1,720,963 research outputs found
Omgeving en leefstijfactoren: al vroeg in het leven van invloed op telomeerlengte
No full textTelomeren zij n de beschermende uiteinden van chromosomen en nemen in lengte af naarmate we verouderen. Telomeren zij n een indicator voor de gevoeligheid om ouderdomsgerelateerde ziekten te ontwikkelen. Verschillen in telomeerlengtes worden voornamelij k verklaard door een complex samen-spel van genetische, leefstij l-en omgevingsfactoren. Eerdere studies toonden aan dat een gezonde leefstij l belangrij k is in termen van ziektepreventie. Recent onderzoek toont aan dat leefstij l ook in verband wordt gebracht met essentiële biologische processen die betrokken zij n bij veroudering, zoals telomeerverkorting. Dit kan gedeeltelij k verklaren waarom er een verband is tussen leefstij l en ontwik-keling van ziekten. Dit benadrukt dat een gezonde leefstij l niet alleen direct bij draagt aan het voorkomen van ziekten, maar ook indirect via biologische processen die de veroudering reguleren en daarbij de gevoeligheid voor het ontstaan van ziekte verminderen. Deze omgevings-en leefstij lfactoren kunnen al voor de geboorte aanzienlij k invloed uitoefenen op de variatie in telomeerlengte bij pasgeborenen. Hoewel bij de geboorte ieder kind even oud is, is dat niet zo als we kij ken naar de biologische leeftij d op basis van de lengte van de telomeren. Met andere woorden, de lengte van de telomeren bij de geboorte vormt één van de mechanismen die verschillen in veroudering en ziektegevoeligheid gedurende het le-ven mee bepalen. Dit benadrukt het belang van een gezonde leefstij l en omgeving voor het bevorderen van een lang en gezond leven vanaf de preconceptie, niet alleen voor onszelf, maar ook voor toekomstige generaties. (NED TIJ DSCHR LEEFSTIJ LGENEESKD 2025;3(2):69-75) 1 PhD-student, 2 hoogleraar faculteit Wetenschappen, 3 gast FWO postdoctoraal onderzoeker, 4 Centrum voor Milieukunde, Universiteit Hasselt, Hasselt, België, 5 departement Maatschappelij ke Gezondheidszorg en Eerstelij nszorg, KU Leuven, Leuven, België. Correspondentie graag richten aan: dhr. prof. dr. T.S. Nawrot, Universiteit Hasselt, Centrum voor Milieukunde, Agoralaan gebouw D, 3590 Diepenbeek, België, tel: +32 490 57 70 13, e-mailadres: [email protected] Belangenconflict: geen gemeld. Financiële ondersteuning: D.S. Martens is houder van een postdoctoraatbeurs bij het Fonds Wetenschap-pelij k Onderzoek-Vlaanderen (FWO 12X9623N). Trefwoorden: gezondheid, leefstij lfactoren, preventie, telomeerlengte, veroudering
Omgeving en leefstijfactoren: al vroeg in het leven van invloed op telomeerlengte
No full textTelomeren zij n de beschermende uiteinden van chromosomen en nemen in lengte af naarmate we verouderen. Telomeren zij n een indicator voor de gevoeligheid om ouderdomsgerelateerde ziekten te ontwikkelen. Verschillen in telomeerlengtes worden voornamelij k verklaard door een complex samen-spel van genetische, leefstij l-en omgevingsfactoren. Eerdere studies toonden aan dat een gezonde leefstij l belangrij k is in termen van ziektepreventie. Recent onderzoek toont aan dat leefstij l ook in verband wordt gebracht met essentiële biologische processen die betrokken zij n bij veroudering, zoals telomeerverkorting. Dit kan gedeeltelij k verklaren waarom er een verband is tussen leefstij l en ontwik-keling van ziekten. Dit benadrukt dat een gezonde leefstij l niet alleen direct bij draagt aan het voorkomen van ziekten, maar ook indirect via biologische processen die de veroudering reguleren en daarbij de gevoeligheid voor het ontstaan van ziekte verminderen. Deze omgevings-en leefstij lfactoren kunnen al voor de geboorte aanzienlij k invloed uitoefenen op de variatie in telomeerlengte bij pasgeborenen. Hoewel bij de geboorte ieder kind even oud is, is dat niet zo als we kij ken naar de biologische leeftij d op basis van de lengte van de telomeren. Met andere woorden, de lengte van de telomeren bij de geboorte vormt één van de mechanismen die verschillen in veroudering en ziektegevoeligheid gedurende het le-ven mee bepalen. Dit benadrukt het belang van een gezonde leefstij l en omgeving voor het bevorderen van een lang en gezond leven vanaf de preconceptie, niet alleen voor onszelf, maar ook voor toekomstige generaties. (NED TIJ DSCHR LEEFSTIJ LGENEESKD 2025;3(2):69-75) 1 PhD-student, 2 hoogleraar faculteit Wetenschappen, 3 gast FWO postdoctoraal onderzoeker, 4 Centrum voor Milieukunde, Universiteit Hasselt, Hasselt, België, 5 departement Maatschappelij ke Gezondheidszorg en Eerstelij nszorg, KU Leuven, Leuven, België. Correspondentie graag richten aan: dhr. prof. dr. T.S. Nawrot, Universiteit Hasselt, Centrum voor Milieukunde, Agoralaan gebouw D, 3590 Diepenbeek, België, tel: +32 490 57 70 13, e-mailadres: [email protected] Belangenconflict: geen gemeld. Financiële ondersteuning: D.S. Martens is houder van een postdoctoraatbeurs bij het Fonds Wetenschap-pelij k Onderzoek-Vlaanderen (FWO 12X9623N). Trefwoorden: gezondheid, leefstij lfactoren, preventie, telomeerlengte, veroudering
