LongeCityNews Last Updated: 18 February 2026 - 02:04 AM

The retina at the back of the eye is the one part of the central nervous system that can be readily visually inspected, including the state of the network of blood vessels that supports it. Capillary networks of tiny blood vessels are dense and actively maintained; as the character of angiogenesis changes for the worse with aging, these networks become less dense and exhibit other signs of damage. Thus imagery of the retina provides a lot of data that can be employed to, for example, produce aging clocks, or act as a proxy measure for other forms of vascular and nervous system aging.

For retinal imagery to be usefully employed as a proxy measure of any specific aspect of vascular aging or central nervous system aging, or specific form of age-related damage, a robust correlation must first be demonstrated. Thus we have papers such as today's example, in which researchers establish links between retinal imagery characteristics and vascular and brain aging. One might expect this to inform efforts to further advance retinal imaging as a relatively low cost diagnostic tool, a way to better establish risk and the need for more costly forms of assessment in older people.

Cross-organ analysis reveals associations between vascular properties of the retina, the carotid and aortic arteries, and the brain

Doctors often use eye scans to check for signs of heart and brain disease, but the exact link between the tiny blood vessels in the eye and those in major organs is unclear. We aimed to systematically map similarities between blood vessels across the entire body. We compared vascular image-derived phenotypes from the brain, carotid artery, aorta, and retina, using UK Biobank sample sizes ranging from 18,808 to 68,740 participants. We examined phenotypic and genetic correlations, as well as common associated genes and pathways.

Here we show that white matter hyperintensities are positively correlated with carotid intima-media thickness (r = 0.03), lumen diameter (r = 0.14), and aortic cross-sectional areas (r = 0.09), but negatively correlated with aortic distensibilities (r ≤ -0.05). Arterial retinal vascular density shows negative correlations with white matter hyperintensities (r = -0.04), intima-media thickness (r = -0.04), lumen diameter (r = -0.06), and aortic areas (r = -0.05), while positively correlating with aortic distensibilities (r = 0.04). Significant correlations also persist after correcting for hypertension.

In summary, we found strong connections with the health of retinal blood vessels mirroring the health of the brain and major arteries. This suggests that some of the same factors influence vessel health across the body. This suggests that an eye scan could be a fast, non-invasive way to get a complete snapshot of a person's overall cardiovascular and brain health. These findings could help doctors identify health issues, such as early artery stiffness or brain aging, much sooner.

Scientists have pitted five diets against each other to see which one is associated with more years of life gained [1].

The clash of the diets

Unhealthy eating is recognized as a globally leading cause of death [2]. Surprisingly, few studies have actually evaluated the gains in life expectancy associated with adherence to a healthy diet. In a new study published in Science Advances, an international group of scientists pitted five leading dietary practices against each other using data from UK Biobank, a huge repository of health-related information on hundreds of thousands of British citizens.

The sample was comprised of 103,649 participants (mean age 58.3 years, 56.4% female) who had completed two or more web-based 24-hour dietary assessments and were free of cardiovascular disease (CVD) and cancer at baseline. Each participant was scored on five dietary pattern indices based on what they reported eating: Alternate Healthy Eating Index (AHEI-2010), Alternate Mediterranean Diet (AMED), healthful Plant-based Diet Index (hPDI), Dietary Approaches to Stop Hypertension (DASH), and Diabetes Risk Reduction Diet (DRRD).

Each score was divided into quintiles. The five scores were moderately-to-highly intercorrelated, meaning that the dietary patterns they capture are often overlapping (which is expected), but not identical. The model was adjusted for race, education, socioeconomic deprivation, smoking status, physical activity, BMI, total energy intake, baseline dyslipidemia, hypertension, diabetes, and, for hPDI, DASH, and DRRD, alcohol consumption.

The researchers also wanted to see how dietary patterns interact with known longevity gene variants. They calculated a longevity polygenic risk score (PRS) from 19 single nucleotide polymorphisms (SNPs) which were significantly associated with longevity in a genome-wide association study (GWAS). This model was additionally adjusted for ten genetic principal components.

The winners and the losers

DRRD showed the strongest association with longevity, as the top quintile had 24% lower mortality than the bottom quintile. The authors attribute this to the fact that DRRD’s scoring algorithm directly includes dietary fiber and glycemic index, the two components that individually showed the strongest associations with mortality: fiber was protective, while high glycemic index was detrimental. Product-wise, sugar-sweetened beverages turned out to be the most harmful, in line with previous research [3].

Other scores followed DRRD closely, with 20% reductions in mortality for the top quintiles of AHEI and AMED compared to the bottom ones, 19% for DASH, and 18% for hPDI. Interestingly, noticeable sex-related differences were observed. When the researchers looked at life expectancy, the top performer for men was DRRD, with 3 years gained between the lowest and the highest quintiles, while for women, it was AMED, with 2.3 years. For both sexes, the least effective diet was hPDI (1.9 and 1.5 years, respectively).

How do “longevity genes” factor in?

The team then analyzed PRS’ association with remaining life expectancy, and it turned out to be slightly lower: 1.4 years for men and 1.7 years for women. However, the PRS was split into tertiles, so the researchers compared the top and bottom tertiles. Importantly, the effects of diet and genetics were roughly additive, with DRRD showing the largest combined gains in both sexes. Being both in the top DRRD quintile and in the top PRS tertile was associated with 3.2 years of additional life expectancy for men and 5.5 years for women.

