Author

Fahd Al-Mulla

View on Semantic Scholar

2 papers indexed here

We haven’t gathered this author’s papers yet. Follow them and we’ll fetch their work.

Not the right person? Other researchers publish under this name.

Open access Aug 2026

Obstructive sleep apnea risk is associated with a diminished cognitive profile: findings from the Canadian longitudinal study on aging

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

Open access Jul 2026

Sucrose-free low-fat diet induces metabolic dysfunction through gut dysbiosis and colonic inflammation in mice

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