Prenatal air pollution exposure in relation to the telomere-mitochondrial axis of aging at birth: A systematic review
No full textBackground
Telomere length (TL) and mitochondrial DNA (mtDNA) are central markers of vital biological mechanisms, including cellular aging. Prenatal air pollution exposure may impact molecular markers of aging leading to adverse health effects.
Objective
To perform a systematic review on human population-based studies investigating the association between prenatal air pollution exposure and TL or mtDNA content at birth.
Methodology
Searches were undertaken on PubMed and Web of Science until July 2023. The framework of the review was based on the PRISMA-P guidelines.
Results
Nineteen studies studied prenatal air pollution and TL or mtDNA content at birth. Studies investigating TL or mtDNA content measured at any other time or did not evaluate prenatal air pollution were excluded. Twelve studies (including 4381 participants with study sample range: 97 to 743 participants) investigated newborn TL and eight studies (including 3081 participants with study sample range: 120 to 743 participants) investigated mtDNA content at birth. Seven studies focused on particulate matter (PM2.5) exposure and newborn TL of which all, except two, showed an inverse association in at least one of the gestational trimesters. Of the eight studies on mtDNA content, four focused on PM2.5 air pollution with two of them reporting an inverse association. For PM2.5 exposure, observations on trimester-specific effects were inconsistent. Current literature showing associations with other prenatal air pollutants (including nitrogen oxides, sulfur dioxide, carbon monoxide and ozone) is inconsistent.
Conclusion
This review provides initial evidence that prenatal PM2.5 exposure impacts the telomere-mitochondrial axis of aging at birth. The current evidence did not reveal harmonious observations for trimester-specific associations nor showed consistent effects of other air pollutants. Future studies should elucidate the specific contribution of prenatal exposure to pollutants other than PM in relation to TL and mtDNA content at birth, and the potential later life health consequences.This study has received funding from the European Union’s Horizon 2020 research and innovation programme ‘SURREAL’ under grant agreement No 956780. TSN holds funding by Methusalem. SD holds funding by National Institutes of Health (NIH U24AG066528). DSM holds a postdoctoral grant by the Research Foundation-Flanders (FWO12X9623N)
Telomere length in early childhood and its association with attention: a study in 4–6 year old children
Full text linkTelomere length (TL), a marker of cellular aging, has been studied in adults with regard to its connection to cognitive function. However, little is known about the association between TL and cognitive development in children. This study investigated the interplay between TL and cognitive functioning in 283 Belgian children aged four to six years of the Environmental Influence on Aging in Early Life (ENVIRONAGE) birth cohort. Child leukocyte TL was measured using qPCR, while cognitive functioning, including attention and memory, was assessed using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Linear regression models were employed to examine the association between TL and cognitive outcomes, adjusting for potential confounders. We found an inverse association between TL and the spatial errors made during the Motor Screening task (p = 0.017), indicating a higher motor accuracy in children with longer telomeres. No significant associations were found between TL and other cognitive outcomes. Our results suggest a specific link between TL and motor accuracy but not with the other cognitive domains
The telomere-mitochondrial axis of aging in newborns
No full textAging starts at the beginning of life as evidenced by high variability in telomere length (TL) and mitochondrial DNA content (mtDNAc) at birth. Whether p53 and PGC-1α are connected to these age-related markers in early life is unclear. In this study, we hypothesized that these hallmarks of aging are associated at birth. In 613 newborns from the ENVIRONAGE birth cohort, p53 and PGC-1α protein levels were measured in cord plasma, while TL and mtDNAc were measured in both cord blood and placental tissue. Cord blood methylation data of genes corresponding to the measured protein levels were available from the Human MethylationEPIC 850K BeadChip array. Pearson correlations and linear regression models were applied while accounting for selected covariates. In cord, a 10% increase in TL was associated with 5.22% (95% CI: 3.26 to 