Determination of the phenotypic age in residents of Mexico City: effect of accelerated ageing on lung function and structure

Abstract

IntroductionPhenotypic age better represents age-related biological dysregulation than chronological age. Recently, a multisystem-based ageing measure, which integrates chronological age and nine biomarkers, was proposed.MethodsPhenotypic age was determined in 774 residents of Mexico City over 60 years old and without respiratory problems. We arbitrarily classified as “accelerated” ageing, those showing >4 years compared with their chronological age, and “slowed” ageing, those with <4 years compared with chronological age. Demographic risk factors were analysed with structured questionnaires. Lung structure was evaluated by high-resolution computed tomography and functional competence was analysed by forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), diffusion capacity of carbon monoxide (DLCO), and the 6-minute walk test (6MWT).ResultsOverall, 13% of this cohort showed accelerated ageing, which was corroborated with four independent biomarkers of ageing, 42% had normal ageing and 46% had slowed ageing. Risk factors associated with accelerated ageing were male sex (OR 4.4, 95% CI 2.4–7.9; p<0.01), diabetes mellitus (OR 9.7, 95% CI 5.5–17.2; p<0.01), and long-term sleep duration (OR 2.9 95% CI 1.34–6.35, p<0.01). Among smokers, there was a slight but significant association with the number of pack-years. Subjects with accelerated ageing showed decreased FVC (p<0.0001), FEV1 (p<0.0001), DLCO (p<0.02) and walking distance in the 6MWT (p=0.0001). Slowed-ageing subjects presented less frequently with emphysematous lesions compared with those with accelerated ageing.ConclusionsA small but significant proportion of residents of Mexico City age rapidly, which is associated with male sex, diabetes, and long-term sleep duration. They exhibit lower levels of lung function and develop emphysema more frequently.

Association of Unhealthy Lifestyle and Childhood Adversity With Acceleration of Aging Among UK Biobank Participants

“…The phenotypic age equation has been widely used in literature over recent years, and it shows that phenotypic age captures morbidity and mortality risk in many populations from different countries . Phenotypic age acceleration was calculated as a residual of phenotypic age adjusted for chronological age by linear regression.…”

“…The phenotypic age equation has been widely used in literature over recent years, and it shows that phenotypic age captures morbidity and mortality risk in many populations from different countries. 31,32 Phenotypic age acceleration was calculated as a residual of phenotypic age adjusted for chronological age by linear regression. Participants with phenotypic age acceleration value greater than 0 were defined as phenotypically older, whereas those with phenotypic age acceleration value less than 0 were defined as phenotypically younger.…”

Differential Genomic Profile in TERT, DSP, and FAM13A Between COPD Patients With Emphysema, IPF, and CPFE Syndrome

“…Recruitment was carried out in the period 2013–2019. The control group from the pulmonary aging cohort was randomly selected ( 18 ), matching the variables of age, sex ratio, and smoking history of the IPF group. All subjects are defined as pulmonary healthy by spirometry (using the reference values of Pérez-Padilla) or imaging ( 20 ).…”

“…In this case-control study, a total of 828 participants divided into three groups of patients were included; COPD smokers (COPD-S), Idiopathic Pulmonary Fibrosis (IPF) patients, and subjects with Combined Pulmonary Fibrosis and Emphysema (CPFE) syndrome diagnosis; as a control groups, smokers without COPD (SWOC), and healthy subjects belonging to the Pulmonary Aging Cohort (PAC) (18,19) over 50 years were included.…”

Cancer Treatment-Induced Accelerated Aging in Cancer Survivors: Biology and Assessment

“…Several clinical and biological measures have been proposed to capture the biological age, including gait speed, grip strength, TUG, 6MW, Fried (Cardiovascular Health Study) Frailty Phenotype, Deficit Accumulation Index/Frailty Index, clinical geriatric assessment, cognitive assessments (e.g., Hopkins Verbal Learning, Controlled Oral Word, the Trail Making Test, etc. ), fatigability, APOE4, 31p recovery time, telomere length, chronic inflammatory biomarkers, maximal oxygen consumption, sarcopenia, phenotypic age, allostatic load, biomarkers of cellular senescence, and aging clocks [ 9 , 10 , 42 , 70 , 71 , 72 ]. In this review, we will focus on three important biomarkers for aging: epigenetic clock, proteomic aging clock, and two critical biomarkers of cellular senescence—p16 IKN4a and ARF (an alternate reading frame protein product of the CDKN2A locus, also known as P14 ARF in humans and P19 ARF in mice) ( Figure 2 ).…”