Intelligence in childhood and atherosclerosis of the carotid and peripheral arteries in later life: the Lothian Birth Cohort 1936.
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ABSTRACT:
SUBMITTER: Gale CR
PROVIDER: S-EPMC4411126 | biostudies-other | 2015
REPOSITORIES: biostudies-other
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Project description:We examined reciprocal, time-ordered associations between age-related changes in fluid intelligence and depressive symptoms. Participants were 1,091 community-dwelling older adults from the Lothian Birth Cohort 1936 study who were assessed repeatedly at 3-year intervals between the ages of 70 and 79 years. On average, fluid intelligence and depressive symptoms worsened with age. There was also a dynamic-coupling effect, in which low fluid intelligence at a given age predicted increasing depressive symptoms across the following 3-year interval, whereas the converse did not hold. Model comparisons showed that this coupling parameter significantly improved overall fit and had a correspondingly moderately strong effect size, accounting on average for an accumulated 0.9 standard-deviation increase in depressive symptoms, following lower cognitive performance, across the observed age range. Adjustment for sociodemographic and health-related covariates did not significantly attenuate this association. This implies that monitoring for cognitive decrements in later life may expedite interventions to reduce related increases in depression risk.
| S-EPMC6291904 | biostudies-other
Project description:BackgroundInformation on childhood determinants of frailty or allostatic load in later life is sparse. We investigated whether lower intelligence and greater socioeconomic disadvantage in childhood increased the risk of frailty and higher allostatic load, and explored the mediating roles of adult socioeconomic position, educational attainment and health behaviours.MethodsParticipants were 876 members of the Lothian Birth Cohort 1936 whose intelligence was assessed at age 11. At age 70, frailty was assessed using the Fried criteria. Measurements were made of fibrinogen, triglyceride, total and high-density lipoprotein cholesterol, albumin, glycated haemoglobin, C reactive protein, body mass index and blood pressure, from which an allostatic load score was calculated.ResultsIn sex-adjusted analyses, lower intelligence and lower social class in childhood were associated with an increased risk of frailty: relative risks (95% CIs) were 1.57 (1.21 to 2.03) for a SD decrease in intelligence and 1.48 (1.12 to 1.96) for a category decrease in social class. In the fully adjusted model, both associations ceased to be significant: relative risks were 1.13 (0.83 to 1.54) and 1.19 (0.86 to 1.61), respectively. Educational attainment had a significant mediating effect. Lower childhood intelligence in childhood, but not social class, was associated with higher allostatic load. The sex-adjusted coefficient for allostatic load for a SD decrease in intelligence was 0.10 (0.07 to 0.14). In the fully adjusted model, this association was attenuated but remained significant (0.05 (0.01 to 0.09)).ConclusionsFurther research will need to investigate the mechanisms whereby lower childhood intelligence is linked to higher allostatic load in later life.
| S-EPMC4820036 | biostudies-literature
Project description:BackgroundPrevious results have been mixed regarding the role of the apolipoprotein E e4 (APOE e4) allele in later-life depression: some studies note that carriers experience greater symptoms and increased risk while others find no such association. However, there are few prospective, population-based studies of the APOE e4-depression association and fewer that examine depressive symptom trajectory and depression risk longitudinally. We examined the association between APOE e4 allele status and longitudinal change in depressive symptoms and depression risk in later-life, over a 12-year follow-up period.MethodsWe used data from 690 participants of the Lothian Birth Cohort 1936 who took part in the Scottish Mental Survey 1947 (aged 11) and were followed-up in later-life over five waves from 2004 to 2019 (aged 70-82). We used APOE e4 allele status to predict longitudinal change in depressive symptom scores and risk of depression (defined by a symptom score threshold or use of depression-related medication). Models were adjusted for sex, childhood cognitive ability, childhood social class, education, adult social class, smoking status and functional limitations at baseline.ResultsDepressive symptom scores increased with age. Once adjusted for covariates, APOE e4 allele status did not significantly predict symptom score trajectories or depression risk. Greater functional limitations at baseline significantly predicted poorer symptom score trajectories and increased depression risk (defined by medications). APOE e4 allele status did not significantly moderate the contribution of sex, education or functional limitations.ConclusionsThere was no evidence that APOE e4 carriers experience an increased risk for later-life depression.
