Previous studies have shown that low-fat diet (LFD) is associated with various health benefits, and that lipid and fatty acid metabolism are linked to telomere shortening. However, no epidemiological studies have examined the association between LFD and telomere length (TL). Dietary information was collected using 24-hour recalls among 6,981 adults from a nationwide cross-sectional study. Diet quality was assessed using overall LFD, healthful LFD (hLFD), and unhealthful LFD (uLFD). TL was measured using quantitative PCR. Linear regression was employed to evaluate the association between LFDs and log-transformed TL, and ordinal logistic regression was performed to assess the association of LFDs with ordinal quintiles of TL in descending order. In both fully adjusted linear and ordinal regression models, higher overall LFD [Tertile 3 vs. Tertile 1: percentage change = 2.48%, 95% confidence interval (CI): 0.60%, 4.40%, Ptrend = 0.003; odds ratio (OR) = 0.79, 95% CI:0.68, 0.93; Ptrend = 0.001] and hLFD [Tertile 3 vs. Tertile 1: percentage change = 2.71%, 95% CI: 0.87%, 4.58%; Ptrend = 0.002; OR = 0.84, 95% CI:0.72, 0.97; Ptrend = 0.003] scores were significantly associated with longer TL. The positive association between hLFD and TL was observed in other racial/ethnic groups, but not in non-Hispanic whites (Pinteraction < 0.005). There was no significant association between uLFD and TL in all the models. Our results suggest that LFD rich in high-quality carbohydrates, unsaturated fat, and plant protein is associated with longer TL, and underscore the need to consider the quality and dietary sources of the macronutrients.

Cognitive decline is a hallmark of brain ageing. Leukocyte telomere length (LTL) has emerged as a candidate biomarker related to brain ageing and neurodegeneration; however, reported associations with cognition and brain structure vary across cohorts. Long‑chain omega‑3 polyunsaturated fatty acids (PUFAs), notably docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), exert anti‑inflammatory and antioxidant effects that may, in some contexts, relate to slower telomere attrition. Here, we synthesize evidence on n‑3 PUFAs, telomere biology, and cognitive outcomes, integrating clinical, epidemiologic, and experimental data. We emphasize biological plausibility (oxidative stress/inflammation, membrane remodeling, mitochondrial function and expression of telomerase reverse transcriptase (TERT) through PI3K/Akt/mTOR, NRF2 and epigenetic modifications) while acknowledging heterogeneous human findings and methodological considerations (assay variability, life‑course timing, cognitive domains, and biomarker stratification). We outline priorities for future studies to clarify causal pathways and inform dietary strategies that support healthy cognitive ageing.

There is widespread agreement that offspring are shaped by the parenting they receive in early childhood. This development is intertwined with offspring’s biological functioning, evidenced by their telomeres length (TL)—a key biomarker of aging. Until recently, most studies have focused on the detrimental implications of negative parenting for offspring’s TL. Contemporary research is oriented toward exploring the possible resilience-promoting effect of positive parenting on the biological aging of the offspring. We conducted a meta-analysis synthesizing the findings regarding the association between parenting quality and offspring’s TL. It examines whether positive parenting delays aging processes and whether such processes are exacerbated by exposure to negative parenting. An analysis of 15 studies (k = 23; N = 3,599, Mmean cohort’s age = 15.5, SD = 17.5) revealed a significant association between positive parenting and offspring’s longer TL (r = .16, 95% CI [.11, .20]). Negative parenting was associated with an increased risk of TL erosion (r = −.17, 95% CI [−.28, −.06]). Moreover, this negative association became more robust as offspring grew older (β = −.01, p < .001). Future investigations would benefit from probing associations between parental quality and offspring’s development. Interventions fostering positive parenting might also scaffold these biological processes.

