UNASSIGNED: Prior studies have incompletely assessed whether the development of cardiometabolic risk factors (CVDRF) (hypertension, hyperlipidemia, and diabetes mellitus) mediates the association between anxiety and depression (anxiety/depression) and cardiovascular disease (CVD).
UNASSIGNED: The authors aimed to evaluate the following: 1) the association between anxiety/depression and incident CVDRFs and whether this association mediates the increased CVD risk; and 2) whether neuro-immune mechanisms and age and sex effects may be involved.
UNASSIGNED: Using a retrospective cohort design, Mass General Brigham Biobank subjects were followed for 10 years. Presence and timing of anxiety/depression, CVDRFs, and CVD were determined using ICD codes. Stress-related neural activity, chronic inflammation, and autonomic function were measured by the assessment of amygdalar-to-cortical activity ratio, high-sensitivity CRP, and heart rate variability. Multivariable regression and mediation analyses were employed.
UNASSIGNED: Among 71,214 subjects (median age 49.6 years; 55.3% female), 27,048 (38.0%) developed CVDRFs during follow-up. Pre-existing anxiety/depression associated with increased risk of incident CVDRF (OR: 1.71 [95% CI: 1.59-1.83], P < 0.001) and with a shorter time to their development (β = -0.486 [95% CI: -0.62 to -0.35], P < 0.001). The development of CVDRFs mediated the association between anxiety/depression and CVD events (log-odds: 0.044 [95% CI: 0.034-0.055], P < 0.05). Neuro-immune pathways contributed to the development of CVDRFs (P < 0.05 each) and significant age and sex effects were noted: younger women experienced the greatest acceleration in the development of CVDRFs after anxiety/depression.
UNASSIGNED: Anxiety/depression accelerate the development of CVDRFs. This association appears to be most notable among younger women and may be mediated by stress-related neuro-immune pathways. Evaluations of tailored preventive measures for individuals with anxiety/depression are needed to reduce CVD risk.

暂无摘要。

BACKGROUND: Fruit consumption has been associated with a lower cardiovascular disease (CVD) risk but the underlying mechanisms are unclear. We investigated the cross-sectional and prospective associations of fruit consumption with markers of adiposity, blood pressure, lipids, low-grade inflammation, glycaemia, and oxidative stress.
METHODS: The main analyses included 365 534 middle-aged adults from the UK Biobank at baseline, of whom 11 510, and 38 988 were included in the first and second follow-up respectively, free from CVD and cancer at baseline. Fruit consumption frequency at baseline was assessed using a questionnaire. We assessed the cross-sectional and prospective associations of fruit with adiposity (body mass index, waist circumference and %body fat), systolic and diastolic blood pressure, lipids (low-density and high-density lipoproteins, triglycerides and apolipoprotein B), glycaemia (haemoglobin A1c), low-grade inflammation (C-reactive protein) and oxidative stress (gamma-glutamyl-transferase) using linear regression models adjusted for socioeconomic and lifestyle factors. Analyses were repeated in a subset with two to five complete 24-h dietary assessments (n = 26 596) allowing for adjustment for total energy intake.
RESULTS: Fruit consumption at baseline generally showed weak inverse associations with adiposity and biomarkers at baseline. Most of these relationships did not persist through follow-up, except for inverse associations with diastolic blood pressure, C-reactive protein, gamma-glutamyl transferase and adiposity. However, for most mechanisms, mean levels varied by less than 0.1 standard deviations (SD) between high and low fruit consumption (> 3 vs < 1 servings/day) in further adjusted models (while the difference was < 0.2 SD for all of them). For example, waist circumference and diastolic blood pressure were 1 cm and 1 mmHg lower in high compared to low fruit intake at the first follow-up (95% confidence interval: -1.8, -0.1 and -1.8, -0.3, respectively). Analyses in the 24-h dietary assessment subset showed overall similar associations.
CONCLUSIONS: We observed very small differences in adiposity and cardiometabolic biomarkers between those who reported high fruit consumption vs low, most of which did not persist over follow-up. Future studies on other mechanisms and detailed assessment of confounding might further elucidate the relevance of fruit to cardiovascular disease.