| S-EPMC9811345 | biostudies-literature
Project description:Objectivesthe 'triad of impairment' phenomenon describes the co-occurrence of age-related cognitive, emotional and physical functioning deficits. We investigated how occupational profile and childhood intelligence contribute to the triad of impairment in late life.Methodswe analysed data of a subsample of the Aberdeen Birth Cohort of 1936 (n = 346). Data were collected on participants' childhood intelligence, late-life cognitive ability, physical functioning, depressive symptoms and main lifetime occupation. We summarised the various occupational and impairment measures into two latent variables, 'occupational profile' and the 'triad of impairment'. We used a series of data reduction approaches and structural equation models (SEMs) of increasing complexity to test both the validity of the models and to understand causal relationships between the life-course risks for the triad of impairment.Resultsoccupational profile had a significant effect on the triad of impairment independent of childhood intelligence. Childhood intelligence was the predominant influence on the triad of impairment and exerted its effect directly and indirectly via its influence on occupation. The direct effect of childhood intelligence exceeded the independent influence of the occupational profile on impairment by a factor of 1.7-1.8 and was greater by a factor of ?4 from the indirect pathway (via occupation).Conclusionschildhood intelligence was the predominant influence on the triad of impairment in late life, independently of the occupational profile. Efforts to reduce impairment in older adults should be informed by a life-course approach with special attention to the early-life environment.
| S-EPMC4916342 | biostudies-literature
Project description:BACKGROUND AND AIMS:While numerous cross-sectional studies have demonstrated an inverse relationship between cardiorespiratory fitness (CRF) and carotid atherosclerosis in middle age, much less is known about the association of midlife CRF with carotid atherosclerosis in later life. METHODS:We studied 1094 participants, free of cardiovascular disease, who completed a maximal exercise test (GXT) for an objective measure of CRF between ages 40 and 59 and carotid ultrasound after the age of 59, with at least five years between studies. Carotid intima media thickness was measured. Assessments were also made regarding the presence of plaque and percent stenosis in four regions: common carotid, bulb, internal carotid and external carotid arteries. Multivariable logistic regression models were constructed to estimate the association of CRF with carotid artery disease. RESULTS:At the time of GXT and carotid scan, participants were aged 50.7?±?5.7 years and 69.3?±?6.4 years, respectively. Almost half of participants had high midlife CRF (48.6%); 41.3% and 10.1% had moderate and low CRF, respectively. Over a mean follow-up period of 18.6?±?8.5 years, the odds of having carotid artery disease in later life in the high CRF group was 0.50 (95% CI: 0.29-0.87) compared with the low CRF group. Each 1 MET increase in CRF was associated with 10% lower odds of having carotid artery disease (OR?=?0.89, 95% CI: 0.80-0.98). CONCLUSIONS:Midlife CRF was inversely associated with carotid artery disease measured almost two decades later. This may represent a mechanistic link between high midlife CRF and reduced risk of stroke in later life.
| S-EPMC6935373 | biostudies-literature
Project description:The identification of biomarkers that discriminate individual ageing trajectories is a principal target of ageing research. Some of the most promising predictors of biological ageing have been developed using DNA methylation. One recent candidate, which tracks age-related phenotypes in addition to chronological age, is 'DNAm PhenoAge'. Here, we performed a phenome-wide association analysis of this biomarker in a cohort of older adults to assess its relationship with a comprehensive set of both historical, and contemporaneously-measured, phenotypes. Higher than expected DNAm PhenoAge compared with chronological age, known as epigenetic age acceleration, was found to associate with a number of blood, cognitive, physical fitness and lifestyle variables, and with mortality. Notably, DNAm PhenoAge, assessed at age 70, was associated with cognitive ability at age 11, and with educational attainment. Adjusting for age 11 cognitive ability attenuated the majority of the cross-sectional later-life associations between DNAm PhenoAge and health outcomes. These results highlight the importance of early life factors on healthy older ageing.
| S-EPMC6883059 | biostudies-literature
Project description:BackgroundLower childhood intelligence test scores are reported in some studies to be associated with higher risk of depression in adulthood. The reasons for the association are unclear. This longitudinal data-linkage study explored the relationship between childhood intelligence (at age ∼11) and risk of depression in later-life (up to age ∼85), and whether childhood family structure and adulthood socio-economic and geographical factors accounted for some of this association.MethodsIntelligence test scores collected in the Scottish Mental Survey 1947 were linked to electronic health records (hospital admissions and prescribing data) between 1980 and 2020 (n = 53,037), to identify diagnoses of depression. Mixed-effect Cox regression models were used to explore the relationship between childhood intelligence test scores and risk of depression in later-life. Analyses were also adjusted for childhood family structure (size of family) and adulthood socio-economic and geographical factors (Carstairs index, urban/rural).ResultsTwenty-seven percent of participants were diagnosed with depression during follow-up (n = 14,063/53,037). Greater childhood intelligence test scores were associated with a reduced risk of depression in an unadjusted analysis (HR = 0.95, 95% CI = 0.93 to 0.97, P < 0.001), and after adjustment for factors experienced in childhood and adulthood (HR = 0.95, 95% CI = 0.91 to 1.00, P = 0.032). When identifying depression using only hospital admissions data, greater childhood intelligence test scores were associated with a reduced risk of depression following unadjusted analysis (HR = 0.86, 95% CI = 0.82 to 0.90, P < 0.001), and after adjusting for risk factors in childhood and adulthood (HR = 0.94, 95% CI = 0.89 to 0.99, P = 0.026). There was no association between childhood cognitive test scores and depression when identifying cases of depression using only prescribed drugs data.ConclusionsThis study provides additional evidence suggesting that higher childhood intelligence predicts reduced risk of later-life depression only when depression is assessed based on hospital admission records. Childhood family structure and adulthood socio-economic and geographical factors did not seem to be substantial confounders.