This study examined associations between pregnancy and infant birth outcomes with child telomere length at age 17 years; and investigated if there are sex differences between pregnancy complications and telomere length. We utilised the population-based prospective Raine cohort study in Western Australia, Australia. 2900 pregnant women were recruited at 16–20 weeks’ gestation (Gen 1), and their children (Gen 2) were followed up over several years. Generalised linear models were used to examine relationships between pregnancy or birth outcomes (gestational diabetes, pre-eclampsia, preterm birth, low birth weight, macrosomia), and as a composite, with telomere length, measured via a DNA sample from blood at 17 years of age. Analyses were adjusted for a range of confounders. Among the 1202 included children, there were no differences in child telomere length for any of the individual maternal or birth weight pregnancy outcomes nor were there any significant interactions between each of the complications (individual or composite) and the sex of the child. However, females born from any of the 5 adverse outcomes had shorter telomeres (estimated mean (SE) = -0.159 (0.061), p = 0.010) than females born in the absence of these complications. Specifically, females born from a pre-eclamptic pregnancy had shorter telomeres than females not born from a pre-eclamptic pregnancy (estimated mean (SE) = -0.166 (0.072), p = 0.022). No relationships were observed in males. Further longitudinal studies are needed to understand mediating factors that are important in predicting offspring telomere length and the necessity to investigate females and males independently.

Objective methods for assessing the cumulative lifetime experience of non-human animals would be valuable. We develop the hypothesis that biological age is a common currency that integrates the overall quality of an animal's lifetime experience across a range of types of exposure. Ageing is the result of the accumulation of somatic damage, and its rate is determined by the balance between experiences that cause damage and experiences that mitigate damage or promote repair. Negative affective states are associated with somatic damage via both direct causal and indirect pathways. Based on these premises, we predict that individuals that are biologically old for their chronological age will, on average, have experienced worse lives than individuals that are biologically younger, both in terms of their overall health and affective experience. Biological age is, thus, an attractive measure of cumulative experience because it requires no subjective decisions either about how a given exposure impacts an animal, or about how different dimensions of welfare should be weighted in an overall assessment. Biological age can be measured objectively using biomarkers. We argue that two biomarkers, namely leukocyte telomere length and hippocampal volume, are valid biomarkers of cumulative experience in humans, with potential for use in non-human vertebrates. We discuss how these biomarkers could be used to assess cumulative experience in animals, highlighting some of the limitations. We conclude that biomarkers of biological age offer a viable objective solution to the assessment of cumulative experience and their application in an animal welfare context deserves further exploration.

Telomere shortening during oocyte growth and development is related to reproductive ageing and infertility. The main mechanism involved in the maintenance of telomeres is based on telomerase activity, a specialized enzyme complex, which is capable of adding TTAGGG repeats at the ends of the chromosomes. Mitochondrial dysfunction may cause progressive shortening of telomeres by promoting the generation of reactive oxygen species. Mitofusin-1 is a protein required for mitochondrial fusion. Mice with the mitofusin-1 (Mfn1) deletion in the oocyte are characterized by accelerated follicular depletion and infertility, associated with defective oocyte maturation and follicular development. We hypothesized whether mitochondrial dysfunction in oocytes with targeted deletion of Mfn1 causes telomere shortening. We analyzed telomere length in oocyte and somatic cells in 3-, 6- and 9-month-old Mfn1−/− and wild-type mice. Immunofluorescence in oocyte mice of TRF1 and H2A.X was assessed to evaluate the interplay between the end-protection functions and the response to DNA damage occurring inside the telomeric repeats. Mitochondrial dysfunction due to the deletion of Mfn1 does not seem to affect telomere length in mouse oocytes.

Se is an indispensable trace element for the human body, and telomere length is considered a marker of biological ageing. Previous studies have shown that dietary Se intake is associated with telomere length. However, the relationship between Se intake and telomere length in patients with diabetes has not been well studied. Therefore, this study aimed to investigate the relationship between dietary Se intake and telomere length in patients with diabetes. We extracted 878 participants with diabetes from the National Health and Nutrition Examination Survey database for 1990–2002. Dietary Se intake was assessed using the 24 h dietary recall method, and telomere length was measured using quantitative PCR. Generalised linear models were constructed to assess the relationship between dietary Se intake and telomere length. After controlling for the confounders, 1 μg increase in dietary Se intake in female patients with diabetes, and telomere length increased by 1·84 base pairs (β = 1·84 (95 % CI: 0·15, 3·53)), there was a line relationship between dietary Se intake and telomere length in female patients with diabetes and telomere length increased with increasing dietary Se intake within the range of 0–250 μg. The study demonstrates that dietary Se intake is significantly associated with telomere length only in the female population with diabetes in the USA. However, further prospective studies are required to confirm this finding.