However, the combined estimates are peculiarly noisy, especially for men. For instance, having a top AMED score and a top PRS gives only 1 year for men, which is actually less than either diet alone (2.2) or PRS alone (1.4). This is probably because the combined estimates come from much smaller slices of the cohort, resulting in noise, rather than due to any negative interaction. The women’s combined numbers behave more sensibly and are roughly additive.

Crucially, these estimates are for a 45-year-old person. The life expectancy benefits of switching to a better diet, naturally, diminish with age, as fewer years remain for the risk reduction to play out, while the risk of dying from something unrelated to diet increases.

While this is a well-executed and carefully sensitivity-tested observational study, a few caveats apply. The effect sizes are modest, and the confidence intervals are wide enough for the true benefit to be as small as about 0.5 years in some comparisons. These are also best-case comparisons that compare top and bottom quintiles, while most people usually do not switch their diets from the worst to the best. Finally, the PRS interaction story is intriguing but might not be statistically robust, leaving room for further research.

Literature

[1] Lv, Y., Song, J., Ding, D., Luo, M., He, F. J., Yuan, C., MacGregor, G. A., Liu, L., & Chen, L. (2026). Healthy dietary patterns, longevity genes, and life expectancy: A prospective cohort study. Science advances, 12(7), eads7559.

[2] Afshin, A., Sur, P. J., Fay, K. A., Cornaby, L., Ferrara, G., Salama, J. S., … & Murray, C. J. (2019). Health effects of dietary risks in 195 countries, 1990–2017: a systematic analysis for the Global Burden of Disease Study 2017. The lancet, 393(10184), 1958-1972.

[3] Imamura, F., O’Connor, L., Ye, Z., Mursu, J., Hayashino, Y., Bhupathiraju, S. N., & Forouhi, N. G. (2015). Consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice and incidence of type 2 diabetes: systematic review, meta-analysis, and estimation of population attributable fraction. Bmj, 351.

Aging is an accumulation of cell and tissue damage, combined with the dysfunctions resulting from that damage. Damaged systems lose function in a haphazard, random fashion that, averaged out over time and across many systems, tends to be proportional to the burden of damage. This is the case whether the system is a simple mechanical device, an organ, or a human. In aging humans and animals one thus observes correlations between most different examples of lost and degraded function, including those that cause mortality.

We assessed the population distribution of age-related functional impairments (ARFIs) and their associations with mortality and life expectancy (LE). We included 12,906 participants (mean age: 62.6 years) from the China Health and Retirement Longitudinal Study. Visual impairment, hearing impairment, cognitive impairment, sleep disorder, depressive symptoms, and disability in activities of daily living (ADL) were assessed. Cox proportional hazards models were used to estimate the associations of ARFIs with all-cause mortality. Life expectancy at age 50 was estimated by the presence and number of key ARFIs.

The six ARFIs exhibit distinct distributions by ages and provinces across China. During the 9-year follow-up, ADL disability, cognitive impairment, and depressive symptoms are independently associated with 64%, 41%, and 20% higher risks of mortality, corresponding to LE losses of 4.45, 3.08, and 1.59 years at the age of 50 years. A greater number of key ARFIs is associated with higher mortality risk in a dose-response manner (hazard ratios: 1.23 for one, 1.42 for two, and 1.86 for three) and greater LE loss (1.63 years for one, 3.37 for two, and 4.96 for three).

Link: https://doi.org/10.1038/s43856-025-01350-3

Evolution optimizes for reproductive success, and thus it should be no surprise to find that reproductive organs influence the entire body, and thus their aging has sizable effects on the aging of other organs. Researchers here review the mechanisms of aging that act to degrade structure and function of the testes, and in turn affect the production of androgens that influence tissue function elsewhere in the body.

The testis, a male-specific organ, plays a critical role in maintaining spermatogenesis and androgen production. As men age, testicular function declines, compromising not only reproductive capacity but also overall health and quality of life. Testicular ageing is characterized by progressive degeneration of the seminiferous epithelium and interstitial compartments, leading to endocrine dysfunction, impaired spermatogenesis, and heightened risk of age-related disease.

Although mechanistic insights are advancing rapidly, most therapeutic studies remain rooted in reductionist single-cell models that overlook the integrated dynamics of the testicular microenvironment. In reality, testicular ageing reflects a coordinated decline of germ cells, Sertoli and Leydig cells, and their niches. This process is driven by interconnected mechanisms, including oxidative stress, defective DNA repair and autophagy, dysregulated endocrine homeostasis, impaired protein quality control, and aberrant activation of ageing-related signalling pathways, which act synergistically.

Testicular ageing is accompanied by a progressive collapse of energy metabolism. Impaired fatty acid utilisation, reduced glucose uptake, and widespread mitochondrial dysfunction collectively drive metabolic remodelling that deteriorates the testicular microenvironment. Moreover, senescent somatic cells acquire a senescence-associated secretory phenotype (SASP), releasing pro-inflammatory cytokines such as IL-6 and IL-1β, while testicular macrophages adopt a pro-inflammatory state that recruits adaptive immune cells. Together, these changes establish a chronic inflammatory microenvironment that reinforces cellular senescence and accelerates testicular ageing.

Priorities for future research include clarifying cell-microenvironment interactions, establishing non-invasive biomarkers for early detection, and resolving metabolic pathways that may guide senolytic strategies. As therapeutic paradigms evolve, emerging interventions - particularly stem-cell-based approaches - may extend beyond the limits of conventional pharmacology to enable more precise and effective mitigation of testicular ageing.

Link: https://doi.org/10.1080/07853890.2026.2624183