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Project description:AIMS/HYPOTHESIS:The aim of this study was to examine whether cognitive function in early and later life, and decline in cognitive function from age 70 to 79 years, are associated with high blood glucose, as measured by HbA1c, at baseline (age 70), and changes in blood glucose from age 70 to 79. METHODS:Participants (n?=?1091) in the Lothian Birth Cohort of 1936 were examined. Fourteen tests were used to assess cognitive functions, grouped into four domains: visuospatial ability, processing speed, memory and crystallised ability. Test results, and measurements of HbA1c and other health variables, were collected at each of four waves of assessment: at the mean age of 70, 73, 76 and 79 years. Data on cognitive function at age 11 was also available for this cohort. Latent growth curve modelling was performed and statistical controls for known risk factors were introduced. RESULTS:Higher age 11 cognitive function predicted lower HbA1c level at age 70 (p?<?0.001). Higher cognitive function at age 70 was related to a comparatively smaller increase in HbA1c levels from age 70 to 79 (p?<?0.001). HbA1c from age 70 to 79 did not have any consistent association with change in cognitive function from age 70 to 79. These associations survived adjustments for age, sex, education, APOE*?4, smoking history, cardiovascular disease history, hypertension history, BMI and corrections for multiple testing. CONCLUSIONS/INTERPRETATION:Our results show that, among older individuals, high blood glucose is consistently predicted by lower cognitive function. Clinical care that examines and tracks cognitive function, while also taking the positive effects of maintaining cognitive function and emulating healthy behaviours associated with higher cognitive function into account, may be one approach for protecting at-risk individuals from elevated blood glucose and subsequent type 2 diabetes mellitus.
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Project description:Media sclerosis (MS) and peripheral artery disease (PAD) may coincide, particularly in type 2 diabetics (T2D) and in patients with chronic kidney disease (CKD). In contrast to non-diabetics, in T2D PAD is more severe and more distal. Although MS is suspected to play a role, the underlying pathophysiological reasons for the differences still remain elusive today. We tested the hypothesis that MS is a promoter of atherosclerosis as it occurs in T2D with PAD by interfering with arterial remodeling using an in-silico simulation. We confirmed that MS aggravates PAD by promoting negative remodeling. We found that the effect is more pronounced in smaller distal arteries compared to larger proximal ones. Our results suggest that the degree of this divergence depends on the ratio between the thickness of the intima relative to the thickness of the media/adventitia of the individually affected arteries.
| S-EPMC6203409 | biostudies-literature
Project description:To determine the extent of thickening of the carotid arterial walls that may be accommodated by outward remodeling.Institutional review board approval was obtained at each participating site, and informed consent was obtained from each participant. All study sites conducted this study in compliance with HIPAA requirements. A total of 2066 participants (age range, 60-85 years) from the Atherosclerosis Risk in Communities (ARIC) study were enrolled in the ARIC Carotid MRI Study. Maximum wall thickness and luminal area were measured with gadolinium-enhanced magnetic resonance (MR) imaging in both common carotid arteries (CCAs) and in one internal carotid artery (ICA) 2 mm above the flow divider. Complete data were available for 1064 ICAs and 3348 CCAs. The association of maximum wall thickness with lumen area was evaluated with linear regression, and adjustments were made for participant age, sex, race, height, and height squared.In the ICA, lumen area was relatively constant across patients with a wall thickness of 1.38 mm or less. In patients with a wall thickness of more than 1.38 mm, however, lumen area decreased linearly as wall thickness increased. Wall area represented a median of 61.9% of the area circumscribed by the vessel at a maximum wall thickness of 1.50 mm +/- 0.05 (standard deviation) and 75.4% at a maximum wall thickness of 4.0 mm +/- 0.10. In the CCA, lumen area was preserved across wall thicknesses less than 2.06 mm, representing 99% of vessels.Atherosclerotic thickening in the ICA appears to be accommodated for vessels with a maximum wall thickness of less than 1.5 mm. Beyond this threshold, greater thickness is associated with a smaller lumen. The CCA appears to accommodate a wall thickness of less than 2.0 mm. These estimates indicate that the carotid arteries are able to compensate for a greater degree of thickening than are the coronary arteries.
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