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Biology subjects

Taba, N.

Publications and source records attributed to Taba, N..

4 recordsLinked to original sources

Circadian rhythms regulate refractive development across species

Myopia is a rapidly escalating global public health challenge, yet the biological mechanisms linking modern lifestyles to abnormal eye growth remain unclear. Circadian rhythms have been implicated in refractive development, but causal evidence is limited. Here, we integrate population-scale human data with an experimental animal model to determine whether circadian misalignment contributes to myopia. In >265,000 individuals from the Estonian and UK Biobanks, late chronotype was consistently associated with myopia. To assess causality, we experimentally disrupted the alignment between behavioural and environmental rhythms in mice by housing them in non-24-hour light-dark schedules. Exposure to a lengthened cycle (T26) induced a myopic shift that was, notably, reversible in early adulthood. Retinal transcriptomics revealed enrichment of mitochondrial and hypoxia-related plasticity pathways, with transcriptional changes distributed across multiple retinal cell classes. Together, these findings identify circadian misalignment as a conserved and modifiable driver of myopia, highlighting opportunities for novel preventive and therapeutic approaches.

neuroscience↗

A catalogue of omics biological ageing clocks reveals substantial commonality and associations with disease risk

Biological age (BA), a measure of functional capacity and prognostic of health outcomes that discriminates between individuals of the same chronological age (chronAge), has been estimated using a variety of biomarkers. Previous comparative studies have mainly used epigenetic models (clocks), we use ~1000 participants to create eleven omics ageing clocks, with correlations of 0.45-0.97 with chronAge, even with substantial sub-setting of biomarkers. These clocks track common aspects of ageing with 94% of the variance in chronAge being shared among clocks. The difference between BA and chronAge - omics clock age acceleration (OCAA) - often associates with health measures. One years OCAA typically has the same effect on risk factors/10-year disease incidence as 0.46/0.45 years of chronAge. Epigenetic and IgG glycomics clocks appeared to track generalised ageing while others capture specific risks. We conclude BA is measurable and prognostic and that future work should prioritise health outcomes over chronAge.

bioinformatics↗

Mendelian randomization identifies the potential causal impact of dietary patterns on circulating blood metabolites

Nutrition plays an important role in the development and progress of several health conditions, but the exact mechanism is often still unclear. Blood metabolites are likely candidates to be mediating these relationships, as their levels are strongly dependent on the frequency of consumption of several foods/drinks. Understanding the causal effect of food on metabolites is thus of extreme importance. To establish these effects we utilized Two-sample Mendelian randomization using the genetic variants associated with dietary traits as instrumental variables. The estimates of single-nucleotide polymorphisms effects on exposures were obtained from a recent genome-wide association study (GWAS) of 25 individual and 15 principal-component dietary traits, whereas the ones for outcomes were obtained from a GWAS of 123 blood metabolites measured by nuclear magnetic resonance spectroscopy. We identified 417 potentially causal links between food and metabolites, replicating previous findings, such as the association between increased oily fish consumption and higher DHA, and highlighting several novel associations. Most of the associations were related to very-low-density, intermediate-density (IDL) and low-density lipoproteins (LDL). For example, we found that constituents of IDL particles and large LDL particles were raised by coffee and alcohol while lowered by an overall healthier diet and fruit consumption. Our results represent one of the first examples of the estimates of long-term causal effects of diet on metabolites and start bridging the gap in the mechanistic understanding linking food consumption to its health consequences.

genomics↗

Using genetics to disentangle the complex relationship between food choices and health status

Despite food choices being one of the most important factors influencing health, efforts to identify individual food groups and dietary patterns that cause disease have been challenging, with traditional nutritional epidemiological approaches plagued by biases and confounding. After identifying 302 individual genetic determinants of dietary intake in 445,779 individuals in the UK Biobank study, we develop a statistical genetics framework that enables us, to directly assess the impact of food choices on health outcomes. We show that the biases which affect observational studies extend also to GWAS, genetic correlations and causal inference through genetics, which can be corrected by applying our methods. Finally, by applying Mendelian Randomization approaches to the corrected results we identify some of the first robust causal associations between eating patterns and cancer, heart disease, obesity, and several other health related risk factors, distinguishing between the effects of specific foods or dietary patterns.

genetics↗