Background: Lipoprotein(a) [Lp(a)] is a genetically determined, pro-atherogenic lipoprotein enriched in oxidized phospholipids and increasingly recognized as a key potential contributor to residual cardiovascular and inflammatory risk. However, data on its distribution and cardiometabolic associations in Middle Eastern populations remain limited. This study aimed to evaluate the prevalence of elevated Lp(a) and its association with type 2 diabetes (T2D), systemic inflammation, and ethnic variation in a multiethnic cohort. Methods: In this cross-sectional study, data from 2083 adults aged ≥ 18 years residing in Kuwait were collected through the Kuwait Diabetes Epidemiology Program (KDEP) at Dasman Diabetes Institute between 2011 and 2014 using random sampling. Plasma Lp(a) concentrations, cardiometabolic parameters, and high-sensitivity C-reactive protein (CRP) were measured. Elevated Lp(a) was defined as ≥ 50 mg/dL according to established clinical guidelines. Associations of elevated Lp(a) with T2D and CRP were assessed using multivariable Poisson regression models to estimate adjusted prevalence ratios. Results: The overall prevalence of elevated Lp(a) was 41.2%, exceeding global estimates. Significant ethnic variation was observed, with Arabs exhibiting the highest prevalence. After adjustment for potential confounders, individuals with T2D had a higher prevalence of elevated Lp(a) (APR = 1.166) and diabetes status significantly modified the association between CRP and elevated Lp(a) interaction (APR = 1.015), thus supporting a link between Lp(a) and systemic inflammation. Conclusions: Elevated Lp(a) was highly prevalent in this multiethnic Middle Eastern population and was independently associated with T2D and systemic inflammation. These findings support the emerging concept that Lp(a) may function as a molecular-inflammatory mediator potentially contributing to residual cardiovascular risk and highlight the importance of incorporating Lp(a) assessment into cardiometabolic risk stratification, particularly in high-risk populations.
Mohammad G. Qaddoumi, A. Albatineh, I. Alkhairi et al.· Biomedicines· 0 citations
Obstructive sleep apnea (OSA) and insomnia are highly prevalent in older adults and both have been linked to cognitive decline. However, it remains unclear whether the physiological burden of OSA or the sleep fragmentation associated with insomnia more strongly predicts cognitive impairment. This study examined whether OSA risk or insomnia better was associated with memory problems and cognitive slowing among community-dwelling older Canadians. Given the cross-sectional design, the study evaluated associations rather than causal relationships.
Data were drawn from 946 participants in the Canadian Longitudinal Study on Aging (CLSA), including 473 individuals reporting a physician-diagnosed memory problem and 473 age- and sex-matched controls. OSA risk was assessed using the validated STOP-BA(N)G questionnaire. At the same time, insomnia was defined using operational research criteria based on sleep onset latency, wake after sleep onset, and duration. Cognitive processing speed was measured via Choice Reaction Time (CRT). General linear models, logistic regression, and discriminant analyses examined associations between sleep parameters and cognitive outcomes, controlling for age, sex, body mass index, income, and diabetes.
Participants with memory problems had significantly higher STOP-BA(N)G scores (
F
(1,931) = 7.10,
p
= 0.008) and slower CRTs (
p
= 0.05) compared to controls. Insomnia alone or comorbid with OSA (COMISA) was not associated with cognitive outcomes. In discriminant analysis, STOP-BA(N)G score (
r
= 0.45) and diabetes (
r
= 0.26) were the strongest predictors of memory problems, correctly classifying 66.6% of cases. Sex-stratified analyses demonstrated that the association between higher STOP-BA(N)G scores and memory problems remained significant in both men and women, although effect sizes were somewhat larger in men.
Higher OSA risk was associated with poorer memory and slower cognitive processing in older adults, whereas insomnia was not associated with these outcomes. Because of the cross-sectional design, causality cannot be inferred. Screening for OSA and metabolic comorbidities in patients with memory complaints may help identify individuals at increased risk of cognitive impairment.
D. Rizzo, M. Baltzan, Mohamed Abu-farha et al.· Frontiers in Psychology· 0 citations
Low-fat diets are widely promoted as health-protective; however, the consequences of removing sucrose within a low-fat dietary framework remain unclear. Here, we investigated the effects of a sucrose-free low-fat diet (SF-LFD) compared with a sucrose-containing low-fat control diet (C-LFD) in mice (n=6/group) over 16 weeks. Despite unchanged body and liver weights, SF-LFD feeding resulted in impaired glucose tolerance, reduced insulin sensitivity, and broad alterations in circulating metabolic hormones, including elevated C-peptide, incretins, ghrelin, and resistin, as well as reduced fasting insulin. 16S rRNA sequencing revealed that SF-LFD markedly disrupted gut microbial diversity and composition, with depletion of short-chain fatty acid–producing commensals, including Lactobacillus murinus and members of the Lachnospiraceae family, and enrichment of taxa associated with inflammatory or stress-adapted states, including Helicobacter ganmani, Odoribacter splanchnicus, and Alistipes species. This dysbiosis was accompanied by pronounced colonic inflammation characterized by crypt architectural disruption, loss of goblet cells, submucosal expansion, increased CD3+ T-cell and F4/80+ macrophage infiltration, and robust upregulation of inflammatory mediators, including Il1b, Il6, Ccl2, Rorγt, and Tbx21. SF-LFD feeding induced hepatic microvesicular steatosis, lobular inflammation, recruitment of F4/80+ and CD11c+ immune cells and increased hepatic expression of IL1b and IL6. Together, these findings suggest that sucrose elimination from a low-fat diet disrupts gut microbiota, impairs metabolic homeostasis, and promotes gut and liver inflammation, revealing an unrecognized dietary trigger of metabolic dysfunction.
N. Almansour, S. Kochumon, Fatema Al-Rashed et al.· Frontiers in Immunology· 0 citations
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