerotic plaques remains unknown. Cytotoxic CD8(+) T lymphocytes represent up to 50% of leukocytes in advanced human plaques and dominate early immune responses in mouse lesions, yet their role in atherosclerosis also remains unresolved. METHODS AND RESULTS: CD8(+) T-lymphocyte depletion by CD8α or CD8ß monoclonal antibody in apolipoprotein E-deficient mice fed a high-fat diet ameliorated atherosclerosis by reducing lipid and macrophage accumulation, apoptosis, necrotic cores, and monocyte chemoattractant protein 1, interleukin 1ß, interferon γ, and vascular cell adhesion molecule 1. Transfer of CD8(+) T cells into lymphocyte-deficient, apolipoprotein E-deficient mice partially reconstituted CD8(+) T cells in lymphoid compartments and was associated with CD8(+) T-cell infiltration in lesions, increased lipid and macrophage accumulation, apoptotic cells, necrotic cores, and interleukin 1ß in atherosclerotic lesions. Transfer of CD8(+) T cells deficient in perforin, granzyme B, or tumor necrosis factor α but not interferon γ failed to increase atherosclerotic lesions despite partial reconstitution in the lymphoid system and the presence in atherosclerotic lesions. Macrophages, smooth muscle cells, and endothelial cells were identified as apoptotic targets. CONCLUSIONS: We conclude that CD8(+) T lymphocytes promote the development of vulnerable atherosclerotic plaques by perforin- and granzyme B-mediated apoptosis of macrophages, smooth muscle cells, and endothelial cells that, in turn, leads to necrotic core formation and further augments inflammation by tumor necrosis factor α secretion.

Decidual-secreted factors alter invasive trophoblast membrane and secreted proteins implying a role for decidual cell regulation of placentation.

Inadequate or inappropriate implantation and placentation during the establishment of human pregnancy is thought to lead to first trimester miscarriage, placental insufficiency and other obstetric complications. To create the placental blood supply, specialized cells, the 'extravillous trophoblast' (EVT) invade through the differentiated uterine endometrium (the decidua) to engraft and remodel uterine spiral arteries. We hypothesized that decidual factors would regulate EVT function by altering the production of EVT membrane and secreted factors. We used a proteomics approach to identify EVT membrane and secreted proteins regulated by decidual cell factors. Human endometrial stromal cells were decidualized in vitro by treatment with estradiol (10(-8) M), medroxyprogesterone acetate (10(-7) M) and cAMP (0.5 mM) for 14 days. Conditioned media (CM) was collected on day 2 (non-decidualized CM) and 14 (decidualized CM) of treatment. Isolated primary EVT cultured on Matrigel™ were treated with media control, non-decidualized or decidualized CM for 16 h. EVT CM was fractionated for proteins <30 kDa using size-exclusion affinity nanoparticles (SEAN) before trypsin digestion and HPLC-MS/MS. 43 proteins produced by EVT were identified; 14 not previously known to be expressed in the placenta and 12 which had previously been associated with diseases of pregnancy including preeclampsia. Profilin 1, lysosome associated membrane glycoprotein 1 (LAMP1), dipeptidyl peptidase 1 (DPP1/cathepsin C) and annexin A2 expression by interstitial EVT in vivo was validated by immunhistochemistry. Decidual CM regulation in vitro was validated by western blotting: decidualized CM upregulated profilin 1 in EVT CM and non-decidualized CM upregulated annexin A2 in EVT CM and pro-DPP1 in EVT cell lysate. Here, non-decidualized factors induced protease expression by EVT suggesting that non-decidualized factors may induce a pro-inflammatory cascade. Preeclampsia is a pro-inflammatory condition. Overall, we have demonstrated the potential of a proteomics approach to identify novel proteins expressed by EVT and to uncover the mechanisms leading to disease states.

Leukemia inhibitory factor enhances endometrial stromal cell decidualization in humans and mice.

Adequate differentiation or decidualization of endometrial stromal cells (ESC) is critical for successful pregnancy in humans and rodents. Here, we investigated the role of leukemia inhibitory factor (LIF) in human and murine decidualization. Ex vivo human (H) ESC decidualization was induced by estrogen (E, 10(-8) M) plus medroxyprogesterone acetate (MPA, 10(-7) M). Exogenous LIF (≥50 ng/ml) induced STAT3 phosphorylation in non-decidualized and decidualized HESC and enhanced E+MPA-induced decidualization (measured by PRL secretion, P<0.05). LIF mRNA in HESC was down-regulated by decidualization treatment (E+MPA) whereas LIF receptor (R) mRNA was up-regulated, suggesting that the decidualization stimulus 'primed' HESC for LIF action, but that factors not present in our in vitro model were required to induce LIF expression. Ex vivo first trimester decidual biopsies secreted >100 pg/mg G-CSF, IL6, IL8, and MCP1. Decidualized HESC secreted IL6, IL8, IL15 and MCP1. LIF (50 ng/ml) up-regulated IL6 and IL15 (P<0.05) secretion in decidualized HESC compared to 0.5 ng/ml LIF. In murine endometrium, LIF and LIFR immunolocalized to decidualized stromal cells on day 5 of gestation (day 0 = day of plug detection). Western blotting confirmed that LIF and the LIFR were up-regulated in intra-implantation sites compared to inter-implantation sites on Day 5 of gestation. To determine the role of LIF during in vivo murine decidualization, intra-peritoneal injections of a long-acting LIF antagonist (PEGLA; 900 or 1200 µg) were given just post-attachment, during the initiation of decidualization on day 4. PEGLA treatment reduced implantation site decidual area (P<0.05) and desmin staining immuno-intensity (P<0.05) compared to control on day 6 of gestation. This study demonstrated that LIF was an important regulator of decidualization in humans and mice and data provides insight into the processes underlying decidualization, which are important for understanding implantation and placentation.