Patients with major depressive disorder (MDD) present features that suggest the involvement of accelerated aging, such as increased circulating inflammatory markers and shorter telomere length (TL). Here we measured T-lymphocytes TL with quantitative fluorescent in situ hybridization (Q-FISH) and plasma levels of inflammatory markers in a cohort of 37 patients with MDD and 36 non-psychiatric controls (C). TL was shorter in MDD compared to C (F=8.52, p=0.005). Patients with treatment resistant (TR) MDD showed higher levels of TNFα compared to non-TR (adjusted p= 0.034) and C (adjusted p=0.025), suggesting that treatment resistance might be associated with increased inflammation compared to non-TR.

Diet is a modifiable risk factor for chronic disease and a potential modulator of telomere length (TL). The study aim was to investigate associations between diet quality and TL in Australian adults after a 12-week dietary intervention with an almond-enriched diet (AED). Participants (overweight/obese, 50–80 years) were randomised to an AED (n 62) or isoenergetic nut-free diet (NFD, n 62) for 12 weeks. Diet quality was assessed using a Dietary Guideline Index (DGI), applied to weighed food records, that consists of ten components reflecting adequacy, variety and quality of core food components and discretionary choices within the diet. TL was measured by quantitative PCR in samples of lymphocytes, neutrophils, and whole blood. There were no significant associations between DGI scores and TL at baseline. Diet quality improved with AED and decreased with NFD after 12 weeks (change from baseline AED + 9·8 %, NFD − 14·3 %; P < 0·001). TL increased in neutrophils (+9·6 bp, P = 0·009) and decreased in whole blood, to a trivial extent (–12·1 bp, P = 0·001), and was unchanged in lymphocytes. Changes did not differ between intervention groups. There were no significant relationships between changes in diet quality scores and changes in lymphocyte, neutrophil or whole blood TL. The inclusion of almonds in the diet improved diet quality scores but had no impact on TL mid-age to older Australian adults. Future studies should investigate the impact of more substantial dietary changes over longer periods of time.

Technical challenges associated with telomere length (TL) measurements have prompted concerns regarding their utility as a biomarker of aging. Several factors influence TL assessment via qPCR, the most common measurement method in epidemiological studies, including storage conditions and DNA extraction method. Here, we tested the impact of power supply during the qPCR assay. Momentary fluctuations in power can affect the functioning of high-performance electronics, including real-time thermocyclers. We investigated if mitigating these fluctuations by using an uninterruptible power supply (UPS) influenced TL assessment via qPCR. Samples run with a UPS had significantly lower standard deviation (p < 0.001) and coefficient of variation (p < 0.001) across technical replicates than those run without a UPS. UPS usage also improved exponential amplification efficiency at the replicate, sample, and plate levels. Together these improvements translated to increased performance across metrics of external validity including correlation with age, within-person correlation across tissues, and correlation between parents and offspring.

Telomere integrity is influenced by oxidative stress. Also, inflammation-related factors, including nutritional factors, could modulate telomere integrity. The relationship between a posteriori-derived dietary patterns and telomere length (TL) has been scarcely investigated. Thus, our objective was to examine the association between empirically derived dietary patterns ascertained through principal component analysis (PCA) and TL in an older adult Spanish population. A total of 886 older adults (>55 years old; 645 males and 241 females) from the Seguimiento Universidad de Navarra (SUN) cohort were included in the study. TL was measured by monochrome multiplex real-time quantitative PCR. Age-adjusted TL was used for all analyses. Dietary patterns were identified by PCA based on thirty predefined candidate food groups collected from a validated 136-food items frequency questionnaire. Generalised linear models were fitted to obtain β-coefficients and their 95 % CI evaluating differences in TL between each of the four upper quintiles of adherence to dietary patterns and the lowest quintile. Sensitivity analyses by rerunning all multiple linear models under different stratifications were performed to evaluate the robustness of our results. Two major dietary patterns were empirically identified, Western dietary pattern (WDP) and Mediterranean dietary pattern (MDP). After adjustment for potential confounders, longer TL was found among subjects in the highest quintile of MDP (β = 0·064; 95 % CI 0·004, 0·123). The WDP showed no significant association with TL. In conclusion, higher adherence to a posteriori-derived MDP was independently associated with longer telomeres in an older adult Spanish population of the SUN project.

