Differences in bone mineral density (BMD) have been observed between adults with Down syndrome (DS) and the general population. The purpose of this article is to describe the prevalence of bone mass disorders in a cohort of adults with DS and their predisposing factors. We performed a cross-sectional study of 104 consecutively recruited adults with DS from an outpatient clinic of a tertiary care hospital in Madrid, Spain. We recorded epidemiological and anthropometric data, nutritional variables, coexisting clinical conditions, and laboratory variables. BMD was measured at the lumbar spine, total hip, and femoral neck using dual-energy X-ray absorptiometry. The prevalence of osteopenia ranged from 48% to 52%, and that of osteoporosis ranged from 19% to 22% depending on the site of measurement (femoral neck or lumbar spine, respectively). Age was the greatest risk factor associated for lower BMD, with similar bone mass accrual curve but with lower peak of BMD than the general population. We conclu...

The objective of this study was to examine the interactions between comorbidity and five lifestyle single habits concerning different subscales of quality of life (QoL). For the study, 302 patients were consecutively recruited at the internal medicine department of a tertiary teaching hospital. Lifestyle habits, comorbidities and QoL were recorded according to validated questionnaires. Five single unhealthy habits, such as tobacco consumption, dietary intake of ultra-processed pastries, raw nuts or carbonated drinks, sleep time and physical activity patterns were selected according to previously published data. The main outcomes of the study were the scores of the eight subscales of the SF-36 QoL survey. The aggregate of unhealthy habits showed statistically significant association to every category in the SF-36 questionnaire, both in the univariate and the multivariate analysis when adjusting by age, sex and comorbidity. An interaction was found between comorbidity and unhealthy habits in both physical and mental summaries of SF-36. In conclusion, the lifestyle assessment according to five unhealthy habits is associated with a worse QoL. The interaction between comorbidity and unhealthy habits is especially clear in diseased patients due to the interplay between illness and lifestyle in the prediction of QoL.

Introduction: MASLD is linked to dyslipidemia, but it remains unclear whether this alteration depends more on disease activity or fibrosis. Objective: To determine whether dyslipidemia is primarily associated with activity and/or fibrosis through standard lipid profile and advanced lipidomics. Methods: A cross-sectional study was conducted including patients with suspected MASLD at a single center. Intraoperative liver biopsies were obtained. Only patients with MASLD were included in the analysis. Histological activity was defined as a NAFLD Activity Score (NAS) ≥5 and fibrosis was staged according to standard criteria. Clinical, biochemical, lipoprotein, and fatty acid profiles were assessed, including nuclear magnetic resonance (NMR) spectroscopy for lipoprotein subfractions and gas chromatography for fatty acids. Multivariable linear regression models were used to evaluate independent associations of activity and fibrosis with lipid parameters. Results: A total of 49 patients were analyzed (mean age 48 years, 46% men, 94% with BMI > 35). Liver biopsies revealed a 30.6% prevalence of activity (NAS ≥ 5) and 36.7% of fibrosis. Higher lipid levels in patients with activity were related to apolipoprotein B, non-HDL cholesterol, and triglycerides in both univariate and multivariate models. Fibrosis was not associated with any lipid parameter. Lipidomics confirmed associations of activity with VLDL+IDL cholesterol (β = 0.474, 95% CI 0.204–0.745, p = 0.001), VLDL+IDL triglycerides (β = 0.454, 95% CI 0.198–0.710, p = 0.001), and VLDL particle concentration (β = 0.409, 95% CI 0.155–0.663, p = 0.002), and showed a trend toward an inverse association with the percentage of large VLDL particles (β=−0.298, 95% CI −0.602–0.006, p = 0.054). Besides, the omega-6/triglycerides ratio was inversely associated with activity (β=−0.345, 95% CI −0.630 to −0.060, p = 0.019). Conclusion: Hepatic inflammatory activity showed strong associations with a non-traditional atherogenic lipidomic profile. These findings suggest that activity, rather than liver fibrosis, may be a key factor in the MASLD atherosclerotic momentum.

The prevalence of cardiovascular diseases (CVDs) is a growing global health concern. Recent advances have demonstrated significant reductions in acute cardiovascular events through the management of modifiable cardiovascular risk factors. However, these factors are responsible for about 50% of the global cardiovascular disease burden. Considering that CVDs are one of the top mortality causes worldwide, the concept of residual cardiovascular risk is an important emerging area of study. Different factors have been proposed as sources of residual risk markers, including non-HDL particles characterization, as well as inflammation measured by serum and imaging technics. Among these, metabolic-associated steatotic liver disease (MASLD) remains controversial. Two opposing viewpoints contend: one positing that fatty liver disease merely reflects classical risk factors and thus adds no additional risk and another asserting that fatty liver disease independently impacts cardiovascular disease incidence. To address this dilemma, one hypothetical approach is to identify specific hepatic energy-yielding mechanisms and assess their impact on the cardiovascular system. Ketogenesis, a metabolic intermediate process particularly linked to energy homeostasis during fasting, might help to link these concepts. Ketogenic metabolism has been shown to vary through MASLD progression. Additionally, newer evidence supports the significance of circulating ketone bodies in cardiovascular risk prediction. Furthermore, ketogenic metabolism modification seems to have a therapeutic impact on cardiovascular and endothelial damage. Describing the relationship, if any, between steatotic liver disease and cardiovascular disease development through ketogenesis impairment might help to clarify MASLD’s role in cardiovascular risk. Furthermore, this evidence might help to solve the controversy surrounding liver steatosis impact in CVD and might lead to a more accurate risk assessment and therapeutic targets in the pursuit of precision medicine.