暂无摘要。

UNASSIGNED: Adverse social determinants of health (SDoH) have been associated with cardiometabolic disease; however, disparities in cardiometabolic outcomes are rarely the result of a single risk factor.
UNASSIGNED: This study aimed to identify and characterize SDoH phenotypes based on patient-reported and neighborhood-level data from the institutional electronic medical record and evaluate the prevalence of diabetes, obesity, and other cardiometabolic diseases by phenotype status.
UNASSIGNED: Patient-reported SDoH were collected (January to December 2020) and neighborhood-level social vulnerability, neighborhood socioeconomic status, and rurality were linked via census tract to geocoded patient addresses. Diabetes status was coded in the electronic medical record using International Classification of Diseases codes; obesity was defined using measured BMI ≥30 kg/m2. Latent class analysis was used to identify clusters of SDoH (eg, phenotypes); we then examined differences in the prevalence of cardiometabolic conditions based on phenotype status using prevalence ratios (PRs).
UNASSIGNED: Complete data were available for analysis for 2380 patients (mean age 53, SD 16 years; n=1405, 59% female; n=1198, 50% non-White). Roughly 8% (n=179) reported housing insecurity, 30% (n=710) reported resource needs (food, health care, or utilities), and 49% (n=1158) lived in a high-vulnerability census tract. We identified 3 patient SDoH phenotypes: (1) high social risk, defined largely by self-reported SDoH (n=217, 9%); (2) adverse neighborhood SDoH (n=1353, 56%), defined largely by adverse neighborhood-level measures; and (3) low social risk (n=810, 34%), defined as low individual- and neighborhood-level risks. Patients with an adverse neighborhood SDoH phenotype had higher prevalence of diagnosed type 2 diabetes (PR 1.19, 95% CI 1.06-1.33), hypertension (PR 1.14, 95% CI 1.02-1.27), peripheral vascular disease (PR 1.46, 95% CI 1.09-1.97), and heart failure (PR 1.46, 95% CI 1.20-1.79).
UNASSIGNED: Patients with the adverse neighborhood SDoH phenotype had higher prevalence of poor cardiometabolic conditions compared to phenotypes determined by individual-level characteristics, suggesting that neighborhood environment plays a role, even if individual measures of socioeconomic status are not suboptimal.

UNASSIGNED: Variants in melanocortin 4 receptor (MC4R) pathway-related genes have been associated with obesity. The association of these variants with cardiometabolic parameters are not fully known.
UNASSIGNED: We compared the severity of obesity and cardiometabolic risk markers in children with MC4R pathway-related clinically reported genetic variants relative to children without these variants.
UNASSIGNED: A retrospective chart review was performed in children with obesity who underwent multigene panel testing for monogenic obesity.
UNASSIGNED: Data on a total of 104 children were examined, with 93 (89%) identified as White. Thirty-nine (37.5%) patients had clinically reported variants in the MC4R pathway, and the remaining 65 patients did not have reported MC4R pathway-related variants. Among the MC4R-related variants, PCSK1 risk alleles were most common, reported in 15 children (14%). The maximum body mass index percent of the 95th percentile was not different between groups (P = .116). Low-density lipoprotein cholesterol (LDL-C) was not different between groups (P = .132). However, subgroup analysis demonstrated higher LDL cholesterol in children with the PCSK1 c.661A>G risk allele relative to those with MC4R-related variant of uncertain significance (P = .047), negative genetic testing (P = .012), and those with non-MC4R related variants (P = .048). The blood pressure, fasting glucose, hemoglobin A1C, total cholesterol, alanine transaminase, and high-density lipoprotein cholesterol were not different between groups.
UNASSIGNED: Variants in the MC4R pathway-related genes were not associated with severity of obesity and cardiometabolic risk markers except for the c.661A>G PCSK1 risk allele, which was associated with higher LDL-C levels.