Telomeres are repeating DNA sequences found on the ends of chromosomes, which shorten with age and are implicated in senescence. Cross-species analyses of telomere shortening rates (TSR) and telomere lengths are important for understanding mechanisms underlying senescence, lifespan and life-history strategies of different species. Whittemore et al. (2019) generated a new dataset on variation in TSR, lifespan and body mass. In phylogenetically uncorrected analyses they found that TSR negatively correlates with lifespan. We re-ran analyses of their dataset using appropriate phylogenetic corrections. We found a strong phylogenetic signal in the association between TSR and body mass. We were able to corroborate Whittemore et al.’s major findings, including while correcting for body mass in a multivariate analysis. Since laboratory mice have different telomere lengths and potentially different telomere dynamics than wild mice, we removed mice from the analysis, which attenuates most associations.

There are limited data on the association between Fe overload and leucocyte telomere length (LTL), known as a useful biomarker of the replicative ageing of cells. The aim of the study was to evaluate associations between Fe-status biomarkers and LTL. A cross-sectional study included 1174 men and women aged 50–79 years who provided blood samples for assays of Fe-status biomarkers including ferritin, transferrin saturation (TSAT), total Fe-binding capacity (TIBC) and relative LTL. They were free of hepatitis, potential infection or Fe deficiency. In multiple linear regression analysis adjusted for potential confounding variables, log-transformed LTL was positively associated with TIBC (adjusted coefficient estimate for its highest quartile: 0·17 (se 0·03), P<0·001) and inversely associated with TSAT (adjusted coefficient estimate for its third and fourth quartiles: −0·09 (se 0·03), P<0·01). These associations were consistent after additional adjustment for serum concentrations of high-sensitivity C-reactive protein, alanine transaminase and aspartate transaminase. In particular, participants with not only abnormally high concentrations (>45 %) but also with high-normal concentrations (35–45 %) of TSAT had shorter LTL compared with those with low-normal concentrations (<30 %) (P<0·05). We also observed that less-active or obese persons with high TSAT concentrations had shorter LTL than others. Our findings that cellular ageing is influenced not only by Fe overload but also by high-normal concentrations of TSAT support the hypothesis regarding the detrimental effects of labile Fe, which has a potent pro-oxidant activity in the body.

Telomere length is widely considered as a marker of biological aging. Clinical studies have reported associations between reduced telomere length and hypertension. The aim of this study was to compare telomere length in hypertensive and normotensive mice at pre-disease and established disease time points to determine whether telomere length differs between the strains before and after the onset of disease. Genomic DNA was extracted from kidney and heart tissues of 4-, 12-, and 20-week-old male hypertensive (BPH/2J) and normotensive (BPN/3J) mice. Relative telomere length (T/S) was measured using quantitative PCR. Age was inversely correlated with telomere length in both strains. In 4-week-old pre-hypertensive animals, no difference in T/S was observed between BPH/2J and BPN/3J animals in kidney or heart tissue (kidney p = 0.14, heart p = 0.06). Once the animals had established disease, at 12 and 20 weeks, BPH/2J mice had significantly shorter telomeres when compared to their age-matched controls in both kidney (12 weeks p < 0.001 and 20 weeks p = 0.004) and heart tissues (12 weeks p < 0.001 and 20 weeks p < 0.001). This is the first study to show that differences in telomere lengths between BPH/2J and BPN/3J mice occur after the development of hypertension and do not cause hypertension in the BPH/2J mice.