7.22; p < 0.0001) higher mtDNAc and -2.66% (95% CI: -5.04 to -0.23%; p = 0.032) lower p53 plasma level. In placenta, a 10% increase in TL was associated with 5.46% (95% CI: 3.82 to 7.13%; p < 0.0001) higher mtDNAc and -2.42% (95% CI: -4.29 to -0.52; p = 0.0098) lower p53 plasma level. Methylation level of TP53 was correlated with TL and mtDNAc in cord blood and with cord plasma p53 level. Our study suggests that p53 may be an important factor both at the protein and methylation level for the telomere-mitochondrial axis of aging at birth.sponsorship: The authors thank the participating women and neonates, as well as the staff of the maternity ward, midwives, and the staff of the clinical laboratory of East-Limburg Hospital in Genk. The ENVIRONAGE birth cohort is supported by the Flemish Scientific Fund (FWO, Grant No. N1518119, No. G082317N and No. 1523817N) and Kom Op Tegen Kanker (KOTK). Dries S. Martens is a postdoctoral fellow funded by the Research Foundation Flanders (FWO, 12X9620N). Bram G. Janssen and Sabine A.S. Langie were the beneficiary of a post-doctoral fellowship (12W3218N and 12L5216N respectively) also provided by the FWO. (Flemish Scientific Fund (FWO)|N1518119, Flemish Scientific Fund (FWO)|G082317N, Flemish Scientific Fund (FWO)|1523817N, Kom Op Tegen Kanker (KOTK), Research Foundation Flanders (FWO)|12X9620N, Research Foundation Flanders (FWO)|12W3218N, Research Foundation Flanders (FWO)|12L5216N)status: Publishe
The association between ambient particulate matter exposure and the telomere–mitochondrial axis of aging in newborns
No full textBackground: Particulate matter (PM) is associated with aging markers at birth, including telomeres and mitochondria. It is unclear whether markers of the core-axis of aging, i.e. tumor suppressor p53 (p53) and peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1α), are associated with prenatal air pollution and whether there are underlying mechanisms. Methods: 556 mother-newborn pairs from the ENVIRONAGE birth cohort were recruited at the East Limburg Hospital in Genk (Belgium). In placenta and cord blood, telomere length (TL) and mitochondrial DNA content (mtDNAc) were measured using quantitative real-time polymerase chain reaction (qPCR). In cord plasma, p53 and PGC-1α protein levels were measured using ELISA. Daily ambient PM2.5 concentrations during gestation were calculated using a spatial temporal interpolation model. Distributed lag models (DLMs) were applied to assess the association between prenatal PM2.5 exposure and each molecular marker. Mediation analysis was performed to test for underlying mechanisms. Results: A 5 µg/m3 increment in PM2.5 exposure was associated with −11.23 % (95 % CI: −17.36 % to −4.65 %, p = 0.0012) and −7.34 % (95 % CI: −11.56 % to −2.92 %, p = 0.0014) lower placental TL during the entire pregnancy and second trimester respectively, and with −12.96 % (95 % CI: −18.84 % to −6.64 %, p < 0.001) lower placental mtDNAc during the third trimester. Furthermore, PM2.5 exposure was associated with a 12.42 % (95 % CI: −1.07 % to 27.74 %, p = 0.059) higher cord plasma p53 protein level and a −3.69 % (95 % CI: −6.97 % to −0.31 %, p = 0.033) lower cord plasma PGC-1α protein level during the third trimester. Placental TL mediated 65 % of the negative and 17 % of the positive association between PM2.5 and placental mtDNAc and cord plasma p53 protein levels, respectively. Conclusion: Ambient PM2.5 exposure during pregnancy is associated with markers of the core-axis of aging, with TL as a mediating factor. This study strengthens the hypothesis of the air pollution induced core-axis of aging, and may unravel a possible underlying mediating mechanism in an early-life epidemiological context
Residential green space is associated with a buffering effect on stress responses during the COVID-19 pandemic in mothers of young children, a prospective study
No full textGreen spaces are associated with increased well-being and reduced risk of developing psychiatric disorders. In this study, we aimed to investigate how residential proximity to green spaces was associated with stress response buffering during the COVID-19 pandemic in a prospective cohort of young mothers. We collected information on stress in 766 mothers (mean age: 36.6 years) from the ENVIRONAGE birth cohort at baseline of the study (from 2010 onwards), and during the COVID-19 pandemic (from December 2020 until May 2021). Self-reported stress responses due to the COVID-19 pandemic were the outcome measure. Green space was quantified in several radiuses around the residence based on high-resolution (1 m2) data. Using ordinal logistic regression, we estimated the odds of better resistance to reported stress, while controlling for age, socio-economic status, stress related to care for children, urbanicity, and household change in income during the