BACKGROUND: Loss-of-control (LOC) eating, or the subjective experience of being unable to stop eating, is a hallmark feature of binge-eating episodes, which are also characterized by consuming an unusually large amount of food. However, regardless of the size of eating episode, LOC-eating may be a risk factor for adverse health outcomes. This systematic review and meta-analysis comprehensively examine the relationship of LOC-eating with cardiometabolic health components and inflammatory markers.
METHODS: Search procedures were conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guidelines in six electronic databases. Studies of adult or youth samples published in English from the year 2000 onward were included. Given heterogeneity in age groups and adjustment for body mass index across studies, these factors were included as meta-regression moderators.
RESULTS: Fifty-eight studies were identified through the literature search. Among individuals with (versus without) LOC-eating, relative risk ratios provided evidence of a greater relative risk for metabolic syndrome, hypertension, and dyslipidemia; standardized mean differences also provided evidence of higher waist circumference and impaired levels of fasting plasma glucose, high-density lipoprotein (HDL)-cholesterol, and triglycerides, but not blood pressure. Age group did not impact cardiometabolic health components. Body mass index differences moderated the effect on waist circumference. A narrative review of inflammatory markers revealed mixed findings linking inflammatory markers to LOC-eating.
CONCLUSIONS: Overall, evidence for the relationship between LOC-eating and impaired cardiometabolic health underscores LOC-eating as an important early intervention target for prevention of serious adverse health outcomes.

暂无摘要。

Cardiometabolic risk factors increase the chance of developing cardiovascular disease (CVD) and type 2 diabetes. Most CVD risk factors are influenced by total and regional obesity. A higher risk of developing CVD may be linked to vitamin D deficiency, which is more prevalent in the older population. With the goal of evaluating the association between vitamin D and cardiometabolic risk factors and total and regional obesity in older adults, this research included 25 (OH) vitamin D3 concentrations and biochemical markers associated with cardiometabolic diseases, as well as total and regional adiposity, which was measured by DXA. A total of 1991 older participants in the PoCOsteo study were included. Overall, 38.5% of participants had vitamin D deficiency. After adjusting for confounders, the results of multiple linear and logistic regression suggested an inverse association between vitamin D and body mass index (P = 0.04), waist circumference (P = 0.001), total fat (P = 0.02), android fat (P = 0.001), visceral fat (P < 0.001), subcutaneous fat (P = 0.01), trunk fat (P = 0.006), arm fat (P = 0.03), high systolic blood pressure (P = 0.004), high total cholesterol (P < 0.001), high LDL-cholesterol (P < 0.001), high serum triglycerides (P = 0.001), and high fasting glucose (P < 0.001). Additionally, higher vitamin D concentrations decreased the risk of dyslipidemia by 2%. Our results showed a significant association between serum vitamin D and a number of cardiometabolic risk factors, including total and regional obesity.

Excess dietary sugar intake increases the risk of unhealthy weight gain, an important cardiometabolic risk factor in children. To further our understanding of this relationship, we performed a narrative review using two approaches. First, research examining dietary sugar intake, its associations with cardiometabolic health, impact of genetics on sweet taste perception and intake, and how genetics moderates the association of dietary sugar intake and cardiometabolic risk factors in preschool-aged children 1.5-5 years old is reviewed. Second, methodological considerations for collecting and analyzing dietary intake of sugar, genetic information, and markers of cardiometabolic health among young children are provided. Our key recommendations include the following for researchers: (1) Further longitudinal research on sugar intake and cardiometabolic risk factors is warranted to inform policy decisions and guidelines for healthy eating in preschool-aged children. (2) Consistency in sugar definitions is needed across research studies to aid with comparisons of results. (3) Select dietary collection tools specific to each study\'s aim and sugar definition(s). (4) Limit subjectivity of dietary assessment tools as this impacts interpretation of study results. (5) Choose non-invasive biomarkers of cardiometabolic disease until the strengths and limitations of available biomarkers in preschool-aged children are clarified. (6) Select approaches that account for the polygenic nature of cardiometabolic disease such as genome risk scores and genome wide association studies to assess how genetics moderates the relationship between dietary sugar intake and cardiometabolic risk. This review highlights potential recommendations that will support a research environment to help inform policy decisions and healthy eating policies to reduce cardiometabolic risk in young children.