Biology subjects

O'Keeffe, L. M.

Publications and source records attributed to O'Keeffe, L. M..

3 recordsLinked to original sources

bioRxiv2019

Age at period cessation and trajectories of cardiovascular risk factors across mid and later life: a prospective cohort study

What is already known about this topicAge at period cessation is associated with cardiovascular disease. Whether age at period cessation adversely affects change in conventional cardiovascular intermediates from mid to later life is not well understood.\n\nWhat this study addsWomen and clinicians concerned about the impact of type and timing of period cessation on conventional cardiovascular intermediates from midlife should be reassured that the impacts over the long term are small.\n\nAbstractO_ST_ABSObjectiveC_ST_ABSTo examine the association between age at period cessation (by type of period cessation) and trajectories of anthropometry, blood pressure, lipids and HBA1c from midlife.\n\nDesignProspective cohort study of women recruited to the Medical Research Council National Survey of Health and Development (NSHD).\n\nSettingPopulation based prospective cohort study.\n\nParticipantsWomen participating in NSHD with a known date of period cessation and at least one measure of each intermediate cardiovascular risk factor.\n\nExposuresAge at period cessation and type of period cessation (hysterectomy compared with natural menopause).\n\nOutcomesRepeated measures of systolic blood pressure, diastolic blood pressure, body mass index (BMI) and waist circumference (WC) from 36 to 69 years and repeated measures of triglyceride, low density lipoprotein cholesterol (LDL-c), high density lipoprotein cholesterol (HDL-c) and glycated haemoglobin (HBA1c) from 53 to 69 years.\n\nResultsWe found no evidence that age at period cessation was associated with trajectories of log triglyceride, LDL-c and HDL-c from 53 to 69 years and trajectories of blood pressure from 36 to 69 years, regardless of whether period cessation occurred naturally or due to hysterectomy. While we found some evidence of associations of age at period cessation with log BMI, log WC and log HBA1C, patterns were not consistent and differences were small at age 69 years, with confidence intervals that spanned the null. For instance, the difference in log WC at age 69 per year increase in age at natural menopause was 0.003 (95% confidence interval, -0.0002, 0.01) while the difference per year increase in age at hysterectomy was -0.002 (95% CI, -0.005, 0.001).\n\nConclusionHow and when women experience period cessation is unlikely to adversely affect conventional cardiovascular risk factors across mid and later life. Women and clinicians concerned about the impact of type and timing of period cessation on conventional cardiovascular intermediates from midlife should be reassured that the impacts over the long term are small.

epidemiology↗

bioRxiv2019

Epigenetic gestational age and trajectories of weight and height during childhood: a prospective cohort study

BackgroundDifferences between an individuals estimated epigenetic gestational age (EGA) and their actual gestational age (GA) are defined as gestational age acceleration (GAA). GAA is associated with increased birthweight and birth length. Whether these associations persist through childhood is yet to be investigated.\n\nMethodsWe examined the association between GAA and trajectories of height and weight from birth to 10 years (n=785) in a British birth cohort study, the Avon Longitudinal Study of Parents and Children (ALSPAC). EGA of participants was estimated using DNA methylation data from cord blood using a recently-developed prediction model. GA of participants was gathered in ALSPAC from clinical records and was measured from last menstrual period (LMP) for most participants. GAA of participants, measured in weeks, was calculated as the residuals from a regression model of EGA on actual GA. Height and weight were obtained from several sources including birth records, research clinics, routine child health clinics, links to health visitor records and parent-reported measures from questionnaires. Analyses were performed using linear spline multilevel models and adjusted for maternal age, maternal pre-pregnancy BMI, maternal smoking during pregnancy and maternal education.\n\nResultsIn adjusted analyses, offspring with a one-week greater GAA were born on average 0.14 kg heavier (95% Confidence Interval (CI) 0.09, 0.19) and 0.55 cm taller (95% CI 0.33, 0.78) at birth. These differences in weight persisted up to approximately age 9 months but thereafter began to attenuate and reduce in magnitude. From age 5 years onwards, the association between GAA and weight reversed such that GAA was associated with lower weight and this association strengthened with age (mean difference at age 10 years -0.60 kg (95% CI, -1.19, -0.01)). Differences in height persisted only up to age 9 months (mean difference at 9 months 0.15 cm, (95% CI -0.09, 0.39)). From age 9 months to age 10 years, offspring with a one-week greater GAA were of comparable height to those with no GAA (mean difference at age 10 years -0.07 cm, (95% CI -0.64, 0.50)).\n\nConclusionsGestational age acceleration is associated with increased birth weight and length and these differences persist to age 9 months. From 5 years onwards, the association of GAA and weight reverses such that by age 10 years greater GAA is associated with lower childhood weight. Further work is required to examine whether the weight effects of GAA strengthen further through adolescence and into early adulthood.

genomics↗

bioRxiv2019

Puberty timing and adiposity change across childhood and adolescence: disentangling cause and consequence

ObjectiveTo better understand if earlier puberty is more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood.\n\nDesignProspective birth cohort study.\n\nSettingPopulation based study of children born in 1991/1992 in Bristol UK (Avon Longitudinal Study of Parents and Children (ALSPAC)).\n\nParticipants4,186 participants (2,176 female and 1,990 male) of predominantly White ethnicity with 18,232 repeated measures throughout follow-up.\n\nExposures & outcomesRepeated measures of height from 5y to 20y to identify puberty timing (age at peak height velocity) and repeated measures of dual-energy X-ray absorptiometry-derived fat mass from age 9y to 18y, modelled separately in females and males using models based on chronological age and time before and after puberty onset.\n\nResultsMean age at peak height velocity was 11.7y (standard deviation (SD)=0.8y) for females and 13.6y (SD=0.9y) for males. In adjusted models of fat mass by chronological age, a one-year later age at peak height velocity was associated with 20.4% (95% Confidence Interval (CI): 18.5% to 22.3%) and 22.8% (95% (CI): 20.7% to 24.8%) lower fat mass in females and males respectively at 9y. These differences were smaller at age 18y: 7.8% (95% (CI):5.9% to 9.6%) and 11.9% (95% (CI): 9.1%, to 14.7%) lower fat mass in females and males respectively per year later age at peak height velocity. Trajectories of fat mass by time before and after puberty onset provided strong evidence for an association of pre-pubertal fat mass with puberty timing, and little evidence of an association of puberty timing with post-pubertal changes in fat mass in females. In males, findings were less clear before puberty though there was some evidence for an association of earlier puberty timing with great post-pubertal gain in fat mass.\n\nConclusionsEarlier puberty is more likely a result of adiposity gain in childhood than a cause of adiposity gain in adulthood in females. In males early to puberty, differences in fat mass after puberty are driven partially by tracking of adiposity from early childhood but also greater gains in post-pubertal adiposity. Reducing levels of childhood adiposity may help prevent both earlier puberty, later life adiposity and their associated adverse social, mental and physical health sequelae.

epidemiology↗