pandemic. In sensitivity analyses we corrected for pre-pandemic stress levels, BMI, physical activity, and changes in health-related habits during the pandemic. We found that for an inter-quartile range contrast in residential green space 300 m and 500 m around the residence, participants were respectively 24% (OR = 1.24, 95%CI: 1.03 to 1.51) and 29% (OR = 1.29, 95%CI: 1.04 to 1.60) more likely to be in a more resistant category, independent of the aforementioned factors. These results remained robust after additionally controlling for pre-pandemic stress levels, BMI, physical activity, smoking status, urbanicity, psychological disorders, and changes in health-related habits during the pandemic. This prospective study in young mothers highlights the importance of proximity to green spaces, especially during challenging times.status: Publishe
Different epigenetic signatures of newborn telomere length and telomere attrition rate in early life
No full textTelomere length (TL) and telomere shortening are biological indicators of aging, and epigenetic associates have been found for TL in adults. However, the role of epigenetic signatures in setting newborn TL and early life telomere dynamics is unknown. In the present study, based on 247 participating newborns from the ENVIRONAGE birth cohort, whole-genome DNA methylation, profiled on the Illumina MethylationEPIC BeadChip microarray, and TL were measured in cord blood. In a follow-up visit at a mean age of 4.58 years, leukocyte TL was evaluated. We combined an epigenome-wide association study and a statistical learning method with re-sampling to select CpGs and their two-way interactions to model baseline (cord blood) TL and early-life telomere attrition rate, where distinct epigenetic signatures were identified for the two outcomes. In addition, a stronger epigenetic regulation was suggested in setting newborn TL than that of telomere dynamics in early life: 47 CpGs and 7 between-CpG interactions explained 76% of the variance in baseline TLs, while 72% of the total variance in telomere attrition rate was explained by 31 CpGs and 5 interactions. Functional enrichment analysis based on the selected CpGs in the two models revealed GLUT4 translocation and immune cell signaling pathways, respectively. These CpGs and interactions, as well as the cellular pathways, are potential novel targets of further investigation of telomere biology and aging
Newborn telomere length predicts later life telomere length: Tracking telomere length from birth to child- and adulthood
No full textBACKGROUND: Telomere length (TL) is considered a biological marker of aging and may indicate age-related disease susceptibility. Adults and children show a fixed ranking and tracking of TL over time. However, the contribution of an individual's initial birth TL to their later life TL is unknown. We evaluated change and tracking of TL from birth to child- and adulthood. METHODS: Telomere length at birth was measured using qPCR in two independent prospective birth cohorts. After a median follow-up period of 4 years in ENVIRONAGE (n = 273) we assessed leukocyte telomere length (LTL) and after 23 years in EFPTS (n = 164) buccal TL was assessed. Correlations and multivariable regression models were applied to study telomere tracking and determinants of TL change from birth onwards. FINDINGS: In children, LTL at the age of 4 correlates with TL at the start of life both in cord blood (r = 0.71, P < 0.0001;) and placenta (r = 0.60, P < 0.0001) and was -11.2% and -33.1% shorter, respectively. In adulthood, buccal TL at the age of 23 correlates with placental TL (r = 0.46, P < 0.0001) and was -35.9% shorter. TL attrition was higher in individuals with longer birth TL. However, based on TL ranking, individuals do not tend to change dramatically from TL rank after 4 or 23 years of follow-up. Finally, longer maternal TL associates with lower telomere attrition in the next generation. INTERPRETATION: The high prediction of newborn TL for later life TL, and stable TL ranking from birth onwards underscores the importance of understanding the initial setting of newborn TL and its significance for later life. FUNDING: European Research Council (ERC-StG310898) and Flemish Scientific Fund (12X9620N).sponsorship: This research was funded by European Research Council (ERCStG310898) and the Flemish Scientific Fund (FWO). Dries Martens holds a postdoctoral grant by the Flemish Scientific Fund (FWO grant 12X9620N). The researchers would like to thank all the ENVIRONAGE follow-up study researchers. (European Research Council|ERCStG310898, Flemish Scientific Fund (FWO), Flemish Scientific Fund (FWO)|12X9620N)status: Publishe
Successful Lung Transplantation from a 94-Years-Old Donor Questions the Discussion on Calendar versus Biological Age
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